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Gene Information
Gene symbol: CD4
Gene name: CD4 molecule
HGNC ID: 1678
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1279667 | To understand better the role of TNF-beta in the regulation of inflammation and type 1 diabetes, we produced transgenic mice in which the murine TNF-beta gene was regulated by the rat insulin II promoter. |
| 2 | 1279667 | The expression of TNF-beta in the pancreas of transgenic mice resulted in a leukocytic inflammatory infiltrate consisting primarily of B220+ IgM+ B cells and CD4+ and CD8+ T cells. |
| 3 | 1286542 | Both the number of CD-4 and CD-8 positive cells increased significantly (p < 0.05), although no change in the CD-4:CD-8 ratio was observed. |
| 4 | 1303681 | No detectable changes in the relative number of CD4+ and CD8+ T-cell subsets in the spleen were seen and there were no obvious differences in splenocyte proliferation rates. |
| 5 | 1309355 | CD4-/CD8-/TCR gamma, delta + T lymphocytes were observed within the islets. |
| 6 | 1309355 | Incubation of the tissue in 15% interleukin 2 induced the migration and initial expansion of the infiltrating cells (66% CD3+ lymphocytes) for up to 2 wk; most T lymphocytes in this initial isolate were CD4+ (92% CD4+ and 7% CD8+). |
| 7 | 1309355 | Long-term anti-CD3 stimulation of this T-lymphocyte population induced the selective growth of CD8+/TCR alpha,beta + (75%) and CD4-/CD8-/TCR gamma,delta + (all V1 delta +) (17%) T lymphocytes. |
| 8 | 1309355 | CD4-/CD8-/TCR gamma, delta + T lymphocytes were observed within the islets. |
| 9 | 1309355 | Incubation of the tissue in 15% interleukin 2 induced the migration and initial expansion of the infiltrating cells (66% CD3+ lymphocytes) for up to 2 wk; most T lymphocytes in this initial isolate were CD4+ (92% CD4+ and 7% CD8+). |
| 10 | 1309355 | Long-term anti-CD3 stimulation of this T-lymphocyte population induced the selective growth of CD8+/TCR alpha,beta + (75%) and CD4-/CD8-/TCR gamma,delta + (all V1 delta +) (17%) T lymphocytes. |
| 11 | 1309355 | CD4-/CD8-/TCR gamma, delta + T lymphocytes were observed within the islets. |
| 12 | 1309355 | Incubation of the tissue in 15% interleukin 2 induced the migration and initial expansion of the infiltrating cells (66% CD3+ lymphocytes) for up to 2 wk; most T lymphocytes in this initial isolate were CD4+ (92% CD4+ and 7% CD8+). |
| 13 | 1309355 | Long-term anti-CD3 stimulation of this T-lymphocyte population induced the selective growth of CD8+/TCR alpha,beta + (75%) and CD4-/CD8-/TCR gamma,delta + (all V1 delta +) (17%) T lymphocytes. |
| 14 | 1346466 | Within T lymphocyte subpopulations, both CD4+ and CD8+ T cells were affected. |
| 15 | 1355504 | The data show that all NOD mice, irrespective of age, sex, and disease progression, possess islet cell-specific CD4+, MHC class II-restricted T cells. |
| 16 | 1359788 | In DP rats, all anti-CD2 MAb except OX53 depleted CD4+ T cells, without depleting natural killer cells or CD8+ T cells. |
| 17 | 1359788 | OX34 injected DR rats were profoundly depleted of CD4+ T cells without evidence of decreased CD8+ T cells, but were not protected against the induction of diabetes by RT6.1+ T-cell depletion and Poly I:C injections. |
| 18 | 1359788 | We conclude that anti-CD2 MAbs protect against BB/Wor autoimmune diabetes by depleting CD4+ T cells, preventing the activation of effector cells, or by blocking CD2/ligand interaction between effector and target cells. |
| 19 | 1359788 | In DP rats, all anti-CD2 MAb except OX53 depleted CD4+ T cells, without depleting natural killer cells or CD8+ T cells. |
| 20 | 1359788 | OX34 injected DR rats were profoundly depleted of CD4+ T cells without evidence of decreased CD8+ T cells, but were not protected against the induction of diabetes by RT6.1+ T-cell depletion and Poly I:C injections. |
| 21 | 1359788 | We conclude that anti-CD2 MAbs protect against BB/Wor autoimmune diabetes by depleting CD4+ T cells, preventing the activation of effector cells, or by blocking CD2/ligand interaction between effector and target cells. |
| 22 | 1359788 | In DP rats, all anti-CD2 MAb except OX53 depleted CD4+ T cells, without depleting natural killer cells or CD8+ T cells. |
| 23 | 1359788 | OX34 injected DR rats were profoundly depleted of CD4+ T cells without evidence of decreased CD8+ T cells, but were not protected against the induction of diabetes by RT6.1+ T-cell depletion and Poly I:C injections. |
| 24 | 1359788 | We conclude that anti-CD2 MAbs protect against BB/Wor autoimmune diabetes by depleting CD4+ T cells, preventing the activation of effector cells, or by blocking CD2/ligand interaction between effector and target cells. |
| 25 | 1385796 | They had a similar distribution into CD4 and CD8 subsets as uninjected controls, and a similar usage and cell surface expression of four T-cell receptor V beta families. |
| 26 | 1388634 | T cell activation is dependent upon calcium influx and protein kinase C activation, with subsequent lymphocyte proliferation dependent upon IL-2. |
| 27 | 1388634 | Analysis of chicken CD3, CD4 and CD8 expression revealed a 39% decrease in peripheral blood CD4+ cells in scleroderma birds, although this decrease was not sufficient to explain the 80-90% decrease observed in proliferation assays and calcium influx. |
| 28 | 1446803 | In this generation of animals, 24% were lymphopenic with decreased numbers of PBL expressing CD5, TCR alpha, and RT6. |
| 29 | 1446803 | Moreover, IEL of the lymphopenic animals exhibited a pattern of staining (increased numbers of TCR alpha beta+CD4+CD8+ and decreased numbers of TCR alpha beta+CD4-CD8+) similar to that of BB DP animals. |
| 30 | 1446802 | CD8 T cells are not required for islet destruction induced by a CD4+ islet-specific T-cell clone. |
| 31 | 1451948 | In order to investigate the role of infiltrating lymphocytes for this altered metabolism, we injected 12- to 13-week-old female NOD mice with monoclonal antibodies directed against either the alpha beta-T cell receptor, CD4+ or CD8+ T cells. |
| 32 | 1451948 | Culture of islets obtained from NOD mice in the presence of the cytokine interleukin-1 beta induced a similar pattern of glucose metabolism as seen earlier in IgG or phosphate-buffered saline treated control NOD mice. |
| 33 | 1485949 | Insulin-dependent diabetes mellitus (IDDM), or type I diabetes, is the end result mainly of a T-cell mediated autoimmune destruction of pancreatic islet beta cells. |
| 34 | 1485949 | The DQ molecules involved in IDDM susceptibility or protection may exert their function either during thymic development of potential self-reactive CD4+ T cells, or by preferential presentation of certain beta-cell derived peptides to CD4+ T cells, or both. |
| 35 | 1510786 | Treatment with IL-1 alpha also inhibited insulitis and hyperglycemia induced by adoptive transfer of pathogenic, polyclonal CD4+8- T cells. |
| 36 | 1510786 | Even after islet-cell destruction, IL-1 alpha injections in diabetic NOD mice normalized plasma glucose levels when administered in combination with insulin, whereas equivalent levels of IL-1 alpha alone did not. |
| 37 | 1510786 | Thus, IL-1 treatment could clinically be an effective immunotherapeutic modality for autoimmune diabetes mellitus by suppressing early disease progression or normalize plasma glucose levels when insulin is present. |
| 38 | 1516628 | Analysis of the roles of CD4+ and CD8+ T cells in autoimmune diabetes of NOD mice using transfer to NOD athymic nude mice. |
| 39 | 1516628 | For the precise analysis of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, these subsets must be transferred into recipients that are completely free of T cells and pathological changes. |
| 40 | 1516628 | To the nude recipients we transferred either one of a highly purified CD4+ or CD8+ T cell subset derived from non-diabetic female NOD mice; any in vivo increase in the contaminating T cell subsets was prevented by injecting the antibody homologous to it. |
| 41 | 1516628 | However, the subsequent transfer of CD8+ T cells into CD4+ T cell-reconstituted recipients induced severe insulitis and hyperglycemia in almost all the recipients. |
| 42 | 1516628 | In these diabetic recipients, we observed severe damage of the pancreatic islets and the infiltration of a large number of CD8+ T cells into the remaining islets; insulin-secreting beta cells were no longer detected. |
| 43 | 1516628 | These results suggest that CD4+ T cells play a predominant role in the development of insulitis and that CD8+ T cells migrate into the islets and are subsequently, with the aid of CD4+ T cells, differentiated into killer cells which act against beta cells. |
| 44 | 1516628 | Analysis of the roles of CD4+ and CD8+ T cells in autoimmune diabetes of NOD mice using transfer to NOD athymic nude mice. |
| 45 | 1516628 | For the precise analysis of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, these subsets must be transferred into recipients that are completely free of T cells and pathological changes. |
| 46 | 1516628 | To the nude recipients we transferred either one of a highly purified CD4+ or CD8+ T cell subset derived from non-diabetic female NOD mice; any in vivo increase in the contaminating T cell subsets was prevented by injecting the antibody homologous to it. |
| 47 | 1516628 | However, the subsequent transfer of CD8+ T cells into CD4+ T cell-reconstituted recipients induced severe insulitis and hyperglycemia in almost all the recipients. |
| 48 | 1516628 | In these diabetic recipients, we observed severe damage of the pancreatic islets and the infiltration of a large number of CD8+ T cells into the remaining islets; insulin-secreting beta cells were no longer detected. |
| 49 | 1516628 | These results suggest that CD4+ T cells play a predominant role in the development of insulitis and that CD8+ T cells migrate into the islets and are subsequently, with the aid of CD4+ T cells, differentiated into killer cells which act against beta cells. |
| 50 | 1516628 | Analysis of the roles of CD4+ and CD8+ T cells in autoimmune diabetes of NOD mice using transfer to NOD athymic nude mice. |
| 51 | 1516628 | For the precise analysis of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, these subsets must be transferred into recipients that are completely free of T cells and pathological changes. |
| 52 | 1516628 | To the nude recipients we transferred either one of a highly purified CD4+ or CD8+ T cell subset derived from non-diabetic female NOD mice; any in vivo increase in the contaminating T cell subsets was prevented by injecting the antibody homologous to it. |
| 53 | 1516628 | However, the subsequent transfer of CD8+ T cells into CD4+ T cell-reconstituted recipients induced severe insulitis and hyperglycemia in almost all the recipients. |
| 54 | 1516628 | In these diabetic recipients, we observed severe damage of the pancreatic islets and the infiltration of a large number of CD8+ T cells into the remaining islets; insulin-secreting beta cells were no longer detected. |
| 55 | 1516628 | These results suggest that CD4+ T cells play a predominant role in the development of insulitis and that CD8+ T cells migrate into the islets and are subsequently, with the aid of CD4+ T cells, differentiated into killer cells which act against beta cells. |
| 56 | 1516628 | Analysis of the roles of CD4+ and CD8+ T cells in autoimmune diabetes of NOD mice using transfer to NOD athymic nude mice. |
| 57 | 1516628 | For the precise analysis of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, these subsets must be transferred into recipients that are completely free of T cells and pathological changes. |
| 58 | 1516628 | To the nude recipients we transferred either one of a highly purified CD4+ or CD8+ T cell subset derived from non-diabetic female NOD mice; any in vivo increase in the contaminating T cell subsets was prevented by injecting the antibody homologous to it. |
| 59 | 1516628 | However, the subsequent transfer of CD8+ T cells into CD4+ T cell-reconstituted recipients induced severe insulitis and hyperglycemia in almost all the recipients. |
| 60 | 1516628 | In these diabetic recipients, we observed severe damage of the pancreatic islets and the infiltration of a large number of CD8+ T cells into the remaining islets; insulin-secreting beta cells were no longer detected. |
| 61 | 1516628 | These results suggest that CD4+ T cells play a predominant role in the development of insulitis and that CD8+ T cells migrate into the islets and are subsequently, with the aid of CD4+ T cells, differentiated into killer cells which act against beta cells. |
| 62 | 1516628 | Analysis of the roles of CD4+ and CD8+ T cells in autoimmune diabetes of NOD mice using transfer to NOD athymic nude mice. |
| 63 | 1516628 | For the precise analysis of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, these subsets must be transferred into recipients that are completely free of T cells and pathological changes. |
| 64 | 1516628 | To the nude recipients we transferred either one of a highly purified CD4+ or CD8+ T cell subset derived from non-diabetic female NOD mice; any in vivo increase in the contaminating T cell subsets was prevented by injecting the antibody homologous to it. |
| 65 | 1516628 | However, the subsequent transfer of CD8+ T cells into CD4+ T cell-reconstituted recipients induced severe insulitis and hyperglycemia in almost all the recipients. |
| 66 | 1516628 | In these diabetic recipients, we observed severe damage of the pancreatic islets and the infiltration of a large number of CD8+ T cells into the remaining islets; insulin-secreting beta cells were no longer detected. |
| 67 | 1516628 | These results suggest that CD4+ T cells play a predominant role in the development of insulitis and that CD8+ T cells migrate into the islets and are subsequently, with the aid of CD4+ T cells, differentiated into killer cells which act against beta cells. |
| 68 | 1533543 | This reduction was predominantly in the CD4 subset, giving rise to a decreased CD4/CD8 lymphocyte ratio. |
| 69 | 1533543 | Those with ICA titres between 5 and 20 JDF units showed abnormalities in both CD3 and CD4 lymphocytes, but not in CD4/CD8 lymphocyte ratio. |
| 70 | 1533543 | The longitudinal study demonstrated that individuals potentially susceptible to the development of type 1 diabetes and who possess high titres of ICA have impairment of CD4/CD8 lymphocyte ratio, mainly due to a reduction in the CD4 subset. |
| 71 | 1533543 | This reduction was predominantly in the CD4 subset, giving rise to a decreased CD4/CD8 lymphocyte ratio. |
| 72 | 1533543 | Those with ICA titres between 5 and 20 JDF units showed abnormalities in both CD3 and CD4 lymphocytes, but not in CD4/CD8 lymphocyte ratio. |
| 73 | 1533543 | The longitudinal study demonstrated that individuals potentially susceptible to the development of type 1 diabetes and who possess high titres of ICA have impairment of CD4/CD8 lymphocyte ratio, mainly due to a reduction in the CD4 subset. |
| 74 | 1533543 | This reduction was predominantly in the CD4 subset, giving rise to a decreased CD4/CD8 lymphocyte ratio. |
| 75 | 1533543 | Those with ICA titres between 5 and 20 JDF units showed abnormalities in both CD3 and CD4 lymphocytes, but not in CD4/CD8 lymphocyte ratio. |
| 76 | 1533543 | The longitudinal study demonstrated that individuals potentially susceptible to the development of type 1 diabetes and who possess high titres of ICA have impairment of CD4/CD8 lymphocyte ratio, mainly due to a reduction in the CD4 subset. |
| 77 | 1539270 | Role of CD4+ and CD8+ T cells in proislet allograft and xenograft rejection. |
| 78 | 1576920 | Both CD4 and CD8 positive cells were in the vicinity of the graft tissue. |
| 79 | 1600853 | The following monoclonal antibodies were used: CD4, CD8, CD57, CD25, HLA-DR. |
| 80 | 1600853 | Interestingly, the patients who exhibited remission presented a statistically higher percentage of positive cells for CD57, HLA-DR and CD25 surface antigens, significantly lower C4 levels and CD4/CD8 ratio and significantly higher IgG levels compared with patients who did not show any remission. |
| 81 | 1600853 | The following monoclonal antibodies were used: CD4, CD8, CD57, CD25, HLA-DR. |
| 82 | 1600853 | Interestingly, the patients who exhibited remission presented a statistically higher percentage of positive cells for CD57, HLA-DR and CD25 surface antigens, significantly lower C4 levels and CD4/CD8 ratio and significantly higher IgG levels compared with patients who did not show any remission. |
| 83 | 1606724 | As measured by flow cytometry, all THI-treated mice had a 60-80% reduction in splenic CD4+ and CD8+ T cells. |
| 84 | 1617115 | Cytofluorometric analysis using specific monoclonal antibodies directed against the T cell antigens Thy-1.2, CD4, CD8, CD4V beta(8.1 + 8.2 + 8.3), and the antigen Mac-1 expressed by mature macrophages and NK cells were used to characterize and quantify the phenotypes of (1) unfractionated and Percoll gradient fractionated in situ islet immune cells isolated from prediabetic and diabetic female NOD mouse spleens. |
| 85 | 1617115 | The percentage of CD8 positive T cells were approximately 10%, and only approximately 4% of the immune cells were Mac-1 positive. |
| 86 | 1617115 | It is concluded that prediabetic NOD mouse in situ islet immune cells are mostly CD4 positive and double negative T cells, and that CD4 and CD8 positive T cells in the intra-islet infiltrate warrants further evaluation as potential effector T cells in target beta-cell destruction. |
| 87 | 1617115 | Cytofluorometric analysis using specific monoclonal antibodies directed against the T cell antigens Thy-1.2, CD4, CD8, CD4V beta(8.1 + 8.2 + 8.3), and the antigen Mac-1 expressed by mature macrophages and NK cells were used to characterize and quantify the phenotypes of (1) unfractionated and Percoll gradient fractionated in situ islet immune cells isolated from prediabetic and diabetic female NOD mouse spleens. |
| 88 | 1617115 | The percentage of CD8 positive T cells were approximately 10%, and only approximately 4% of the immune cells were Mac-1 positive. |
| 89 | 1617115 | It is concluded that prediabetic NOD mouse in situ islet immune cells are mostly CD4 positive and double negative T cells, and that CD4 and CD8 positive T cells in the intra-islet infiltrate warrants further evaluation as potential effector T cells in target beta-cell destruction. |
| 90 | 1623929 | We here show that it is possible to re-establish self tolerance in an animal model of insulin-dependent diabetes mellitus without prior deletion of CD4+ T cells using a short course of therapy with a non-lytic monoclonal antibody to the CD4 adhesion receptor on T cells. |
| 91 | 1628775 | Distinct difference in beta-cell destruction between CD4+ and CD8+ T-cell clones derived from lymphocytes infiltrating the islets of NOD mice. |
| 92 | 1628775 | Six CD4+ and three CD8+ islet-reactive T-cell clones were established from lymphocytes infiltrating the pancreatic islets of NOD mice. |
| 93 | 1628775 | CD8+ CTLs could not be isolated from islets of NOD mice less than 10 wk of age, even if the islets showed lymphocytic infiltration, whereas CD4+ T-cells could be isolated from islets of these younger NOD mice. |
| 94 | 1628775 | On the basis of these observations, we concluded that CD4+ and CD8+ T-cells interact differently with beta-cells at different stages in T-cell--mediated beta-cell destruction. |
| 95 | 1628775 | CD4+ T-cells may secrete cytokines, which in turn activate effector cell populations, whereas CD8+ T-cells may act as a final effector directly involved in beta-cell destruction. |
| 96 | 1628775 | Distinct difference in beta-cell destruction between CD4+ and CD8+ T-cell clones derived from lymphocytes infiltrating the islets of NOD mice. |
| 97 | 1628775 | Six CD4+ and three CD8+ islet-reactive T-cell clones were established from lymphocytes infiltrating the pancreatic islets of NOD mice. |
| 98 | 1628775 | CD8+ CTLs could not be isolated from islets of NOD mice less than 10 wk of age, even if the islets showed lymphocytic infiltration, whereas CD4+ T-cells could be isolated from islets of these younger NOD mice. |
| 99 | 1628775 | On the basis of these observations, we concluded that CD4+ and CD8+ T-cells interact differently with beta-cells at different stages in T-cell--mediated beta-cell destruction. |
| 100 | 1628775 | CD4+ T-cells may secrete cytokines, which in turn activate effector cell populations, whereas CD8+ T-cells may act as a final effector directly involved in beta-cell destruction. |
| 101 | 1628775 | Distinct difference in beta-cell destruction between CD4+ and CD8+ T-cell clones derived from lymphocytes infiltrating the islets of NOD mice. |
| 102 | 1628775 | Six CD4+ and three CD8+ islet-reactive T-cell clones were established from lymphocytes infiltrating the pancreatic islets of NOD mice. |
| 103 | 1628775 | CD8+ CTLs could not be isolated from islets of NOD mice less than 10 wk of age, even if the islets showed lymphocytic infiltration, whereas CD4+ T-cells could be isolated from islets of these younger NOD mice. |
| 104 | 1628775 | On the basis of these observations, we concluded that CD4+ and CD8+ T-cells interact differently with beta-cells at different stages in T-cell--mediated beta-cell destruction. |
| 105 | 1628775 | CD4+ T-cells may secrete cytokines, which in turn activate effector cell populations, whereas CD8+ T-cells may act as a final effector directly involved in beta-cell destruction. |
| 106 | 1628775 | Distinct difference in beta-cell destruction between CD4+ and CD8+ T-cell clones derived from lymphocytes infiltrating the islets of NOD mice. |
| 107 | 1628775 | Six CD4+ and three CD8+ islet-reactive T-cell clones were established from lymphocytes infiltrating the pancreatic islets of NOD mice. |
| 108 | 1628775 | CD8+ CTLs could not be isolated from islets of NOD mice less than 10 wk of age, even if the islets showed lymphocytic infiltration, whereas CD4+ T-cells could be isolated from islets of these younger NOD mice. |
| 109 | 1628775 | On the basis of these observations, we concluded that CD4+ and CD8+ T-cells interact differently with beta-cells at different stages in T-cell--mediated beta-cell destruction. |
| 110 | 1628775 | CD4+ T-cells may secrete cytokines, which in turn activate effector cell populations, whereas CD8+ T-cells may act as a final effector directly involved in beta-cell destruction. |
| 111 | 1628775 | Distinct difference in beta-cell destruction between CD4+ and CD8+ T-cell clones derived from lymphocytes infiltrating the islets of NOD mice. |
| 112 | 1628775 | Six CD4+ and three CD8+ islet-reactive T-cell clones were established from lymphocytes infiltrating the pancreatic islets of NOD mice. |
| 113 | 1628775 | CD8+ CTLs could not be isolated from islets of NOD mice less than 10 wk of age, even if the islets showed lymphocytic infiltration, whereas CD4+ T-cells could be isolated from islets of these younger NOD mice. |
| 114 | 1628775 | On the basis of these observations, we concluded that CD4+ and CD8+ T-cells interact differently with beta-cells at different stages in T-cell--mediated beta-cell destruction. |
| 115 | 1628775 | CD4+ T-cells may secrete cytokines, which in turn activate effector cell populations, whereas CD8+ T-cells may act as a final effector directly involved in beta-cell destruction. |
| 116 | 1670607 | CD8+ T cell homing to the pancreas in the nonobese diabetic mouse is CD4+ T cell-dependent. |
| 117 | 1670607 | The adoptive transfer of type I diabetes in nonobese diabetic mice requires the contribution of both CD4+ and CD8+ T cells. |
| 118 | 1670607 | None of the animals injected with either CD4+ or CD8+ T cells became overtly diabetic during the 30 days of observation whereas 8 of 23 mice inoculated with a mixture of the two subsets developed glycosuria and hyperglycemia. |
| 119 | 1670607 | However, insulitis was found in 6 of the 13 mice injected with CD4+ T cells whereas only 1 of the 9 mice injected with CD8+ T cells showed marginal infiltration of the pancreas. |
| 120 | 1670607 | CD4+ T cells, which have the capacity to home to the pancreas, promote in turn the influx of CD8+ effector T cells that do not by themselves accumulate in this organ. |
| 121 | 1670607 | CD8+ T cell homing to the pancreas in the nonobese diabetic mouse is CD4+ T cell-dependent. |
| 122 | 1670607 | The adoptive transfer of type I diabetes in nonobese diabetic mice requires the contribution of both CD4+ and CD8+ T cells. |
| 123 | 1670607 | None of the animals injected with either CD4+ or CD8+ T cells became overtly diabetic during the 30 days of observation whereas 8 of 23 mice inoculated with a mixture of the two subsets developed glycosuria and hyperglycemia. |
| 124 | 1670607 | However, insulitis was found in 6 of the 13 mice injected with CD4+ T cells whereas only 1 of the 9 mice injected with CD8+ T cells showed marginal infiltration of the pancreas. |
| 125 | 1670607 | CD4+ T cells, which have the capacity to home to the pancreas, promote in turn the influx of CD8+ effector T cells that do not by themselves accumulate in this organ. |
| 126 | 1670607 | CD8+ T cell homing to the pancreas in the nonobese diabetic mouse is CD4+ T cell-dependent. |
| 127 | 1670607 | The adoptive transfer of type I diabetes in nonobese diabetic mice requires the contribution of both CD4+ and CD8+ T cells. |
| 128 | 1670607 | None of the animals injected with either CD4+ or CD8+ T cells became overtly diabetic during the 30 days of observation whereas 8 of 23 mice inoculated with a mixture of the two subsets developed glycosuria and hyperglycemia. |
| 129 | 1670607 | However, insulitis was found in 6 of the 13 mice injected with CD4+ T cells whereas only 1 of the 9 mice injected with CD8+ T cells showed marginal infiltration of the pancreas. |
| 130 | 1670607 | CD4+ T cells, which have the capacity to home to the pancreas, promote in turn the influx of CD8+ effector T cells that do not by themselves accumulate in this organ. |
| 131 | 1670607 | CD8+ T cell homing to the pancreas in the nonobese diabetic mouse is CD4+ T cell-dependent. |
| 132 | 1670607 | The adoptive transfer of type I diabetes in nonobese diabetic mice requires the contribution of both CD4+ and CD8+ T cells. |
| 133 | 1670607 | None of the animals injected with either CD4+ or CD8+ T cells became overtly diabetic during the 30 days of observation whereas 8 of 23 mice inoculated with a mixture of the two subsets developed glycosuria and hyperglycemia. |
| 134 | 1670607 | However, insulitis was found in 6 of the 13 mice injected with CD4+ T cells whereas only 1 of the 9 mice injected with CD8+ T cells showed marginal infiltration of the pancreas. |
| 135 | 1670607 | CD4+ T cells, which have the capacity to home to the pancreas, promote in turn the influx of CD8+ effector T cells that do not by themselves accumulate in this organ. |
| 136 | 1670607 | CD8+ T cell homing to the pancreas in the nonobese diabetic mouse is CD4+ T cell-dependent. |
| 137 | 1670607 | The adoptive transfer of type I diabetes in nonobese diabetic mice requires the contribution of both CD4+ and CD8+ T cells. |
| 138 | 1670607 | None of the animals injected with either CD4+ or CD8+ T cells became overtly diabetic during the 30 days of observation whereas 8 of 23 mice inoculated with a mixture of the two subsets developed glycosuria and hyperglycemia. |
| 139 | 1670607 | However, insulitis was found in 6 of the 13 mice injected with CD4+ T cells whereas only 1 of the 9 mice injected with CD8+ T cells showed marginal infiltration of the pancreas. |
| 140 | 1670607 | CD4+ T cells, which have the capacity to home to the pancreas, promote in turn the influx of CD8+ effector T cells that do not by themselves accumulate in this organ. |
| 141 | 1675318 | A possible target antigen was suggested by the proliferation of CD4 T cells from a newly diagnosed patient in response to a 38 kD polypeptide of the insulin-secretory-granule membrane. |
| 142 | 1677834 | Abnormalities within CD4 and CD8 T lymphocytes subsets in type 1 (insulin-dependent) diabetes. |
| 143 | 1677834 | Monoclonal antibodies labelled with various fluorochromes were used here to define the percentages of subsets, and especially to divide CD4+ (helper/inducer) and CD8+ (suppressor/cytotoxic) cells into phenotypic subgroups. |
| 144 | 1677834 | Blood samples were analysed from 25 patients (age 10.1 +/- 3.7 years) with recently diagnosed insulin-dependent diabetes mellitus (IDDM) and 25 age- and sex-matched control subjects. |
| 145 | 1677834 | The percentages of CD4+ cells and CD4+CD45RA+ cells described as naive T helper cells or suppressor/inducers were increased in the IDDM patients (P less than 0.05 and P less than 0.05. |
| 146 | 1677834 | The percentage of CD8+CD11b+ cells containing suppressor/effector lymphocytes was decreased in the IDDM patients as compared with the controls (P less than 0.01) but no significant difference was seen in total CD8+ cells. |
| 147 | 1677834 | Abnormalities within CD4 and CD8 T lymphocytes subsets in type 1 (insulin-dependent) diabetes. |
| 148 | 1677834 | Monoclonal antibodies labelled with various fluorochromes were used here to define the percentages of subsets, and especially to divide CD4+ (helper/inducer) and CD8+ (suppressor/cytotoxic) cells into phenotypic subgroups. |
| 149 | 1677834 | Blood samples were analysed from 25 patients (age 10.1 +/- 3.7 years) with recently diagnosed insulin-dependent diabetes mellitus (IDDM) and 25 age- and sex-matched control subjects. |
| 150 | 1677834 | The percentages of CD4+ cells and CD4+CD45RA+ cells described as naive T helper cells or suppressor/inducers were increased in the IDDM patients (P less than 0.05 and P less than 0.05. |
| 151 | 1677834 | The percentage of CD8+CD11b+ cells containing suppressor/effector lymphocytes was decreased in the IDDM patients as compared with the controls (P less than 0.01) but no significant difference was seen in total CD8+ cells. |
| 152 | 1677834 | Abnormalities within CD4 and CD8 T lymphocytes subsets in type 1 (insulin-dependent) diabetes. |
| 153 | 1677834 | Monoclonal antibodies labelled with various fluorochromes were used here to define the percentages of subsets, and especially to divide CD4+ (helper/inducer) and CD8+ (suppressor/cytotoxic) cells into phenotypic subgroups. |
| 154 | 1677834 | Blood samples were analysed from 25 patients (age 10.1 +/- 3.7 years) with recently diagnosed insulin-dependent diabetes mellitus (IDDM) and 25 age- and sex-matched control subjects. |
| 155 | 1677834 | The percentages of CD4+ cells and CD4+CD45RA+ cells described as naive T helper cells or suppressor/inducers were increased in the IDDM patients (P less than 0.05 and P less than 0.05. |
| 156 | 1677834 | The percentage of CD8+CD11b+ cells containing suppressor/effector lymphocytes was decreased in the IDDM patients as compared with the controls (P less than 0.01) but no significant difference was seen in total CD8+ cells. |
| 157 | 1679332 | Pancreatic T lymphocytes from NOD-Wehi mice, which have an incidence of spontaneous diabetes of less than 5%, had a CD4:CD8 ratio of 1.25 +/- 0.23 compared with 2.44 +/- 0.31 for peripheral blood lymphocytes. |
| 158 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 159 | 1679332 | T lymphocytes bearing IL-2 receptors increased two- to three-fold in number and their secretion of GM-CSF/IL-3 and IFN-gamma increased to a maximum on day 7. |
| 160 | 1679332 | Pancreatic insulin content and mRNA levels declined sharply between days 10 and 12, at which time the majority of pancreatic T lymphocytes in hyperglycaemic mice were CD8+ (CD4:CD8 ratio 0.63 +/- 0.04 compared to 4.14 +/- 1.05 in peripheral blood). |
| 161 | 1679332 | The pancreatic T lymphocyte CD4:CD8 ratio in prediabetic NOD-Lt mice, which have an incidence of spontaneous diabetes of about 60% at 150 days, was similar to that in untreated NOD-Wehi mice, but 25% of their pancreatic CD8 T lymphocytes were IL-2-receptor positive. |
| 162 | 1679332 | The earliest change after cyclophosphamide was an increase in activated, predominantly CD4+ T lymphocytes; with the development of beta cell destruction and hyperglycaemia, pancreatic T lymphocytes were, as in human IDDM, predominantly CD8+. |
| 163 | 1679332 | Pancreatic T lymphocytes from NOD-Wehi mice, which have an incidence of spontaneous diabetes of less than 5%, had a CD4:CD8 ratio of 1.25 +/- 0.23 compared with 2.44 +/- 0.31 for peripheral blood lymphocytes. |
| 164 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 165 | 1679332 | T lymphocytes bearing IL-2 receptors increased two- to three-fold in number and their secretion of GM-CSF/IL-3 and IFN-gamma increased to a maximum on day 7. |
| 166 | 1679332 | Pancreatic insulin content and mRNA levels declined sharply between days 10 and 12, at which time the majority of pancreatic T lymphocytes in hyperglycaemic mice were CD8+ (CD4:CD8 ratio 0.63 +/- 0.04 compared to 4.14 +/- 1.05 in peripheral blood). |
| 167 | 1679332 | The pancreatic T lymphocyte CD4:CD8 ratio in prediabetic NOD-Lt mice, which have an incidence of spontaneous diabetes of about 60% at 150 days, was similar to that in untreated NOD-Wehi mice, but 25% of their pancreatic CD8 T lymphocytes were IL-2-receptor positive. |
| 168 | 1679332 | The earliest change after cyclophosphamide was an increase in activated, predominantly CD4+ T lymphocytes; with the development of beta cell destruction and hyperglycaemia, pancreatic T lymphocytes were, as in human IDDM, predominantly CD8+. |
| 169 | 1679332 | Pancreatic T lymphocytes from NOD-Wehi mice, which have an incidence of spontaneous diabetes of less than 5%, had a CD4:CD8 ratio of 1.25 +/- 0.23 compared with 2.44 +/- 0.31 for peripheral blood lymphocytes. |
| 170 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 171 | 1679332 | T lymphocytes bearing IL-2 receptors increased two- to three-fold in number and their secretion of GM-CSF/IL-3 and IFN-gamma increased to a maximum on day 7. |
| 172 | 1679332 | Pancreatic insulin content and mRNA levels declined sharply between days 10 and 12, at which time the majority of pancreatic T lymphocytes in hyperglycaemic mice were CD8+ (CD4:CD8 ratio 0.63 +/- 0.04 compared to 4.14 +/- 1.05 in peripheral blood). |
| 173 | 1679332 | The pancreatic T lymphocyte CD4:CD8 ratio in prediabetic NOD-Lt mice, which have an incidence of spontaneous diabetes of about 60% at 150 days, was similar to that in untreated NOD-Wehi mice, but 25% of their pancreatic CD8 T lymphocytes were IL-2-receptor positive. |
| 174 | 1679332 | The earliest change after cyclophosphamide was an increase in activated, predominantly CD4+ T lymphocytes; with the development of beta cell destruction and hyperglycaemia, pancreatic T lymphocytes were, as in human IDDM, predominantly CD8+. |
| 175 | 1679332 | Pancreatic T lymphocytes from NOD-Wehi mice, which have an incidence of spontaneous diabetes of less than 5%, had a CD4:CD8 ratio of 1.25 +/- 0.23 compared with 2.44 +/- 0.31 for peripheral blood lymphocytes. |
| 176 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 177 | 1679332 | T lymphocytes bearing IL-2 receptors increased two- to three-fold in number and their secretion of GM-CSF/IL-3 and IFN-gamma increased to a maximum on day 7. |
| 178 | 1679332 | Pancreatic insulin content and mRNA levels declined sharply between days 10 and 12, at which time the majority of pancreatic T lymphocytes in hyperglycaemic mice were CD8+ (CD4:CD8 ratio 0.63 +/- 0.04 compared to 4.14 +/- 1.05 in peripheral blood). |
| 179 | 1679332 | The pancreatic T lymphocyte CD4:CD8 ratio in prediabetic NOD-Lt mice, which have an incidence of spontaneous diabetes of about 60% at 150 days, was similar to that in untreated NOD-Wehi mice, but 25% of their pancreatic CD8 T lymphocytes were IL-2-receptor positive. |
| 180 | 1679332 | The earliest change after cyclophosphamide was an increase in activated, predominantly CD4+ T lymphocytes; with the development of beta cell destruction and hyperglycaemia, pancreatic T lymphocytes were, as in human IDDM, predominantly CD8+. |
| 181 | 1679332 | Pancreatic T lymphocytes from NOD-Wehi mice, which have an incidence of spontaneous diabetes of less than 5%, had a CD4:CD8 ratio of 1.25 +/- 0.23 compared with 2.44 +/- 0.31 for peripheral blood lymphocytes. |
| 182 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 183 | 1679332 | T lymphocytes bearing IL-2 receptors increased two- to three-fold in number and their secretion of GM-CSF/IL-3 and IFN-gamma increased to a maximum on day 7. |
| 184 | 1679332 | Pancreatic insulin content and mRNA levels declined sharply between days 10 and 12, at which time the majority of pancreatic T lymphocytes in hyperglycaemic mice were CD8+ (CD4:CD8 ratio 0.63 +/- 0.04 compared to 4.14 +/- 1.05 in peripheral blood). |
| 185 | 1679332 | The pancreatic T lymphocyte CD4:CD8 ratio in prediabetic NOD-Lt mice, which have an incidence of spontaneous diabetes of about 60% at 150 days, was similar to that in untreated NOD-Wehi mice, but 25% of their pancreatic CD8 T lymphocytes were IL-2-receptor positive. |
| 186 | 1679332 | The earliest change after cyclophosphamide was an increase in activated, predominantly CD4+ T lymphocytes; with the development of beta cell destruction and hyperglycaemia, pancreatic T lymphocytes were, as in human IDDM, predominantly CD8+. |
| 187 | 1688592 | The levels of expression of CD4, TCR-alpha beta within each thymocyte subset were comparable in BBn and BBd animals as were the anti-TCR-induced proliferative responses of their CD4+8- and CD4-8+ thymocytes. |
| 188 | 1696864 | The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. |
| 189 | 1696864 | Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. |
| 190 | 1696864 | However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. |
| 191 | 1696864 | Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. |
| 192 | 1696864 | In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. |
| 193 | 1696864 | An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. |
| 194 | 1696864 | The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. |
| 195 | 1696864 | Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. |
| 196 | 1696864 | However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. |
| 197 | 1696864 | Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. |
| 198 | 1696864 | In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. |
| 199 | 1696864 | An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. |
| 200 | 1696864 | The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. |
| 201 | 1696864 | Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. |
| 202 | 1696864 | However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. |
| 203 | 1696864 | Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. |
| 204 | 1696864 | In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. |
| 205 | 1696864 | An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. |
| 206 | 1696864 | The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. |
| 207 | 1696864 | Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. |
| 208 | 1696864 | However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. |
| 209 | 1696864 | Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. |
| 210 | 1696864 | In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. |
| 211 | 1696864 | An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. |
| 212 | 1696864 | The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. |
| 213 | 1696864 | Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. |
| 214 | 1696864 | However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. |
| 215 | 1696864 | Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. |
| 216 | 1696864 | In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. |
| 217 | 1696864 | An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. |
| 218 | 1727731 | T-lymphocyte lines specific for glutamic acid decarboxylase (GAD) the 64K beta-cell antigen of IDDM. |
| 219 | 1727731 | Insulin-dependent diabetes mellitus (IDDM) is viewed as a thymus-dependent autoimmune disease, although the specific beta-cell autoantigen or autoantigens remain unknown. |
| 220 | 1727731 | In this study, we describe the isolation of GAD-specific T-lymphocyte lines from BB rats, an animal model of IDDM. |
| 221 | 1727731 | GAD-specific T lymphocytes were obtained by culture with interleukin 2 and repeated stimulation with GAD in the presence of BB rat thymic antigen-presenting cells. |
| 222 | 1727731 | Four stable, CD4+, MHC (RT1u)-restricted T-lymphocyte lines were isolated. |
| 223 | 1727731 | They proliferate selectively in the presence of GAD and secrete interleukin 2 and interferon-gamma. |
| 224 | 1737783 | Human CD4, a monomeric T cell surface glycoprotein, is required for T helper cell activation and is also the receptor for the human immunodeficiency virus. |
| 225 | 1823558 | Flowcytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from the spleens of anti-asialo GM1 antibody-injected mice but no suppression of CD8+ and CD4+ cells could be demonstrated. |
| 226 | 1826279 | We demonstrate here that an altered (with respect to control BALB/cJ mice) thymic T-lymphocyte maturation reflected by a depletion (approximately 12%) of CD4+CD8+ T lymphocytes and a reciprocal increase in CD4-CD8- T lymphocytes precedes the onset of diabetes. |
| 227 | 1826279 | By onset of diabetes, an even greater decrease (approximately 35%) of CD4+CD8+ and a reciprocal increase of CD4-CD8- T lymphocytes were apparent and accompanied by the same depletion (3%) of V beta 8 lo T lymphocytes. |
| 228 | 1826279 | Administration of cyclophosphamide (CY), which accelerates the appearance of diabetes in NOD mice, caused similar depletions of CD4+CD8+ and V beta 8lo thymic T lymphocytes. |
| 229 | 1826279 | We demonstrate here that an altered (with respect to control BALB/cJ mice) thymic T-lymphocyte maturation reflected by a depletion (approximately 12%) of CD4+CD8+ T lymphocytes and a reciprocal increase in CD4-CD8- T lymphocytes precedes the onset of diabetes. |
| 230 | 1826279 | By onset of diabetes, an even greater decrease (approximately 35%) of CD4+CD8+ and a reciprocal increase of CD4-CD8- T lymphocytes were apparent and accompanied by the same depletion (3%) of V beta 8 lo T lymphocytes. |
| 231 | 1826279 | Administration of cyclophosphamide (CY), which accelerates the appearance of diabetes in NOD mice, caused similar depletions of CD4+CD8+ and V beta 8lo thymic T lymphocytes. |
| 232 | 1826279 | We demonstrate here that an altered (with respect to control BALB/cJ mice) thymic T-lymphocyte maturation reflected by a depletion (approximately 12%) of CD4+CD8+ T lymphocytes and a reciprocal increase in CD4-CD8- T lymphocytes precedes the onset of diabetes. |
| 233 | 1826279 | By onset of diabetes, an even greater decrease (approximately 35%) of CD4+CD8+ and a reciprocal increase of CD4-CD8- T lymphocytes were apparent and accompanied by the same depletion (3%) of V beta 8 lo T lymphocytes. |
| 234 | 1826279 | Administration of cyclophosphamide (CY), which accelerates the appearance of diabetes in NOD mice, caused similar depletions of CD4+CD8+ and V beta 8lo thymic T lymphocytes. |
| 235 | 1826646 | Depletion of CD8+ T lymphocytes from the PBMC of healthy subjects abolished their suppressive capacity, while depletion of CD4+ T lymphocytes and pre-incubation with CD3 monoclonal antibodies had no effect. |
| 236 | 1827712 | To investigate the possible role of CD4+ T lymphocyte immunoregulatory abnormalities in the pathogenesis of human insulin-dependent diabetes mellitus (IDD), we studied the in vitro function of CD4+ helper/inducer and suppressor/inducer T-cell subpopulations in 25 high risk non-diabetic individuals who tested positive for islet-cell antibodies (ICA). |
| 237 | 1827815 | This T cell defect is not due to a difference in the level of CD3 and IL-2R expression by NOD and BALB/c thymocytes, and both NOD CD4+ CD8- and CD4- CD8+ mature thymic T cells respond poorly to Con A. |
| 238 | 1838123 | The subsets of Leu11+Leu7+, Leu11-Leu7+ and Leu7+Leu2+ were decreased significantly in peripheral Natural Killer cells. |
| 239 | 1838123 | The CD4/CD8 ratio, and the IL2+Leu2+ subset, showed a negative regressions with HbA1, and the diabetic duration, respectively. |
| 240 | 1865367 | Both Lyt2+ (CD8+) and L3T4+ (CD4+) enriched T cell populations showed a labeling response to Con A. |
| 241 | 1865761 | Dual-color analysis of lymphocyte subpopulations demonstrated that acute (2 hour) restraint stress suppressed mitogen-stimulated increases in [Ca2+]i in CD4+ T cells, but enhanced [Ca2+]i in CD8+ T cells. |
| 242 | 1865761 | Within T lymphocyte subpopulations, both acute and chronic stress predominantly affected CD4+ T cells, which may induce a functional reversal of the CD4/CD8 ratios in vivo. |
| 243 | 1865761 | Dual-color analysis of lymphocyte subpopulations demonstrated that acute (2 hour) restraint stress suppressed mitogen-stimulated increases in [Ca2+]i in CD4+ T cells, but enhanced [Ca2+]i in CD8+ T cells. |
| 244 | 1865761 | Within T lymphocyte subpopulations, both acute and chronic stress predominantly affected CD4+ T cells, which may induce a functional reversal of the CD4/CD8 ratios in vivo. |
| 245 | 1899142 | The role of CD4+ and CD8+ T cells in the destruction of islet grafts by spontaneously diabetic mice. |
| 246 | 1899142 | In disease-transfer experiments, the activation of diabetes has been reported to require participation of both CD4+ and CD8+ T-cell subsets. |
| 247 | 1899142 | These findings seem to indicate that the CD4+ cells are the helper cells for the activation of cytotoxic CD8+ cells that directly destroy islet beta cells in type I diabetes. |
| 248 | 1899142 | In this report we challenge this interpretation because of two observations: (i) Destruction of syngeneic islet grafts by spontaneously diabetic NOD mice (disease recurrence) is CD4+ and not CD8+ T-cell dependent. |
| 249 | 1899142 | The role of CD4+ and CD8+ T cells in the destruction of islet grafts by spontaneously diabetic mice. |
| 250 | 1899142 | In disease-transfer experiments, the activation of diabetes has been reported to require participation of both CD4+ and CD8+ T-cell subsets. |
| 251 | 1899142 | These findings seem to indicate that the CD4+ cells are the helper cells for the activation of cytotoxic CD8+ cells that directly destroy islet beta cells in type I diabetes. |
| 252 | 1899142 | In this report we challenge this interpretation because of two observations: (i) Destruction of syngeneic islet grafts by spontaneously diabetic NOD mice (disease recurrence) is CD4+ and not CD8+ T-cell dependent. |
| 253 | 1899142 | The role of CD4+ and CD8+ T cells in the destruction of islet grafts by spontaneously diabetic mice. |
| 254 | 1899142 | In disease-transfer experiments, the activation of diabetes has been reported to require participation of both CD4+ and CD8+ T-cell subsets. |
| 255 | 1899142 | These findings seem to indicate that the CD4+ cells are the helper cells for the activation of cytotoxic CD8+ cells that directly destroy islet beta cells in type I diabetes. |
| 256 | 1899142 | In this report we challenge this interpretation because of two observations: (i) Destruction of syngeneic islet grafts by spontaneously diabetic NOD mice (disease recurrence) is CD4+ and not CD8+ T-cell dependent. |
| 257 | 1899142 | The role of CD4+ and CD8+ T cells in the destruction of islet grafts by spontaneously diabetic mice. |
| 258 | 1899142 | In disease-transfer experiments, the activation of diabetes has been reported to require participation of both CD4+ and CD8+ T-cell subsets. |
| 259 | 1899142 | These findings seem to indicate that the CD4+ cells are the helper cells for the activation of cytotoxic CD8+ cells that directly destroy islet beta cells in type I diabetes. |
| 260 | 1899142 | In this report we challenge this interpretation because of two observations: (i) Destruction of syngeneic islet grafts by spontaneously diabetic NOD mice (disease recurrence) is CD4+ and not CD8+ T-cell dependent. |
| 261 | 1902177 | In humans and non-obese diabetic mice (NOD), insulin-dependent diabetes mellitus (IDDM) results from a spontaneous T cell-dependent autoimmune destruction of the insulin-producing pancreatic beta cells. |
| 262 | 1902177 | To resolve the cellular basis of this intricate network of pathogenic CD4+ and CD8+ T cells and the role of T cells in suppressive immune phenomena. |
| 263 | 1902177 | A CD4+ T cell clone, IS-3S7D, proliferates in response to islet antigen(s) and its transfer into prediabetic NOD mice promotes the rapid onset of IDDM. |
| 264 | 1902177 | An interleukin 2 (IL 2)-dependent noncytolytic, V beta 11+ CD8+. |
| 265 | 1902177 | The present study, which documents the presence of CD4+ diabetogenic T cell clones and CD8+ T cell clones that dampen autoimmunity, gives tangible evidence that opposing autoimmune processes may determine whether an autoimmune-prone host develops frank disease. |
| 266 | 1902177 | In humans and non-obese diabetic mice (NOD), insulin-dependent diabetes mellitus (IDDM) results from a spontaneous T cell-dependent autoimmune destruction of the insulin-producing pancreatic beta cells. |
| 267 | 1902177 | To resolve the cellular basis of this intricate network of pathogenic CD4+ and CD8+ T cells and the role of T cells in suppressive immune phenomena. |
| 268 | 1902177 | A CD4+ T cell clone, IS-3S7D, proliferates in response to islet antigen(s) and its transfer into prediabetic NOD mice promotes the rapid onset of IDDM. |
| 269 | 1902177 | An interleukin 2 (IL 2)-dependent noncytolytic, V beta 11+ CD8+. |
| 270 | 1902177 | The present study, which documents the presence of CD4+ diabetogenic T cell clones and CD8+ T cell clones that dampen autoimmunity, gives tangible evidence that opposing autoimmune processes may determine whether an autoimmune-prone host develops frank disease. |
| 271 | 1902177 | In humans and non-obese diabetic mice (NOD), insulin-dependent diabetes mellitus (IDDM) results from a spontaneous T cell-dependent autoimmune destruction of the insulin-producing pancreatic beta cells. |
| 272 | 1902177 | To resolve the cellular basis of this intricate network of pathogenic CD4+ and CD8+ T cells and the role of T cells in suppressive immune phenomena. |
| 273 | 1902177 | A CD4+ T cell clone, IS-3S7D, proliferates in response to islet antigen(s) and its transfer into prediabetic NOD mice promotes the rapid onset of IDDM. |
| 274 | 1902177 | An interleukin 2 (IL 2)-dependent noncytolytic, V beta 11+ CD8+. |
| 275 | 1902177 | The present study, which documents the presence of CD4+ diabetogenic T cell clones and CD8+ T cell clones that dampen autoimmunity, gives tangible evidence that opposing autoimmune processes may determine whether an autoimmune-prone host develops frank disease. |
| 276 | 1902501 | All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. |
| 277 | 1903736 | The development of insulin-dependent diabetes mellitus in non-obese diabetic mice: the role of CD4+ and CD8+ T cells. |
| 278 | 1907661 | Concanavalin A (Con A) administered in vivo inhibited the development of insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic mice. |
| 279 | 1907661 | The treatment increased the frequency of "blast-sized" cells in vivo and decreased the CD4+/CD8+ ratio among resting splenocytes. |
| 280 | 1948748 | Indirect immunofluorescence and monoclonal antibodies to leukocytic differentiated antigens CD3, CD4, CD8, CD22, CD25, CD71 and HLA-DR were used. |
| 281 | 1948748 | It has been demonstrated that the pre-nephrotic stage of DN is marked by the normal content of the main subpopulations of peripheral lymphocytes (CD3, CD4, CD8 and CD22-positive). |
| 282 | 1948748 | Indirect immunofluorescence and monoclonal antibodies to leukocytic differentiated antigens CD3, CD4, CD8, CD22, CD25, CD71 and HLA-DR were used. |
| 283 | 1948748 | It has been demonstrated that the pre-nephrotic stage of DN is marked by the normal content of the main subpopulations of peripheral lymphocytes (CD3, CD4, CD8 and CD22-positive). |
| 284 | 1975826 | CD4+CD8- Th cells from DBA/1 LacJ mice with type II collagen arthritis expressed low levels of type n K+ channels, and CD4-CD8+ T cells (cytotoxic) showed small numbers of type l or n' K+ channels, like their phenotypic counterparts in normal mice. |
| 285 | 2018977 | Of particular interest was the RT6+ T cell subset, that appears to have important immunoregulatory properties in a rat model of autoimmune insulin-dependent diabetes mellitus. |
| 286 | 2018977 | Analysis of other lymphocyte subpopulations demonstrated a decrease of CD4+ and CD5+ cells, whereas B cells as well as CD8+, IL-2 receptor+, and MHC class II+ subsets showed no consistent correlation with the onset or resolution of the autoimmune process. |
| 287 | 2022315 | However, within T cell subpopulations, CD4+ but not CD8+ cells were affected. |
| 288 | 2022315 | Adrenalectomy abolished this effect of morphine in CD4+ T but not CD4-, CD8- spleen cells (most likely Thy 1.2- B cells). |
| 289 | 2022315 | Moreover, simultaneous administration of the opiate antagonist naltrexone blocked the effect of morphine in CD4-, CD8- spleen cells, but not in CD4+ T cells. |
| 290 | 2022315 | However, within T cell subpopulations, CD4+ but not CD8+ cells were affected. |
| 291 | 2022315 | Adrenalectomy abolished this effect of morphine in CD4+ T but not CD4-, CD8- spleen cells (most likely Thy 1.2- B cells). |
| 292 | 2022315 | Moreover, simultaneous administration of the opiate antagonist naltrexone blocked the effect of morphine in CD4-, CD8- spleen cells, but not in CD4+ T cells. |
| 293 | 2022315 | However, within T cell subpopulations, CD4+ but not CD8+ cells were affected. |
| 294 | 2022315 | Adrenalectomy abolished this effect of morphine in CD4+ T but not CD4-, CD8- spleen cells (most likely Thy 1.2- B cells). |
| 295 | 2022315 | Moreover, simultaneous administration of the opiate antagonist naltrexone blocked the effect of morphine in CD4-, CD8- spleen cells, but not in CD4+ T cells. |
| 296 | 2041484 | Are syntax errors due to the amino acid sequence of neuroleukin involved in the pathogenesis of the acquired immunodeficiency syndrome (AIDS) and insulin dependent diabetes mellitus (IDDM)? |
| 297 | 2041484 | In AIDS the basic defect would be the human specific inability to distinguish between the amino acid sequence of neuroleukin and peptides derived from the gp120 envelope protein of HIV, resulting in a slowly progressing failure of the CD4+ T cell-mediated immunity. |
| 298 | 2041484 | In the ensuing dialogue neuroleukin secreted by T cells would imply a continuous demand for insulin secretion to pancreatic beta cells resulting in diabetes. |
| 299 | 2091903 | Cell-mediated immunity (CMI) included delayed type skin test (MULTITEST CMI), total lymphocyte count and lymphocyte subpopulations (CD3, CD4 and CD8) were determined. |
| 300 | 2104186 | No differences were detected between the three groups with respect to total T-lymphocytes (CD3), helper T-lymphocytes (CD4), suppressor cytotoxic T-lymphocytes (CD8), or the inducer of suppressor (Leu 3+/Leu 8+) subset of T-lymphocytes. |
| 301 | 2113565 | Differential roles of Mac-1+ cells, and CD4+ and CD8+ T lymphocytes in primary nonfunction and classic rejection of islet allografts. |
| 302 | 2113565 | Selective immunodepletion of host CD4+ and CD8+ T lymphocytes significantly extended the time of classic rejection but did not significantly affect the rate of primary nonfunction. |
| 303 | 2113565 | Differential roles of Mac-1+ cells, and CD4+ and CD8+ T lymphocytes in primary nonfunction and classic rejection of islet allografts. |
| 304 | 2113565 | Selective immunodepletion of host CD4+ and CD8+ T lymphocytes significantly extended the time of classic rejection but did not significantly affect the rate of primary nonfunction. |
| 305 | 2123429 | Abnormalities of CD4+ T lymphocyte proliferative responses from patients with recently diagnosed insulin-dependent diabetes mellitus. |
| 306 | 2123429 | To investigate the abnormalities of cell-mediated immunity in patients with recently diagnosed insulin-dependent diabetes mellitus (IDDM), we studied the responses of the two major T lymphocyte subsets from peripheral blood lymphocytes (PBL) to mitogen stimulation. |
| 307 | 2123429 | CD4+ and CD8+ T cells were isolated and were subsequently stimulated with three specific lymphocyte mitogens, namely Phytohemagglutinin (PHA), Concanavalin A (Con A) and Pokeweek mitogen (PWM). |
| 308 | 2123429 | The responses of CD8+ T cells from IDDM patients and from controls were not significantly different. |
| 309 | 2123429 | However, CD4+ T cells from IDDM patients showed significantly depressed responses to PHA and Con A and to a much lesser extent to PWM. |
| 310 | 2123429 | These data provide new information regarding the CD4+ T lymphocyte abnormalities found in patients with IDDM. |
| 311 | 2123429 | Abnormalities of CD4+ T lymphocyte proliferative responses from patients with recently diagnosed insulin-dependent diabetes mellitus. |
| 312 | 2123429 | To investigate the abnormalities of cell-mediated immunity in patients with recently diagnosed insulin-dependent diabetes mellitus (IDDM), we studied the responses of the two major T lymphocyte subsets from peripheral blood lymphocytes (PBL) to mitogen stimulation. |
| 313 | 2123429 | CD4+ and CD8+ T cells were isolated and were subsequently stimulated with three specific lymphocyte mitogens, namely Phytohemagglutinin (PHA), Concanavalin A (Con A) and Pokeweek mitogen (PWM). |
| 314 | 2123429 | The responses of CD8+ T cells from IDDM patients and from controls were not significantly different. |
| 315 | 2123429 | However, CD4+ T cells from IDDM patients showed significantly depressed responses to PHA and Con A and to a much lesser extent to PWM. |
| 316 | 2123429 | These data provide new information regarding the CD4+ T lymphocyte abnormalities found in patients with IDDM. |
| 317 | 2123429 | Abnormalities of CD4+ T lymphocyte proliferative responses from patients with recently diagnosed insulin-dependent diabetes mellitus. |
| 318 | 2123429 | To investigate the abnormalities of cell-mediated immunity in patients with recently diagnosed insulin-dependent diabetes mellitus (IDDM), we studied the responses of the two major T lymphocyte subsets from peripheral blood lymphocytes (PBL) to mitogen stimulation. |
| 319 | 2123429 | CD4+ and CD8+ T cells were isolated and were subsequently stimulated with three specific lymphocyte mitogens, namely Phytohemagglutinin (PHA), Concanavalin A (Con A) and Pokeweek mitogen (PWM). |
| 320 | 2123429 | The responses of CD8+ T cells from IDDM patients and from controls were not significantly different. |
| 321 | 2123429 | However, CD4+ T cells from IDDM patients showed significantly depressed responses to PHA and Con A and to a much lesser extent to PWM. |
| 322 | 2123429 | These data provide new information regarding the CD4+ T lymphocyte abnormalities found in patients with IDDM. |
| 323 | 2123429 | Abnormalities of CD4+ T lymphocyte proliferative responses from patients with recently diagnosed insulin-dependent diabetes mellitus. |
| 324 | 2123429 | To investigate the abnormalities of cell-mediated immunity in patients with recently diagnosed insulin-dependent diabetes mellitus (IDDM), we studied the responses of the two major T lymphocyte subsets from peripheral blood lymphocytes (PBL) to mitogen stimulation. |
| 325 | 2123429 | CD4+ and CD8+ T cells were isolated and were subsequently stimulated with three specific lymphocyte mitogens, namely Phytohemagglutinin (PHA), Concanavalin A (Con A) and Pokeweek mitogen (PWM). |
| 326 | 2123429 | The responses of CD8+ T cells from IDDM patients and from controls were not significantly different. |
| 327 | 2123429 | However, CD4+ T cells from IDDM patients showed significantly depressed responses to PHA and Con A and to a much lesser extent to PWM. |
| 328 | 2123429 | These data provide new information regarding the CD4+ T lymphocyte abnormalities found in patients with IDDM. |
| 329 | 2132756 | Results indicate that: 1) the first islet-infiltrating leukocytes are class II+, Ig- monocytes and CD8+ T lymphocytes, 2) after a slight decrease in the CD8+ cell population, an influx of CD4+ T lymphocytes occurs, accompanied by increasing numbers of CD8+ T cells, as well as IgM+ and IgG+ B lymphocytes, 3) whereas all the IgM+ B cells appear to be CD5+, between 70-95% of IgG+ B cells express CD5, and 4) throughout the response, the class II+, IgG-cell population remains relatively constant. |
| 330 | 2137753 | Activated CD4+ and CD8+ T-lymphocytes in newly diagnosed type 1 diabetes: a prospective study. |
| 331 | 2137753 | The overall percentage of activated T-lymphocytes (CD4+ + CD8+ cells) was (mean +/- SE) 3.1 +/- 0.5% at diagnosis, 2.1 +/- 0.3% at 1 month and 2.2 +/- 0.5% at 7 months test. |
| 332 | 2137753 | Among the CD4+ cells the percentage of activated cells fell from diagnosis (2.8 +/- 0.7%), to 1 month (1.5 +/- 0.3%, p less than 0.05), and 7 months (1.5 +/- 0.4%, p less than 0.05), whereas among the CD8+ cells they remained unchanged (3.3 +/- 0.6, 2.5 +/- 0.5 and 3.1 +/- 0.6%). |
| 333 | 2137753 | The percentage of activated CD4+ cells at diagnosis, and of CD8+ cells at all times, were higher (p less than 0.02) than in control subjects (CD4+, 0.8 +/- 0.2%; CD8+, 1.2 +/- 0.2%). |
| 334 | 2137753 | In conclusion, the activated T-lymphocytes present in Type 1 diabetic patients at diagnosis are equally increased among CD4+ and CD8+ cells, but after 7 months the increase is predominantly in CD8+ cells. |
| 335 | 2137753 | Activated CD4+ and CD8+ T-lymphocytes in newly diagnosed type 1 diabetes: a prospective study. |
| 336 | 2137753 | The overall percentage of activated T-lymphocytes (CD4+ + CD8+ cells) was (mean +/- SE) 3.1 +/- 0.5% at diagnosis, 2.1 +/- 0.3% at 1 month and 2.2 +/- 0.5% at 7 months test. |
| 337 | 2137753 | Among the CD4+ cells the percentage of activated cells fell from diagnosis (2.8 +/- 0.7%), to 1 month (1.5 +/- 0.3%, p less than 0.05), and 7 months (1.5 +/- 0.4%, p less than 0.05), whereas among the CD8+ cells they remained unchanged (3.3 +/- 0.6, 2.5 +/- 0.5 and 3.1 +/- 0.6%). |
| 338 | 2137753 | The percentage of activated CD4+ cells at diagnosis, and of CD8+ cells at all times, were higher (p less than 0.02) than in control subjects (CD4+, 0.8 +/- 0.2%; CD8+, 1.2 +/- 0.2%). |
| 339 | 2137753 | In conclusion, the activated T-lymphocytes present in Type 1 diabetic patients at diagnosis are equally increased among CD4+ and CD8+ cells, but after 7 months the increase is predominantly in CD8+ cells. |
| 340 | 2137753 | Activated CD4+ and CD8+ T-lymphocytes in newly diagnosed type 1 diabetes: a prospective study. |
| 341 | 2137753 | The overall percentage of activated T-lymphocytes (CD4+ + CD8+ cells) was (mean +/- SE) 3.1 +/- 0.5% at diagnosis, 2.1 +/- 0.3% at 1 month and 2.2 +/- 0.5% at 7 months test. |
| 342 | 2137753 | Among the CD4+ cells the percentage of activated cells fell from diagnosis (2.8 +/- 0.7%), to 1 month (1.5 +/- 0.3%, p less than 0.05), and 7 months (1.5 +/- 0.4%, p less than 0.05), whereas among the CD8+ cells they remained unchanged (3.3 +/- 0.6, 2.5 +/- 0.5 and 3.1 +/- 0.6%). |
| 343 | 2137753 | The percentage of activated CD4+ cells at diagnosis, and of CD8+ cells at all times, were higher (p less than 0.02) than in control subjects (CD4+, 0.8 +/- 0.2%; CD8+, 1.2 +/- 0.2%). |
| 344 | 2137753 | In conclusion, the activated T-lymphocytes present in Type 1 diabetic patients at diagnosis are equally increased among CD4+ and CD8+ cells, but after 7 months the increase is predominantly in CD8+ cells. |
| 345 | 2137753 | Activated CD4+ and CD8+ T-lymphocytes in newly diagnosed type 1 diabetes: a prospective study. |
| 346 | 2137753 | The overall percentage of activated T-lymphocytes (CD4+ + CD8+ cells) was (mean +/- SE) 3.1 +/- 0.5% at diagnosis, 2.1 +/- 0.3% at 1 month and 2.2 +/- 0.5% at 7 months test. |
| 347 | 2137753 | Among the CD4+ cells the percentage of activated cells fell from diagnosis (2.8 +/- 0.7%), to 1 month (1.5 +/- 0.3%, p less than 0.05), and 7 months (1.5 +/- 0.4%, p less than 0.05), whereas among the CD8+ cells they remained unchanged (3.3 +/- 0.6, 2.5 +/- 0.5 and 3.1 +/- 0.6%). |
| 348 | 2137753 | The percentage of activated CD4+ cells at diagnosis, and of CD8+ cells at all times, were higher (p less than 0.02) than in control subjects (CD4+, 0.8 +/- 0.2%; CD8+, 1.2 +/- 0.2%). |
| 349 | 2137753 | In conclusion, the activated T-lymphocytes present in Type 1 diabetic patients at diagnosis are equally increased among CD4+ and CD8+ cells, but after 7 months the increase is predominantly in CD8+ cells. |
| 350 | 2137753 | Activated CD4+ and CD8+ T-lymphocytes in newly diagnosed type 1 diabetes: a prospective study. |
| 351 | 2137753 | The overall percentage of activated T-lymphocytes (CD4+ + CD8+ cells) was (mean +/- SE) 3.1 +/- 0.5% at diagnosis, 2.1 +/- 0.3% at 1 month and 2.2 +/- 0.5% at 7 months test. |
| 352 | 2137753 | Among the CD4+ cells the percentage of activated cells fell from diagnosis (2.8 +/- 0.7%), to 1 month (1.5 +/- 0.3%, p less than 0.05), and 7 months (1.5 +/- 0.4%, p less than 0.05), whereas among the CD8+ cells they remained unchanged (3.3 +/- 0.6, 2.5 +/- 0.5 and 3.1 +/- 0.6%). |
| 353 | 2137753 | The percentage of activated CD4+ cells at diagnosis, and of CD8+ cells at all times, were higher (p less than 0.02) than in control subjects (CD4+, 0.8 +/- 0.2%; CD8+, 1.2 +/- 0.2%). |
| 354 | 2137753 | In conclusion, the activated T-lymphocytes present in Type 1 diabetic patients at diagnosis are equally increased among CD4+ and CD8+ cells, but after 7 months the increase is predominantly in CD8+ cells. |
| 355 | 2138777 | With anti-I-Ak monoclonal antibody (specific for I-Ak,f,r,s beta and produced by clone 11-5-2), and fluorescein isothiocyanate-conjugated goat anti-mouse IgG as second-step antibody, we found that SCICs from both sexes aberrantly expressed class II MHC molecules, which was not altered after SCICs were cultured for 24 hr or 120 hr in the presence of 10 ng of recombinant murine interferon gamma per ml. |
| 356 | 2138777 | Monoclonal antibodies to class II MHC and CD4 antigens blocked the proliferative response. |
| 357 | 2138777 | Results from control autologous and allogeneic mixed lymphocyte reactions suggest that the responder CD4 T cells are autoreactive self-class II MHC restricted. |
| 358 | 2138777 | With anti-I-Ak monoclonal antibody (specific for I-Ak,f,r,s beta and produced by clone 11-5-2), and fluorescein isothiocyanate-conjugated goat anti-mouse IgG as second-step antibody, we found that SCICs from both sexes aberrantly expressed class II MHC molecules, which was not altered after SCICs were cultured for 24 hr or 120 hr in the presence of 10 ng of recombinant murine interferon gamma per ml. |
| 359 | 2138777 | Monoclonal antibodies to class II MHC and CD4 antigens blocked the proliferative response. |
| 360 | 2138777 | Results from control autologous and allogeneic mixed lymphocyte reactions suggest that the responder CD4 T cells are autoreactive self-class II MHC restricted. |
| 361 | 2146283 | The increased binding in vitro of CD3 CD4 T-lymphocytes from type 1 (insulin-dependent) diabetic patients to beta-cell membrane antigens compared to lymphocytes from control subjects was previously shown to be a marker of cell-mediated immunity, called diabetic rosettes. |
| 362 | 2162302 | Most of the cells expressing Ly-6C were Thy-1.2+, CD4+, and CD8- and proliferated after stimulation with HK1.4. |
| 363 | 2162302 | To further understand the failure of NOD splenocytes to express Ly-6C, freshly isolated cells were stimulated with alpha/beta-interferon (IFN-alpha/beta) and IFN-gamma. |
| 364 | 2179951 | Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 365 | 2179951 | We show that the genes for tumor necrosis factor alpha and granzyme A, a serine protease associated with cytoplasmic granules of cytotoxic cells, are expressed during the development of spontaneous diabetes mellitus in the nonobese diabetic mouse. |
| 366 | 2179951 | Tumor necrosis factor alpha expression is exclusively observed in the intra-islet infiltrate, predominantly in lymphocytes adjacent to insulin-producing beta cells, the targets of the autoimmune destruction, implying that tumor necrosis factor alpha expression is induced locally--i.e., in the islet. |
| 367 | 2179951 | A considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells. |
| 368 | 2187189 | Repopulation of the atrophied thymus in diabetic rats by insulin-like growth factor I. |
| 369 | 2187189 | We describe here that the weight and the architecture of the thymus of diabetic rats is restored towards normal not only by insulin but also by insulin-like growth factor I (IGF-I) treatment. |
| 370 | 2187189 | In contrast to insulin, this effect of IGF-I occurs despite persisting hyperglycemia and adrenal hyperplasia. |
| 371 | 2187189 | Insulin, as well as IGF-I treatment of diabetic rats increased [3H]thymidine incorporation by thymocytes. |
| 372 | 2187189 | In addition, a major deficiency of thymocytes expressing simultaneously the W3/25 and the Ox8 antigens (corresponding to immature human CD4+/CD8+ thymocytes) was observed. |
| 373 | 2187189 | These changes were restored towards normal by insulin as well as by IGF-I treatment. |
| 374 | 2187189 | We conclude that IGF-I has important effects on the thymocyte number and the presence of CD4+/CD8+ immature cells in the thymus of diabetic rats despite persisting hyperglycemia. |
| 375 | 2187189 | Repopulation of the atrophied thymus in diabetic rats by insulin-like growth factor I. |
| 376 | 2187189 | We describe here that the weight and the architecture of the thymus of diabetic rats is restored towards normal not only by insulin but also by insulin-like growth factor I (IGF-I) treatment. |
| 377 | 2187189 | In contrast to insulin, this effect of IGF-I occurs despite persisting hyperglycemia and adrenal hyperplasia. |
| 378 | 2187189 | Insulin, as well as IGF-I treatment of diabetic rats increased [3H]thymidine incorporation by thymocytes. |
| 379 | 2187189 | In addition, a major deficiency of thymocytes expressing simultaneously the W3/25 and the Ox8 antigens (corresponding to immature human CD4+/CD8+ thymocytes) was observed. |
| 380 | 2187189 | These changes were restored towards normal by insulin as well as by IGF-I treatment. |
| 381 | 2187189 | We conclude that IGF-I has important effects on the thymocyte number and the presence of CD4+/CD8+ immature cells in the thymus of diabetic rats despite persisting hyperglycemia. |
| 382 | 2204602 | Insulin induced proliferation of blood mononuclear cells, numbers of blood B and T cells, of blood lymphocytes bearing interleukin 2 receptors or HLA class II molecules were assayed at diagnosis and one year later in children with insulin-dependent diabetes mellitus (IDDM) and in healthy children. |
| 383 | 2204602 | T cells of the helper/inducer (CD4+) phenotype and interleukin 2 receptor positive lymphocytes were increased both at diagnosis and one year later. |
| 384 | 2459088 | Here we report three CD4+ T lymphocyte clones (TLCs) generated from a DR3,4; DQw2,w3.1 responder stimulated with cells from a DR3,4; DQw2,w3.2 donor, and using a modified cloning procedure involving enrichment of IL-2 receptor-positive T cell during priming. |
| 385 | 2480383 | By means of immunohistochemical analysis, we were able to detect perforin Ag in a small subpopulation of CD8+/Thy-1+/asialo GM1-/CD4- lymphocytes in the pancreatic islets of animals undergoing both spontaneous and adoptive transfer-mediated insulitis. |
| 386 | 2492007 | The role of T-lymphocyte subpopulations in the rejection of fetal pig proislet (islet precursor) xenografts in mice was examined with in vivo administration of monoclonal antibodies (MoAbs) to CD4+ (GK 1.5) and CD8+ (49-11.1) T-lymphocyte subsets. |
| 387 | 2502462 | Persistent reduction of CD4/CD8 lymphocyte ratio and cell activation before the onset of type 1 (insulin-dependent) diabetes. |
| 388 | 2502462 | Lymphocytes were phenotyped using a panel of monoclonal antibodies which recognise CD3, CD4, CD8 lymphocytes, K/NK cells, HLA Class II products and IL-2 receptors (IL-2r). |
| 389 | 2502462 | They all possessed CF-ICA and five out of six showed a persistent reduction (less than 1.5) of the CD4/CD8 lymphocyte ratio before the clinical onset of the disease. |
| 390 | 2502462 | We conclude that imbalance of lymphocyte immunoregulatory subsets is present before the onset of Type 1 diabetes in susceptible individuals; the persistence of a reduced CD4/CD8 lymphocyte ratio may reflect the ongoing process leading to B-cell destruction. |
| 391 | 2502462 | Persistent reduction of CD4/CD8 lymphocyte ratio and cell activation before the onset of type 1 (insulin-dependent) diabetes. |
| 392 | 2502462 | Lymphocytes were phenotyped using a panel of monoclonal antibodies which recognise CD3, CD4, CD8 lymphocytes, K/NK cells, HLA Class II products and IL-2 receptors (IL-2r). |
| 393 | 2502462 | They all possessed CF-ICA and five out of six showed a persistent reduction (less than 1.5) of the CD4/CD8 lymphocyte ratio before the clinical onset of the disease. |
| 394 | 2502462 | We conclude that imbalance of lymphocyte immunoregulatory subsets is present before the onset of Type 1 diabetes in susceptible individuals; the persistence of a reduced CD4/CD8 lymphocyte ratio may reflect the ongoing process leading to B-cell destruction. |
| 395 | 2502462 | Persistent reduction of CD4/CD8 lymphocyte ratio and cell activation before the onset of type 1 (insulin-dependent) diabetes. |
| 396 | 2502462 | Lymphocytes were phenotyped using a panel of monoclonal antibodies which recognise CD3, CD4, CD8 lymphocytes, K/NK cells, HLA Class II products and IL-2 receptors (IL-2r). |
| 397 | 2502462 | They all possessed CF-ICA and five out of six showed a persistent reduction (less than 1.5) of the CD4/CD8 lymphocyte ratio before the clinical onset of the disease. |
| 398 | 2502462 | We conclude that imbalance of lymphocyte immunoregulatory subsets is present before the onset of Type 1 diabetes in susceptible individuals; the persistence of a reduced CD4/CD8 lymphocyte ratio may reflect the ongoing process leading to B-cell destruction. |
| 399 | 2502462 | Persistent reduction of CD4/CD8 lymphocyte ratio and cell activation before the onset of type 1 (insulin-dependent) diabetes. |
| 400 | 2502462 | Lymphocytes were phenotyped using a panel of monoclonal antibodies which recognise CD3, CD4, CD8 lymphocytes, K/NK cells, HLA Class II products and IL-2 receptors (IL-2r). |
| 401 | 2502462 | They all possessed CF-ICA and five out of six showed a persistent reduction (less than 1.5) of the CD4/CD8 lymphocyte ratio before the clinical onset of the disease. |
| 402 | 2502462 | We conclude that imbalance of lymphocyte immunoregulatory subsets is present before the onset of Type 1 diabetes in susceptible individuals; the persistence of a reduced CD4/CD8 lymphocyte ratio may reflect the ongoing process leading to B-cell destruction. |
| 403 | 2506278 | In order to address the roles of CD4+ and CD8+ T cells in pancreatic islet rejection, we used an adoptive transfer model in which H-2b nude mice were reconstituted with negatively selected H-2b CD4+ or CD8+ T cell subpopulations and engrafted with fully allogeneic pancreatic islet grafts. |
| 404 | 2506278 | We found that primary (unprimed) CD4+ T cells mediated the rejection of pancreatic islet grafts, whereas, primary CD8+ T cells failed to do so, even though both T cell subpopulations were competent to reject skin allografts. |
| 405 | 2506278 | These data indicate that primary CD4+ T cells are necessary for rejection of allogeneic pancreatic islet grafts, whereas primary CD8+ T lymphocytes are not. |
| 406 | 2506278 | In order to address the roles of CD4+ and CD8+ T cells in pancreatic islet rejection, we used an adoptive transfer model in which H-2b nude mice were reconstituted with negatively selected H-2b CD4+ or CD8+ T cell subpopulations and engrafted with fully allogeneic pancreatic islet grafts. |
| 407 | 2506278 | We found that primary (unprimed) CD4+ T cells mediated the rejection of pancreatic islet grafts, whereas, primary CD8+ T cells failed to do so, even though both T cell subpopulations were competent to reject skin allografts. |
| 408 | 2506278 | These data indicate that primary CD4+ T cells are necessary for rejection of allogeneic pancreatic islet grafts, whereas primary CD8+ T lymphocytes are not. |
| 409 | 2506278 | In order to address the roles of CD4+ and CD8+ T cells in pancreatic islet rejection, we used an adoptive transfer model in which H-2b nude mice were reconstituted with negatively selected H-2b CD4+ or CD8+ T cell subpopulations and engrafted with fully allogeneic pancreatic islet grafts. |
| 410 | 2506278 | We found that primary (unprimed) CD4+ T cells mediated the rejection of pancreatic islet grafts, whereas, primary CD8+ T cells failed to do so, even though both T cell subpopulations were competent to reject skin allografts. |
| 411 | 2506278 | These data indicate that primary CD4+ T cells are necessary for rejection of allogeneic pancreatic islet grafts, whereas primary CD8+ T lymphocytes are not. |
| 412 | 2507922 | To determine the mechanism of the protective effect of I-E, we have produced cloned CD4+ and CD8+ T-cell lines from islets of recently diabetic NOD mice. |
| 413 | 2507922 | Both CD4+ and CD8+ cloned T cells bear receptors encoded by a V beta 5 gene segment, known to be deleted during development in I-E expressing mice. |
| 414 | 2507922 | To determine the mechanism of the protective effect of I-E, we have produced cloned CD4+ and CD8+ T-cell lines from islets of recently diabetic NOD mice. |
| 415 | 2507922 | Both CD4+ and CD8+ cloned T cells bear receptors encoded by a V beta 5 gene segment, known to be deleted during development in I-E expressing mice. |
| 416 | 2526634 | The percent CD4+ and CD8+ T cells were not significantly different from control. |
| 417 | 2527266 | The percentage of CD4 and CD8 cells in the spleen was transiently reduced after injection and the frequency of Pgp-1+-high cells (putative memory cells) was increased 2 to 4 wk postinjection, suggesting that in vivo administration of the antibody caused some T cells to divide as well as transiently reducing T cell numbers. |
| 418 | 2527266 | Protection from diabetes did not follow neonatal elimination of T cells with CD4 and CD8 antibodies, nor the injection of a TCR subset antibody, F23.1. |
| 419 | 2527266 | The percentage of CD4 and CD8 cells in the spleen was transiently reduced after injection and the frequency of Pgp-1+-high cells (putative memory cells) was increased 2 to 4 wk postinjection, suggesting that in vivo administration of the antibody caused some T cells to divide as well as transiently reducing T cell numbers. |
| 420 | 2527266 | Protection from diabetes did not follow neonatal elimination of T cells with CD4 and CD8 antibodies, nor the injection of a TCR subset antibody, F23.1. |
| 421 | 2530249 | Sulfated beef insulin treatment elicits CD8+ T cells that may abrogate immunologic insulin resistance in type I diabetes. |
| 422 | 2530249 | Insulin A-loop specific CD4+ T cells from these patients did not respond to SBI. |
| 423 | 2530249 | This occurred in parallel to the appearance of her insulin-specific CD8+ T cells, which inhibited the response of her A-loop-specific CD4+ T cells to insulin. |
| 424 | 2530249 | A transient increase in her CD8+ anti-insulin antibody activity coincided with a relative lack of her CD8+ T cell activity. |
| 425 | 2530249 | CD8+ T cells that regulate T cell responsiveness to insulin are probably present but difficult to detect in most type I diabetes patients. |
| 426 | 2530249 | Our data demonstrate that CD8+ T cells play an important role in controlling peripheral tolerance to insulin and may abrogate IIR in a diabetic patient treated with SBI. |
| 427 | 2530249 | Sulfated beef insulin treatment elicits CD8+ T cells that may abrogate immunologic insulin resistance in type I diabetes. |
| 428 | 2530249 | Insulin A-loop specific CD4+ T cells from these patients did not respond to SBI. |
| 429 | 2530249 | This occurred in parallel to the appearance of her insulin-specific CD8+ T cells, which inhibited the response of her A-loop-specific CD4+ T cells to insulin. |
| 430 | 2530249 | A transient increase in her CD8+ anti-insulin antibody activity coincided with a relative lack of her CD8+ T cell activity. |
| 431 | 2530249 | CD8+ T cells that regulate T cell responsiveness to insulin are probably present but difficult to detect in most type I diabetes patients. |
| 432 | 2530249 | Our data demonstrate that CD8+ T cells play an important role in controlling peripheral tolerance to insulin and may abrogate IIR in a diabetic patient treated with SBI. |
| 433 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 434 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 435 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 436 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 437 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 438 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 439 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 440 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 441 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 442 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 443 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 444 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 445 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 446 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 447 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 448 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 449 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 450 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 451 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 452 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 453 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 454 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 455 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 456 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 457 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 458 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 459 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 460 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 461 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 462 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 463 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 464 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 465 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 466 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 467 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 468 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 469 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 470 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 471 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 472 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 473 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 474 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 475 | 2570740 | Defective immunoregulation in primary biliary cirrhosis: CD4+, Leu-8+ T cells have abnormal activation and suppressor function in vitro. |
| 476 | 2570740 | The proportion of CD4+ T cells expressing the Leu-8 and CD45R antigens was normal in patients with primary biliary cirrhosis. |
| 477 | 2570740 | The capacity of CD4+, Leu-8- T cells to provide helper function for pokeweed mitogen-stimulated immunoglobulin synthesis by B cells in vitro was similar in patients and controls. |
| 478 | 2570740 | However, in contrast to normal individuals and patients with other liver diseases, CD4+, Leu-8+ T cells from six of 10 patients with primary biliary cirrhosis did not suppress, but enhanced immunoglobulin synthesis. |
| 479 | 2570740 | Whereas treatment of CD4+ T cells from normal individuals with anti-Leu-8 monoclonal antibody enhanced their suppressor function, similar treatment of CD4+ T cells from patients with primary biliary cirrhosis did not increase their suppressor function. |
| 480 | 2570740 | To determine whether the abnormal regulatory function of CD4+, Leu-8+ T cells was due to a defect of cell activation, the proliferative response of CD4+ T cell subpopulations to mitogenic stimulation was examined. |
| 481 | 2570740 | The proliferative responses of CD4+, Leu-8- T cells from patients with primary biliary cirrhosis and controls were similar, but the proliferative responses of CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis were lower than those of control cells. |
| 482 | 2644144 | Effect of cyclosporin on interleukin 2-related T-lymphocyte parameters in IDDM patients. |
| 483 | 2644144 | Seventy patients aged 15-40 yr with recent-onset insulin-dependent diabetes mellitus (IDDM) were entered into a double-blind trial, in which they were randomly assigned to either cyclosporin (7.5 mg.kg-1.day-1) or to placebo and were monitored for 1 yr for various phenotypic and functional parameters of T-lymphocyte-mediated immunity. |
| 484 | 2644144 | Before treatment, the proportions of total T-lymphocytes (CD3+) and helper-inducer T-lymphocytes (CD4+) were normal, whereas significantly decreased values of suppressor/cytotoxic T-lymphocytes (CD8+), as compared with normal controls, were found in 31% of the patients. |
| 485 | 2644144 | The interleukin 2 (IL-2)-receptor expression was significantly increased in IDDM patients compared with control subjects, although the single values were low: patients, 2.02 +/- 0.41%; controls, 0.88 +/- 0.25% (means +/- SE). |
| 486 | 2644144 | Circulating levels of soluble IL-2 receptor were also significantly increased in IDDM patients compared with controls: patients, 372.3 +/- 25.4 U/ml; controls, 235.5 +/- 29.3 U/ml (means +/- SE). |
| 487 | 2654321 | Patients who had been included in a randomized double-blind placebo-controlled trial on the efficacy of cyclosporin A (CyA) in producing remissions in insulin-dependent diabetes mellitus (IDDM) type I were investigated for humoral and cellular immunologic parameters. |
| 488 | 2654321 | Whereas metabolic derangement before the initiation of insulin treatment led to small but significant decreases in the percentage of CD4-positive lymphocytes as well as of the activity of natural killer (NK) cells and antibody-dependent cellular cytotoxicity (ADCC), the administration of CyA did not influence any of the immunologic parameters tested, which included proliferative lymphocyte responses to mitogens and alloantigens and serum concentrations of immunoglobulins G, A and M. |
| 489 | 2687874 | CD4 is a T-cell surface glycoprotein and serves as the receptor for the human immunodeficiency virus. |
| 490 | 2693822 | Diabetic patients with the disease duration less than 1 year (group 1 eight patients with diabetes mellitus type I and group 2 seven patients with diabetes mellitus type II) and 8 healthy donors were examined for subpopulations of lymphocytes (CD 3-, CD 4-, CD 8-, CD 20-positive cells, CD4/CD8), expression of activation markers on peripheral blood mononuclears investigated with monoclonal antibodies of BMA and OKT series, and serum neopterin concentration. |
| 491 | 2693822 | Group I patients had low CD4/CD8 and increased number of CD 8 cells, 1a/DR-positive lymphocytes (28.6 +/- 7%), OKT9-positive lymphocytes (8.0 +/- 4.7%), activated neopterin synthesis registered neither in group 2 patients nor donors. |
| 492 | 2693822 | Diabetic patients with the disease duration less than 1 year (group 1 eight patients with diabetes mellitus type I and group 2 seven patients with diabetes mellitus type II) and 8 healthy donors were examined for subpopulations of lymphocytes (CD 3-, CD 4-, CD 8-, CD 20-positive cells, CD4/CD8), expression of activation markers on peripheral blood mononuclears investigated with monoclonal antibodies of BMA and OKT series, and serum neopterin concentration. |
| 493 | 2693822 | Group I patients had low CD4/CD8 and increased number of CD 8 cells, 1a/DR-positive lymphocytes (28.6 +/- 7%), OKT9-positive lymphocytes (8.0 +/- 4.7%), activated neopterin synthesis registered neither in group 2 patients nor donors. |
| 494 | 2695566 | No differences in total lymphocyte count, percentage of B cells, percentage of total T cells (CD3), helper-inducer T cells (CD4) or cytotoxic-suppressor cells (CD8), lymphocyte blastogenesis assays, or pokeweed mitogen-induced IgG secretion in T & B cell co-cultures were detected before therapy. |
| 495 | 2962799 | Normalization of the CD4/CD8 lymphocyte ratio and increased B lymphocytes in long standing diabetic patients following therapy with thymopentin. |
| 496 | 2962799 | A double blind study with thymopentin (TP5) and placebo was performed in 49 patients affected by Type 1 and Type 2 diabetes of long duration characterized by a reduction of the CD4/CD8 (helper/suppressor) lymphocyte ratio. |
| 497 | 2962799 | Data showed a statistically significant increase of the CD4/CD8 lymphocyte ratio (p less than 0.02) and of the percentage of B lymphocytes (p less than 0.001) only in the TP5 receiving group. |
| 498 | 2962799 | Normalization of the CD4/CD8 lymphocyte ratio and increased B lymphocytes in long standing diabetic patients following therapy with thymopentin. |
| 499 | 2962799 | A double blind study with thymopentin (TP5) and placebo was performed in 49 patients affected by Type 1 and Type 2 diabetes of long duration characterized by a reduction of the CD4/CD8 (helper/suppressor) lymphocyte ratio. |
| 500 | 2962799 | Data showed a statistically significant increase of the CD4/CD8 lymphocyte ratio (p less than 0.02) and of the percentage of B lymphocytes (p less than 0.001) only in the TP5 receiving group. |
| 501 | 2962799 | Normalization of the CD4/CD8 lymphocyte ratio and increased B lymphocytes in long standing diabetic patients following therapy with thymopentin. |
| 502 | 2962799 | A double blind study with thymopentin (TP5) and placebo was performed in 49 patients affected by Type 1 and Type 2 diabetes of long duration characterized by a reduction of the CD4/CD8 (helper/suppressor) lymphocyte ratio. |
| 503 | 2962799 | Data showed a statistically significant increase of the CD4/CD8 lymphocyte ratio (p less than 0.02) and of the percentage of B lymphocytes (p less than 0.001) only in the TP5 receiving group. |
| 504 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 505 | 2972427 | Twenty-five recently diagnosed insulin-dependent diabetic patients were screened for the presence of activated T lymphocytes using the anti-IL-2 receptor monoclonal antibody; thirteen had elevated levels of activated T lymphocytes. |
| 506 | 2972427 | The activated cells were mostly confined to the CD4 subset, with the CD4/CD8 ratio in IL-2 receptor expressing cells averaging 5 +/- 1 (s.d.) compared with 1.3 +/- 0.3 for all T cells. |
| 507 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 508 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 509 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 510 | 2972427 | Twenty-five recently diagnosed insulin-dependent diabetic patients were screened for the presence of activated T lymphocytes using the anti-IL-2 receptor monoclonal antibody; thirteen had elevated levels of activated T lymphocytes. |
| 511 | 2972427 | The activated cells were mostly confined to the CD4 subset, with the CD4/CD8 ratio in IL-2 receptor expressing cells averaging 5 +/- 1 (s.d.) compared with 1.3 +/- 0.3 for all T cells. |
| 512 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 513 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 514 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 515 | 2972427 | Twenty-five recently diagnosed insulin-dependent diabetic patients were screened for the presence of activated T lymphocytes using the anti-IL-2 receptor monoclonal antibody; thirteen had elevated levels of activated T lymphocytes. |
| 516 | 2972427 | The activated cells were mostly confined to the CD4 subset, with the CD4/CD8 ratio in IL-2 receptor expressing cells averaging 5 +/- 1 (s.d.) compared with 1.3 +/- 0.3 for all T cells. |
| 517 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 518 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 519 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 520 | 2972427 | Twenty-five recently diagnosed insulin-dependent diabetic patients were screened for the presence of activated T lymphocytes using the anti-IL-2 receptor monoclonal antibody; thirteen had elevated levels of activated T lymphocytes. |
| 521 | 2972427 | The activated cells were mostly confined to the CD4 subset, with the CD4/CD8 ratio in IL-2 receptor expressing cells averaging 5 +/- 1 (s.d.) compared with 1.3 +/- 0.3 for all T cells. |
| 522 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 523 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 524 | 3010443 | However, in the presence of CD4+ T cells, CD8+ cells were able to mount a substantial proliferation when stimulated with soluble antigens. |
| 525 | 3071440 | Neither CD3+ (pan) T-lymphocytes, CD4+ (helper) T-cells, CD8+ (suppressor/cytotoxic) T-cells, the relation between CD4+ and CD8+ T-cells, nor the total amount of lymphocytes, changed significantly between the first, second, and third examination. |
| 526 | 3135758 | The infiltrates within native pancreatic islets and islet grafts were comprised predominantly of Ia+ cells (dendritic cells and macrophages) CD4+ cells (helper/inducer lymphocytes and macrophages), CD5+ (pan-T) cells and smaller numbers of CD8+ (cytotoxic/suppressor and NK) cells. |
| 527 | 3259951 | The T-cell surface glycoprotein CD4 plays an important role in mediating cellular immunity and serves as the receptor for human immunodeficiency virus. |
| 528 | 3280182 | Children with newly diagnosed insulin-dependent diabetes mellitus (IDDM) had increased numbers of CD25 positive lymphocytes in peripheral blood and peripheral blood mononuclear cells responded to insulin antigens by proliferation. |
| 529 | 3280182 | The CD25 positivity and insulin proliferation were associated to the duration of symptoms before the diagnosis of IDDM. |
| 530 | 3280182 | Children with IDDM also had increased numbers of CD4 positive T cells in peripheral blood. |
| 531 | 3286489 | The results indicate that the cells responding to insulin were T cells mainly of the helper (CD4+) phenotype and that they required adherent cells of the monocyte/macrophage lineage for proliferation to occur. |
| 532 | 3293350 | An increased percentage of T cells (CD3+ cells) expressing class II antigens was seen in 19 out of 25 patients and class II expression was observed on cells within both the CD4+ and CD8+ T cell subsets. |
| 533 | 3500476 | In the course of characterizing human T-cell tumors with an immature (CD4-, CD8-) surface phenotype, we detected a 2-kilobase alpha-related transcript. |
| 534 | 3652617 | The ultrastructure of peripheral blood lymphocyte subsets and activated lymphocytes from 5 patients with recent onset insulin-dependent diabetes as identified by monoclonal antibodies (CD4, CD8 and 4F2) and labelled with gold coupled goat anti-mouse IgG are described and depicted. |
| 535 | 7482726 | This contrasts with the dependence of islet allograft rejection on both CD4+ and CD8+ T cells. |
| 536 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 537 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 538 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 539 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 540 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 541 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 542 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 543 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 544 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 545 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 546 | 7510012 | Immunohistochemical staining showed abundant insulin-positive cells at the graft site, with small numbers of CD4- and CD8-positive cells present in the vicinity of the normal-appearing islets. |
| 547 | 7512875 | Flow cytometric analysis of lymphocyte subsets in blood and spleen also showed no significant differences, but in the thymus the percentage of immature CD4/CD8 "double positive" cells increased while the more mature CD3"high", and CD4 or CD8 "single-positive" cells decreased. |
| 548 | 7512990 | An adoptive transfer model of insulin-dependent diabetes mellitus (IDDM) in the nonobese diabetic mouse was used to examine the roles of alpha 4-integrin, vascular cell adhesion molecule 1 (VCAM-1); and intercellular adhesion molecule 1 (ICAM-1) in the pathogenesis of autoimmune diabetes. |
| 549 | 7512990 | Antibodies specific for ICAM-1 had little effect on the onset or incidence of IDDM. |
| 550 | 7512990 | In addition, the cascade of events leading to T cell transit across endothelium may be different for CD4 and CD8 cells, and may differ depending on the endothelium involved. |
| 551 | 7515343 | Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. |
| 552 | 7515343 | The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. |
| 553 | 7515343 | In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. |
| 554 | 7515343 | The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. |
| 555 | 7515343 | However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). |
| 556 | 7515343 | Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. |
| 557 | 7515343 | Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. |
| 558 | 7515343 | The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. |
| 559 | 7515343 | In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. |
| 560 | 7515343 | The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. |
| 561 | 7515343 | However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). |
| 562 | 7515343 | Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. |
| 563 | 7515343 | Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. |
| 564 | 7515343 | The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. |
| 565 | 7515343 | In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. |
| 566 | 7515343 | The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. |
| 567 | 7515343 | However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). |
| 568 | 7515343 | Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. |
| 569 | 7515343 | Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. |
| 570 | 7515343 | The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. |
| 571 | 7515343 | In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. |
| 572 | 7515343 | The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. |
| 573 | 7515343 | However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). |
| 574 | 7515343 | Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. |
| 575 | 7515343 | Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. |
| 576 | 7515343 | The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. |
| 577 | 7515343 | In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. |
| 578 | 7515343 | The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. |
| 579 | 7515343 | However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). |
| 580 | 7515343 | Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. |
| 581 | 7515343 | Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. |
| 582 | 7515343 | The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. |
| 583 | 7515343 | In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. |
| 584 | 7515343 | The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. |
| 585 | 7515343 | However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). |
| 586 | 7515343 | Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. |
| 587 | 7519242 | Higher autoantibody levels and recognition of a linear NH2-terminal epitope in the autoantigen GAD65, distinguish stiff-man syndrome from insulin-dependent diabetes mellitus. |
| 588 | 7519242 | Thus, destruction of pancreatic beta cells, which results in insulin-dependent diabetes mellitus (IDDM), and impairment of GABA-ergic synaptic transmission in Stiff-Man syndrome (SMS) are both characterized by circulating autoantibodies to GAD65. |
| 589 | 7519242 | Here we report the characterization of humoral autoimmune responses to GAD65 in 35 SMS patients, of whom 13 (37%) also had IDDM. |
| 590 | 7519242 | All SMS patients immunoprecipitated native GAD65 and the main titers were orders of magnitude higher than in IDDM patients. |
| 591 | 7519242 | Furthermore, in contrast to the situation in IDDM, autoantibodies in 35 of 35 (100%) of SMS patients recognized denatured GAD65 on Western blots. |
| 592 | 7519242 | The first pattern, detected in 25 of 35 SMS patients (71%), of whom 11 had IDDM (44%), was predominantly reactive with a linear NH2-terminal epitope residing in the first eight amino acids of GAD65. |
| 593 | 7519242 | The second epitope pattern may represent epitope spreading in the GAD65 molecule, but may also include some cases of epitope recognition associated with IDDM resistant HLA-haplotypes. |
| 594 | 7519242 | The principal NH2-terminal linear epitope in GAD65 distinguishes the reactivity of SMS and IDDM autoantibodies and may be a determinant of pathogenicity for GABA-ergic neurons. |
| 595 | 7519242 | The greater magnitude and distinct specificity of the humoral response to GAD65 in SMS may reflect a biased involvement of the T helper cell type 2 (Th2) subset of CD4+ T cells and antibody responses, whereas IDDM is likely mediated by the Th1 subset of CD4+ T cells and cytotoxic T cell responses. |
| 596 | 7525431 | Reduced numbers of CD8+ T cells and B cell-expression of Leu-8 antigen in peripheral blood of patients with primary biliary cirrhosis. |
| 597 | 7525431 | In PBC the proportion of PBMC that were CD4+ was normal; in contrast, the proportion that were CD8+ was decreased (p < 0.01). |
| 598 | 7525431 | These findings suggest that in peripheral blood of PBC patients reduced numbers of T cells may occur due to a selective intrahepatic sequestration of CD8+ T cells, and that the decreased expression of Leu-8 antigen by B cells may be associated with their participation in autoimmune processes. |
| 599 | 7534735 | A CD8+ T-lymphocyte-mediated and CD4+ T-lymphocyte-independent autoimmune diabetes of early onset in transgenic mice. |
| 600 | 7534735 | While transgenic mice expressing tumour necrosis factor-alpha under the control of the beta-cell-specific insulin promoter display a marked lymphocytic infiltration of the islets, they never develop insulin-dependent diabetes mellitus (IDDM). |
| 601 | 7534735 | These results indicate that while tumour necrosis factor-alpha induced lymphocytic infiltration is not sufficient to effect beta-cell destruction, locally co-stimulated islet-infiltrating CD8+ T lymphocytes could play a critical role in the development of IDDM. |
| 602 | 7540575 | Transgenic mice that express mouse B7-1 (mB7-1, recently designated CD80) on their pancreatic beta-cells maintain normal islet architecture, have normal pancreatic insulin content, and only rarely spontaneously develop insulitis and diabetes. |
| 603 | 7540575 | While this insulitis resolved in the nontransgenic mice, the islet-infiltrating CD4+ and CD8+ T-cells in the transgenic mice were associated with complete beta-cell destruction. |
| 604 | 7545875 | Autorecognition of many self-proteins by CD4+ T lymphocytes is restricted by the products of class II immune response genes of the major histocompatibility complex (MHC), and in human type I diabetes such a MHC association has been described. |
| 605 | 7545875 | The present study uses a rat MHC class II (RT1.Bl) peptide binding motif to predict potentially autoreactive CD4+ T cell epitopes in two key islet beta-cell constituents: the enzyme glutamic acid decarboxylase (GAD) and the insulin precursor hormone proinsulin (PI). |
| 606 | 7545875 | Seventeen-amino-acid-long peptide fragments of GAD and PI containing the binding motif were synthesized and used to generate peptide-specific, MHC class II-restricted, CD4+ T cell lines. |
| 607 | 7545875 | Once established, the T cell lines specific for rat islet GAD and PI were adoptively transferred to naive, MHC-compatible rats. |
| 608 | 7545875 | Autorecognition of many self-proteins by CD4+ T lymphocytes is restricted by the products of class II immune response genes of the major histocompatibility complex (MHC), and in human type I diabetes such a MHC association has been described. |
| 609 | 7545875 | The present study uses a rat MHC class II (RT1.Bl) peptide binding motif to predict potentially autoreactive CD4+ T cell epitopes in two key islet beta-cell constituents: the enzyme glutamic acid decarboxylase (GAD) and the insulin precursor hormone proinsulin (PI). |
| 610 | 7545875 | Seventeen-amino-acid-long peptide fragments of GAD and PI containing the binding motif were synthesized and used to generate peptide-specific, MHC class II-restricted, CD4+ T cell lines. |
| 611 | 7545875 | Once established, the T cell lines specific for rat islet GAD and PI were adoptively transferred to naive, MHC-compatible rats. |
| 612 | 7545875 | Autorecognition of many self-proteins by CD4+ T lymphocytes is restricted by the products of class II immune response genes of the major histocompatibility complex (MHC), and in human type I diabetes such a MHC association has been described. |
| 613 | 7545875 | The present study uses a rat MHC class II (RT1.Bl) peptide binding motif to predict potentially autoreactive CD4+ T cell epitopes in two key islet beta-cell constituents: the enzyme glutamic acid decarboxylase (GAD) and the insulin precursor hormone proinsulin (PI). |
| 614 | 7545875 | Seventeen-amino-acid-long peptide fragments of GAD and PI containing the binding motif were synthesized and used to generate peptide-specific, MHC class II-restricted, CD4+ T cell lines. |
| 615 | 7545875 | Once established, the T cell lines specific for rat islet GAD and PI were adoptively transferred to naive, MHC-compatible rats. |
| 616 | 7554346 | Increased and decreased relative risk for non-insulin-dependent diabetes mellitus conferred by HLA class II and by CD4 alleles. |
| 617 | 7554346 | In this study the association of HLA class II alleles and genotypes and the association of CD4 and CD3 polymorphisms were assessed in a large number of Belgian non-insulin-dependent diabetes mellitus patients. |
| 618 | 7554346 | These results therefore suggest that HLA class II and CD4 genes might independently contribute to the susceptibility for non-insulin-dependent diabetes mellitus and that these alleles and genotypes might identify subgroups of patients with different susceptibilities. |
| 619 | 7554346 | Increased and decreased relative risk for non-insulin-dependent diabetes mellitus conferred by HLA class II and by CD4 alleles. |
| 620 | 7554346 | In this study the association of HLA class II alleles and genotypes and the association of CD4 and CD3 polymorphisms were assessed in a large number of Belgian non-insulin-dependent diabetes mellitus patients. |
| 621 | 7554346 | These results therefore suggest that HLA class II and CD4 genes might independently contribute to the susceptibility for non-insulin-dependent diabetes mellitus and that these alleles and genotypes might identify subgroups of patients with different susceptibilities. |
| 622 | 7554346 | Increased and decreased relative risk for non-insulin-dependent diabetes mellitus conferred by HLA class II and by CD4 alleles. |
| 623 | 7554346 | In this study the association of HLA class II alleles and genotypes and the association of CD4 and CD3 polymorphisms were assessed in a large number of Belgian non-insulin-dependent diabetes mellitus patients. |
| 624 | 7554346 | These results therefore suggest that HLA class II and CD4 genes might independently contribute to the susceptibility for non-insulin-dependent diabetes mellitus and that these alleles and genotypes might identify subgroups of patients with different susceptibilities. |
| 625 | 7578872 | In parallel studies, normal Swiss male mice given stz at a similar dose developed diabetes (10/10) associated with insulitis which consisted predominantly of CD4, CD8 and MAC-1 cells. |
| 626 | 7578887 | The percentage of CD4+PBL was higher in NOD/Smrf females than males, was intermediate in [NOD X NON] F1 mice and approximated a 1:1 distribution in F1 mice backcrossed to either NOD or NON parental strains, suggesting primary control of the phenotype by an incompletely dominant gene, but not excluding additional effects by other genes. |
| 627 | 7578887 | We term this primary gene Tlf(T lymphocyte frequency) because it also influenced the percentage of CD8+ T cells, although to lesser extent and independently from the MHC previously shown to lower the CD8+ T cell fraction in NON mice. |
| 628 | 7578887 | Dihydrotestosterone simultaneously lowered CD4+ PBL levels and prevented diabetes in NOD females while, in vitro, it had a differential effect on Con A elicited cytokines, increasing IL-2 22% and decreasing IL-4 39% (p < 0.0001). |
| 629 | 7578887 | The percentage of CD4+PBL was higher in NOD/Smrf females than males, was intermediate in [NOD X NON] F1 mice and approximated a 1:1 distribution in F1 mice backcrossed to either NOD or NON parental strains, suggesting primary control of the phenotype by an incompletely dominant gene, but not excluding additional effects by other genes. |
| 630 | 7578887 | We term this primary gene Tlf(T lymphocyte frequency) because it also influenced the percentage of CD8+ T cells, although to lesser extent and independently from the MHC previously shown to lower the CD8+ T cell fraction in NON mice. |
| 631 | 7578887 | Dihydrotestosterone simultaneously lowered CD4+ PBL levels and prevented diabetes in NOD females while, in vitro, it had a differential effect on Con A elicited cytokines, increasing IL-2 22% and decreasing IL-4 39% (p < 0.0001). |
| 632 | 7586687 | Insulin-like growth factor-1 (IGF-1) protects NOD mice from insulitis and diabetes. |
| 633 | 7586687 | The percentages of CD4+ and CD8+ T cells in the spleen of experimental mice were similar. |
| 634 | 7587921 | This study was undertaken to determine whether this reduced lymphocyte proliferation is mediated by a decreased production of cytokine or decreased expression of interleukin-2 receptor (IL-2R). |
| 635 | 7587921 | However, the production of IL-1 beta, IL-2 and interferon-gamma, the percentages of pan T cells (CD3), T helper cells (CD4), T suppressor cells (CD8), the ratio of CD4/CD8 and the expression of CR1 and Fc receptors for immunoglobulin G (Fc gamma RII and Fc gamma RIII) were not significantly different between NIDDM patients and healthy subjects. |
| 636 | 7587921 | These findings suggest that decreased expression of CR3 on monocytes, decreased lymphocyte proliferation and decreased IL-2R expression despite a higher production of TNF-alpha may explain the impaired cell-mediated immunity seen in NIDDM patients. |
| 637 | 7589146 | Autoimmune gastritis, induced by day-3 thymectomy of BALB/c mice, is a destructive CD4+ T cell-mediated disease characterized by leukocyte infiltrates in the gastric mucosa, loss of parietal and chief cells and anti-gastric H/K ATPase autoantibodies. |
| 638 | 7589848 | Aberrant activation of CD8+ T-cell and CD8+ T-cell subsets in patients with newly diagnosed IDDM. |
| 639 | 7589848 | Two- and three-color cytofluorimetric techniques were used to study the expression patterns of the activation antigen HLA-DR on peripheral blood immunoregulatory T-cells from 25 patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM) and 14 age- and sex-matched control subjects. |
| 640 | 7589848 | In control subjects, basal activation of CD4+ and CD8+ lymphocytes accounted for the low percentage levels of activated T-cells. |
| 641 | 7589848 | In contrast, the majority of IDDM patients showed an unbalanced activation of CD4+ and CD8+ lymphocytes with predominant activation of the CD8+ lymphocyte subset. |
| 642 | 7589848 | The composition of the activated T-cell fraction was dependent on the composition of the total (activated + nonactivated) T-cell population, as indicated by the positive correlation between the CD4+/CD8+ T-cell ratios in these two cell populations (r = 0.714; P < 0.001). |
| 643 | 7589848 | Analysis of the CD11b-defined subsets revealed predominant activation of CD8+ CD11b- (cytotoxic) T-cells; CD8+ CD16+ HLA-DR+ natural killer cells were unchanged. |
| 644 | 7589848 | The distribution of HLA-DR+ cells among subsets of CD4+ T-cells differed from the pattern in the CD8+ population in that selective activation of CD4+ CD45RA- (memory, helper-inducer) cells accounted for the small increase in activated CD4+ cells. |
| 645 | 7589848 | Aberrant activation of CD8+ T-cell and CD8+ T-cell subsets in patients with newly diagnosed IDDM. |
| 646 | 7589848 | Two- and three-color cytofluorimetric techniques were used to study the expression patterns of the activation antigen HLA-DR on peripheral blood immunoregulatory T-cells from 25 patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM) and 14 age- and sex-matched control subjects. |
| 647 | 7589848 | In control subjects, basal activation of CD4+ and CD8+ lymphocytes accounted for the low percentage levels of activated T-cells. |
| 648 | 7589848 | In contrast, the majority of IDDM patients showed an unbalanced activation of CD4+ and CD8+ lymphocytes with predominant activation of the CD8+ lymphocyte subset. |
| 649 | 7589848 | The composition of the activated T-cell fraction was dependent on the composition of the total (activated + nonactivated) T-cell population, as indicated by the positive correlation between the CD4+/CD8+ T-cell ratios in these two cell populations (r = 0.714; P < 0.001). |
| 650 | 7589848 | Analysis of the CD11b-defined subsets revealed predominant activation of CD8+ CD11b- (cytotoxic) T-cells; CD8+ CD16+ HLA-DR+ natural killer cells were unchanged. |
| 651 | 7589848 | The distribution of HLA-DR+ cells among subsets of CD4+ T-cells differed from the pattern in the CD8+ population in that selective activation of CD4+ CD45RA- (memory, helper-inducer) cells accounted for the small increase in activated CD4+ cells. |
| 652 | 7589848 | Aberrant activation of CD8+ T-cell and CD8+ T-cell subsets in patients with newly diagnosed IDDM. |
| 653 | 7589848 | Two- and three-color cytofluorimetric techniques were used to study the expression patterns of the activation antigen HLA-DR on peripheral blood immunoregulatory T-cells from 25 patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM) and 14 age- and sex-matched control subjects. |
| 654 | 7589848 | In control subjects, basal activation of CD4+ and CD8+ lymphocytes accounted for the low percentage levels of activated T-cells. |
| 655 | 7589848 | In contrast, the majority of IDDM patients showed an unbalanced activation of CD4+ and CD8+ lymphocytes with predominant activation of the CD8+ lymphocyte subset. |
| 656 | 7589848 | The composition of the activated T-cell fraction was dependent on the composition of the total (activated + nonactivated) T-cell population, as indicated by the positive correlation between the CD4+/CD8+ T-cell ratios in these two cell populations (r = 0.714; P < 0.001). |
| 657 | 7589848 | Analysis of the CD11b-defined subsets revealed predominant activation of CD8+ CD11b- (cytotoxic) T-cells; CD8+ CD16+ HLA-DR+ natural killer cells were unchanged. |
| 658 | 7589848 | The distribution of HLA-DR+ cells among subsets of CD4+ T-cells differed from the pattern in the CD8+ population in that selective activation of CD4+ CD45RA- (memory, helper-inducer) cells accounted for the small increase in activated CD4+ cells. |
| 659 | 7589848 | Aberrant activation of CD8+ T-cell and CD8+ T-cell subsets in patients with newly diagnosed IDDM. |
| 660 | 7589848 | Two- and three-color cytofluorimetric techniques were used to study the expression patterns of the activation antigen HLA-DR on peripheral blood immunoregulatory T-cells from 25 patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM) and 14 age- and sex-matched control subjects. |
| 661 | 7589848 | In control subjects, basal activation of CD4+ and CD8+ lymphocytes accounted for the low percentage levels of activated T-cells. |
| 662 | 7589848 | In contrast, the majority of IDDM patients showed an unbalanced activation of CD4+ and CD8+ lymphocytes with predominant activation of the CD8+ lymphocyte subset. |
| 663 | 7589848 | The composition of the activated T-cell fraction was dependent on the composition of the total (activated + nonactivated) T-cell population, as indicated by the positive correlation between the CD4+/CD8+ T-cell ratios in these two cell populations (r = 0.714; P < 0.001). |
| 664 | 7589848 | Analysis of the CD11b-defined subsets revealed predominant activation of CD8+ CD11b- (cytotoxic) T-cells; CD8+ CD16+ HLA-DR+ natural killer cells were unchanged. |
| 665 | 7589848 | The distribution of HLA-DR+ cells among subsets of CD4+ T-cells differed from the pattern in the CD8+ population in that selective activation of CD4+ CD45RA- (memory, helper-inducer) cells accounted for the small increase in activated CD4+ cells. |
| 666 | 7589882 | Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients. |
| 667 | 7589882 | No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). |
| 668 | 7589882 | We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (< 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. |
| 669 | 7589882 | When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3+ and CD4+ CD45R0+ T-cell populations was reduced significantly in IDDM patients (46.8 +/- 15.4 vs 79.6 +/- 11.7; 25.7 +/- 3.8 vs 47.15 +/- 5.7, respectively; p < 0.001). |
| 670 | 7589882 | Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. |
| 671 | 7590418 | The factors determining the outcome of human fetal islet transplantation in patients with insulin-dependent diabetes mellitus (IDDM) remain unclarified. |
| 672 | 7590418 | After transplantation we evaluated simultaneously the level of metabolic control through HbA1c values determined by chromatography, the capacity of insulin secretion through the C-peptide levels (determined by radioimmunoassay) before and 6 minutes after 1 mg glucagon i.v. stimulation, and the ratio between CD4+ and CD8+ lymphocytes determined by immunofluorescence using monoclonal antibodies. |
| 673 | 7590418 | However, the loss of islet function was preceded by the increase in CD4+/CD8+ ratio, thus reflecting the presumable accumulation of CD4+ inducer T-lymphocytes. |
| 674 | 7590418 | When the islet secretion capacity was destroyed, we found a decrease in CD4+/CD8+ ratio, reflecting the recruitment of CD8+ effector cells. |
| 675 | 7590418 | The factors determining the outcome of human fetal islet transplantation in patients with insulin-dependent diabetes mellitus (IDDM) remain unclarified. |
| 676 | 7590418 | After transplantation we evaluated simultaneously the level of metabolic control through HbA1c values determined by chromatography, the capacity of insulin secretion through the C-peptide levels (determined by radioimmunoassay) before and 6 minutes after 1 mg glucagon i.v. stimulation, and the ratio between CD4+ and CD8+ lymphocytes determined by immunofluorescence using monoclonal antibodies. |
| 677 | 7590418 | However, the loss of islet function was preceded by the increase in CD4+/CD8+ ratio, thus reflecting the presumable accumulation of CD4+ inducer T-lymphocytes. |
| 678 | 7590418 | When the islet secretion capacity was destroyed, we found a decrease in CD4+/CD8+ ratio, reflecting the recruitment of CD8+ effector cells. |
| 679 | 7590418 | The factors determining the outcome of human fetal islet transplantation in patients with insulin-dependent diabetes mellitus (IDDM) remain unclarified. |
| 680 | 7590418 | After transplantation we evaluated simultaneously the level of metabolic control through HbA1c values determined by chromatography, the capacity of insulin secretion through the C-peptide levels (determined by radioimmunoassay) before and 6 minutes after 1 mg glucagon i.v. stimulation, and the ratio between CD4+ and CD8+ lymphocytes determined by immunofluorescence using monoclonal antibodies. |
| 681 | 7590418 | However, the loss of islet function was preceded by the increase in CD4+/CD8+ ratio, thus reflecting the presumable accumulation of CD4+ inducer T-lymphocytes. |
| 682 | 7590418 | When the islet secretion capacity was destroyed, we found a decrease in CD4+/CD8+ ratio, reflecting the recruitment of CD8+ effector cells. |
| 683 | 7612149 | Lymphocytes were also characterized for the expression of CD4 and CD8 T cell markers and, within each population, for the expression of activation markers (CD25, CD69) and adhesion markers (CD51, CD54, CD11b, CD49e, L-selectin). |
| 684 | 7612149 | Significantly increased levels of CD4+CD8+ double-positive and CD4-CD8- double-negative T cell populations were observed in the infiltrating lymphocytes as compared with peripheral lymphocytes. |
| 685 | 7612149 | In addition, within both CD4 and CD8 subpopulations isolated from islet infiltrates, CD11b+ and CD49e+ cells were increased with respect to the same subset of cells isolated from the periphery. |
| 686 | 7612149 | In contrast, the level of cells that expressed L-selectin was significantly higher in the periphery for both CD4+ and CD8+ cells than for infiltrating cells. |
| 687 | 7612149 | Lymphocytes were also characterized for the expression of CD4 and CD8 T cell markers and, within each population, for the expression of activation markers (CD25, CD69) and adhesion markers (CD51, CD54, CD11b, CD49e, L-selectin). |
| 688 | 7612149 | Significantly increased levels of CD4+CD8+ double-positive and CD4-CD8- double-negative T cell populations were observed in the infiltrating lymphocytes as compared with peripheral lymphocytes. |
| 689 | 7612149 | In addition, within both CD4 and CD8 subpopulations isolated from islet infiltrates, CD11b+ and CD49e+ cells were increased with respect to the same subset of cells isolated from the periphery. |
| 690 | 7612149 | In contrast, the level of cells that expressed L-selectin was significantly higher in the periphery for both CD4+ and CD8+ cells than for infiltrating cells. |
| 691 | 7612149 | Lymphocytes were also characterized for the expression of CD4 and CD8 T cell markers and, within each population, for the expression of activation markers (CD25, CD69) and adhesion markers (CD51, CD54, CD11b, CD49e, L-selectin). |
| 692 | 7612149 | Significantly increased levels of CD4+CD8+ double-positive and CD4-CD8- double-negative T cell populations were observed in the infiltrating lymphocytes as compared with peripheral lymphocytes. |
| 693 | 7612149 | In addition, within both CD4 and CD8 subpopulations isolated from islet infiltrates, CD11b+ and CD49e+ cells were increased with respect to the same subset of cells isolated from the periphery. |
| 694 | 7612149 | In contrast, the level of cells that expressed L-selectin was significantly higher in the periphery for both CD4+ and CD8+ cells than for infiltrating cells. |
| 695 | 7612149 | Lymphocytes were also characterized for the expression of CD4 and CD8 T cell markers and, within each population, for the expression of activation markers (CD25, CD69) and adhesion markers (CD51, CD54, CD11b, CD49e, L-selectin). |
| 696 | 7612149 | Significantly increased levels of CD4+CD8+ double-positive and CD4-CD8- double-negative T cell populations were observed in the infiltrating lymphocytes as compared with peripheral lymphocytes. |
| 697 | 7612149 | In addition, within both CD4 and CD8 subpopulations isolated from islet infiltrates, CD11b+ and CD49e+ cells were increased with respect to the same subset of cells isolated from the periphery. |
| 698 | 7612149 | In contrast, the level of cells that expressed L-selectin was significantly higher in the periphery for both CD4+ and CD8+ cells than for infiltrating cells. |
| 699 | 7621990 | Intrathymic transplantation of islet antigen affects CD8+ diabetogenic T-cells resulting in tolerance to autoimmune IDDM. |
| 700 | 7621990 | Normally, islet antigens that are involved in insulin-dependent diabetes mellitus (IDDM) are not present in the thymus, but we have previously shown that transplantation of islets expressing relevant antigens into the thymus at the time of T-cell maturation results in prevention of IDDM in the multidose streptozotocin model of diabetes mellitus (MDSDM). |
| 701 | 7621990 | Although both CD4+ and CD8+ T-cells are involved in the pathogenesis of this disease, the cells affected by intrathymic transplantation of islets are unknown. |
| 702 | 7621990 | Streptozotocin (STZ)-treated syngeneic islets were transplanted into the thymuses of C57BL/KsJ mice, and CD4+, CD8+, or both subsets of cells were transiently depleted with monoclonal antibodies (mAbs). |
| 703 | 7621990 | Intrathymic transplantation of islet antigen affects CD8+ diabetogenic T-cells resulting in tolerance to autoimmune IDDM. |
| 704 | 7621990 | Normally, islet antigens that are involved in insulin-dependent diabetes mellitus (IDDM) are not present in the thymus, but we have previously shown that transplantation of islets expressing relevant antigens into the thymus at the time of T-cell maturation results in prevention of IDDM in the multidose streptozotocin model of diabetes mellitus (MDSDM). |
| 705 | 7621990 | Although both CD4+ and CD8+ T-cells are involved in the pathogenesis of this disease, the cells affected by intrathymic transplantation of islets are unknown. |
| 706 | 7621990 | Streptozotocin (STZ)-treated syngeneic islets were transplanted into the thymuses of C57BL/KsJ mice, and CD4+, CD8+, or both subsets of cells were transiently depleted with monoclonal antibodies (mAbs). |
| 707 | 7647584 | Markers of cell-mediated immune activation were studied in 32 Chinese patients with recent-onset insulin-dependent diabetes mellitus (IDDM) as compared with 12 patients with recent-onset non-insulin-dependent diabetes mellitus (NIDDM) and 34 normal subjects. |
| 708 | 7647584 | Sera were assessed for soluble markers of T-cell activation (sCD4, sCD8, sIL-2R); the cytokines (IL-1 beta, TNF-alpha, IL-2, IL-6), and T-cell subsets were also determined. |
| 709 | 7647584 | Three IDDM patients had detectable IL-1 beta and this weakly so (< 3.5 pg/ml). |
| 710 | 7647584 | However, the other cytokine data and the frequency of activated T-cells, CD4+, CD8+ T-cell subsets and CD4:CD8 ratio showed no significant differences among the IDDM, NIDDM and normal subjects. |
| 711 | 7660685 | The uniform finding is that T cells are made hyporesponsive, and that the most likely mechanism is one of active suppression mediated through the selective activation of T cells, of either CD4+ or CD8+ phenotype, that make cytokines which in turn can suppress pathological T cells responsible for the disease lesions. |
| 712 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 713 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 714 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 715 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 716 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 717 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 718 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 719 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 720 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 721 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 722 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 723 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 724 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 725 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 726 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 727 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 728 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 729 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 730 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 731 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 732 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 733 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 734 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 735 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 736 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 737 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 738 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 739 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 740 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 741 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 742 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 743 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 744 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 745 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 746 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 747 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 748 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 749 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 750 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 751 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 752 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 753 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 754 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 755 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 756 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 757 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 758 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 759 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 760 | 7684344 | Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients. |
| 761 | 7684344 | The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes. |
| 762 | 7684344 | CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations. |
| 763 | 7684344 | Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004). |
| 764 | 7684344 | This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014). |
| 765 | 7684344 | The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects. |
| 766 | 7684344 | Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells. |
| 767 | 7696203 | Local production of human IL-6 promotes insulitis but retards the onset of insulin-dependent diabetes mellitus in non-obese diabetic mice. |
| 768 | 7696203 | Immunohistochemistry reveals these cells to be predominantly CD4+, CD8+, B220+ cells. |
| 769 | 7696203 | Transgenic rat insulin promoter-IL-6 mice were therefore also made on an inbred NOD background. |
| 770 | 7714099 | Activation of T lymphocyte subsets by synthetic TSH receptor peptides and recombinant glutamate decarboxylase in autoimmune thyroid disease and insulin-dependent diabetes. |
| 771 | 7714099 | In this context, we have measured the proliferative responses of peripheral blood mononuclear cells (PBMC) to the synthetic peptides corresponding to the extracellular domain of the TSH receptor (TSHR) and recombinant glutamate decarboxylase (GAD65) by means of 3H thymidine incorporation. |
| 772 | 7714099 | We have also studied the antigenic activation of CD4+ and CD8+ T lymphocytes by measuring human leukocyte antigen-DR (HLA-DR) expression on the cell surface by flow cytometric analysis. |
| 773 | 7714099 | PBMC obtained from 47 patients with Graves' disease (GD) [including 19 hyperthyroid GD (hyper GD)], 18 with Hashimoto's thyroiditis (HT), 7 with nontoxic nodular goiter (NG), 18 with insulin-dependent diabetes (IDDM), and 20 normal controls (N), were cultured for 7 days in the presence or absence of the pool peptides representing 3 different segments of TSHR or GAD65 at final concentration of 30 micrograms/mL or 10 micrograms/mL. |
| 774 | 7714099 | The proportion of subjects whose PBMC gave a positive proliferative response with a stimulation index (SI) of over 2.3 (i.e. above the mean +2 SD for N) to TSHR peptides was significantly higher in the hyper GD group than among euthyroid GD (eu GD), HT, IDDM, and N group. |
| 775 | 7714099 | The CD4+ T lymphocytes from hyper GD group were significantly more activated by TSHR peptides compared to eu GD, HT, IDDM, and N, and this induction correlated to their thyroid hormone levels. |
| 776 | 7714099 | Quite differently, the activation of CD8+ T lymphocytes from both hyper GD and eu GD group in response to TSHR peptides was impaired compared to HT, IDDM, and the N group; in contrast to the findings with CD4+ T lymphocytes, this was independent of thyroid hormone levels. |
| 777 | 7714099 | On the other hand, while the CD8+ T lymphocytes from GD and N groups were activated equally by GAD65, the activation of CD8+ T lymphocytes from the IDDM group by GAD65 was impaired compared to the GD and N groups. |
| 778 | 7714099 | In conclusion, the activation of CD8+ T lymphocytes from GD and IDDM by relevant antigens (i.e. |
| 779 | 7714099 | TSHR peptides for GD and GAD65 for IDDM) was impaired, but not by irrelevant antigens (i.e. |
| 780 | 7714099 | GAD65 for GD and TSHR peptides for IDDM). |
| 781 | 7714099 | There was also a modest stimulation of CD8+ T cells from all groups by tetanus toxoid and cardiac myosin light chain peptide, both irrelevant antigens. |
| 782 | 7714099 | Activation of T lymphocyte subsets by synthetic TSH receptor peptides and recombinant glutamate decarboxylase in autoimmune thyroid disease and insulin-dependent diabetes. |
| 783 | 7714099 | In this context, we have measured the proliferative responses of peripheral blood mononuclear cells (PBMC) to the synthetic peptides corresponding to the extracellular domain of the TSH receptor (TSHR) and recombinant glutamate decarboxylase (GAD65) by means of 3H thymidine incorporation. |
| 784 | 7714099 | We have also studied the antigenic activation of CD4+ and CD8+ T lymphocytes by measuring human leukocyte antigen-DR (HLA-DR) expression on the cell surface by flow cytometric analysis. |
| 785 | 7714099 | PBMC obtained from 47 patients with Graves' disease (GD) [including 19 hyperthyroid GD (hyper GD)], 18 with Hashimoto's thyroiditis (HT), 7 with nontoxic nodular goiter (NG), 18 with insulin-dependent diabetes (IDDM), and 20 normal controls (N), were cultured for 7 days in the presence or absence of the pool peptides representing 3 different segments of TSHR or GAD65 at final concentration of 30 micrograms/mL or 10 micrograms/mL. |
| 786 | 7714099 | The proportion of subjects whose PBMC gave a positive proliferative response with a stimulation index (SI) of over 2.3 (i.e. above the mean +2 SD for N) to TSHR peptides was significantly higher in the hyper GD group than among euthyroid GD (eu GD), HT, IDDM, and N group. |
| 787 | 7714099 | The CD4+ T lymphocytes from hyper GD group were significantly more activated by TSHR peptides compared to eu GD, HT, IDDM, and N, and this induction correlated to their thyroid hormone levels. |
| 788 | 7714099 | Quite differently, the activation of CD8+ T lymphocytes from both hyper GD and eu GD group in response to TSHR peptides was impaired compared to HT, IDDM, and the N group; in contrast to the findings with CD4+ T lymphocytes, this was independent of thyroid hormone levels. |
| 789 | 7714099 | On the other hand, while the CD8+ T lymphocytes from GD and N groups were activated equally by GAD65, the activation of CD8+ T lymphocytes from the IDDM group by GAD65 was impaired compared to the GD and N groups. |
| 790 | 7714099 | In conclusion, the activation of CD8+ T lymphocytes from GD and IDDM by relevant antigens (i.e. |
| 791 | 7714099 | TSHR peptides for GD and GAD65 for IDDM) was impaired, but not by irrelevant antigens (i.e. |
| 792 | 7714099 | GAD65 for GD and TSHR peptides for IDDM). |
| 793 | 7714099 | There was also a modest stimulation of CD8+ T cells from all groups by tetanus toxoid and cardiac myosin light chain peptide, both irrelevant antigens. |
| 794 | 7714099 | Activation of T lymphocyte subsets by synthetic TSH receptor peptides and recombinant glutamate decarboxylase in autoimmune thyroid disease and insulin-dependent diabetes. |
| 795 | 7714099 | In this context, we have measured the proliferative responses of peripheral blood mononuclear cells (PBMC) to the synthetic peptides corresponding to the extracellular domain of the TSH receptor (TSHR) and recombinant glutamate decarboxylase (GAD65) by means of 3H thymidine incorporation. |
| 796 | 7714099 | We have also studied the antigenic activation of CD4+ and CD8+ T lymphocytes by measuring human leukocyte antigen-DR (HLA-DR) expression on the cell surface by flow cytometric analysis. |
| 797 | 7714099 | PBMC obtained from 47 patients with Graves' disease (GD) [including 19 hyperthyroid GD (hyper GD)], 18 with Hashimoto's thyroiditis (HT), 7 with nontoxic nodular goiter (NG), 18 with insulin-dependent diabetes (IDDM), and 20 normal controls (N), were cultured for 7 days in the presence or absence of the pool peptides representing 3 different segments of TSHR or GAD65 at final concentration of 30 micrograms/mL or 10 micrograms/mL. |
| 798 | 7714099 | The proportion of subjects whose PBMC gave a positive proliferative response with a stimulation index (SI) of over 2.3 (i.e. above the mean +2 SD for N) to TSHR peptides was significantly higher in the hyper GD group than among euthyroid GD (eu GD), HT, IDDM, and N group. |
| 799 | 7714099 | The CD4+ T lymphocytes from hyper GD group were significantly more activated by TSHR peptides compared to eu GD, HT, IDDM, and N, and this induction correlated to their thyroid hormone levels. |
| 800 | 7714099 | Quite differently, the activation of CD8+ T lymphocytes from both hyper GD and eu GD group in response to TSHR peptides was impaired compared to HT, IDDM, and the N group; in contrast to the findings with CD4+ T lymphocytes, this was independent of thyroid hormone levels. |
| 801 | 7714099 | On the other hand, while the CD8+ T lymphocytes from GD and N groups were activated equally by GAD65, the activation of CD8+ T lymphocytes from the IDDM group by GAD65 was impaired compared to the GD and N groups. |
| 802 | 7714099 | In conclusion, the activation of CD8+ T lymphocytes from GD and IDDM by relevant antigens (i.e. |
| 803 | 7714099 | TSHR peptides for GD and GAD65 for IDDM) was impaired, but not by irrelevant antigens (i.e. |
| 804 | 7714099 | GAD65 for GD and TSHR peptides for IDDM). |
| 805 | 7714099 | There was also a modest stimulation of CD8+ T cells from all groups by tetanus toxoid and cardiac myosin light chain peptide, both irrelevant antigens. |
| 806 | 7729614 | The time required to transfer insulin-dependent diabetes mellitus (IDDM) using islet-infiltrating lymphocytes from young prediabetic mice (25 +/- 9 days) was not statistically different from the time required to transfer IDDM using splenocytes from overtly diabetic mice (32 +/- 5 days). |
| 807 | 7729614 | Cotransfer of splenocyte cells or CD4+, but not CD8+ spleen cells, from 60- to 80-day-old prediabetic female NOD mice together with either splenocytes from diabetic mice or islet-infiltrating lymphocytes from prediabetic NOD mice delayed the rapid transfer of IDDM, suggesting that CD4+ cells mediated immunoregulation. |
| 808 | 7756046 | Serum osteocalcin was found to be lower in patients who, according to the Centers for Disease Control (CDC) classification, had greater disease severity, and showed a positive correlation with the number of CD4+ T lymphocytes. |
| 809 | 7790825 | We report the isolation of a panel of CD4+ T helper type 1 autoreactive T cell clones from the spleen of unprimed nonobese diabetic mice, a murine model of human insulin-dependent diabetes mellitus. |
| 810 | 7792922 | Long-term dual treatment may be required to inactivate CD4+ and CD8+ T cells in the NOD/Lt mouse to prevent both autoimmune disease recurrence and rejection. |
| 811 | 7798703 | The number of lymphocytes and their subsets (CD3+, CD+, CD8+, 4/8 ratio, IL-2R+) did not significantly differ between the groups, but in GI patients, the number of OKIa1 positive lymphocytes were significantly lower than in GII the day before and 7 days after the operation. |
| 812 | 7798703 | IL-2 production in GII was significantly correlated to the number of CD4 positive lymphocytes, but this was not true in GI. |
| 813 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 814 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 815 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 816 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 817 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 818 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 819 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 820 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 821 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 822 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 823 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 824 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 825 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 826 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 827 | 7819154 | beta 2-Microglobulin (beta 2m)-deficient non-obese diabetic (NOD) mice were established by crossing beta 2m-deficient 129/Sv mice with NOD mice, and used to examine the possible involvement of MHC class I molecules and CD8+ T cells in the development of insulitis and diabetes. |
| 828 | 7819154 | These findings support the notion that the expression of MHC class I molecules and/or CD8+ T cells plays an essential role in the infiltration of CD4+ T cells in islets as well as the development of diabetes in NOD mice. |
| 829 | 7834277 | Improved risk assessment for insulin-dependent diabetes mellitus by analysis of amino acids in HLA-DQ and DRB1 loci. |
| 830 | 7834277 | Polymorphisms in HLA class II genes have been shown to contribute to susceptibility or protection against insulin-dependent diabetes mellitus (IDDM). |
| 831 | 7834277 | In the present study the role of HLA class II haplotypes and the role of DQ alpha Arg52, DQ beta Asp57 and of polymorphic amino acids, located in the antigen-binding groove and the CD4-binding domain of the DR beta 1 chain, were studied in 210 unrelated Caucasian IDDM patients and 205 controls. |
| 832 | 7834277 | Our findings confirm that protection against IDDM is provided by HLA-DQ loci but that susceptibility for IDDM is provided by both HLA-DRB1 and DQB1 loci. |
| 833 | 7835983 | The precise role of immune cells in beta cell killing and their manner of invasion of pancreatic islets in insulin-dependent diabetes mellitus (IDDM) are unclear. |
| 834 | 7835983 | Immunohistochemical analysis showed that the islet engrafted cells were of CD4 and CD8 phenotype. |
| 835 | 7836934 | T cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice. |
| 836 | 7836934 | Administration of interleukin 12 (IL-12), a key cytokine which guides the development of T helper type 1 (Th1) CD4+ T cells, induces rapid onset of IDDM in NOD, but not in BALB/c mice. |
| 837 | 7836934 | CD4+ pancreas-infiltrating T cells, after activation by insolubilized anti T cell receptor antibody, secrete high levels of interferon gamma and low levels of IL-4. |
| 838 | 7836934 | Therefore, IL-12 administration accelerates IDDM development in genetically susceptible NOD mice, and this correlates with increased Th1 cytokine production by islet-infiltrating cells. |
| 839 | 7836934 | T cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice. |
| 840 | 7836934 | Administration of interleukin 12 (IL-12), a key cytokine which guides the development of T helper type 1 (Th1) CD4+ T cells, induces rapid onset of IDDM in NOD, but not in BALB/c mice. |
| 841 | 7836934 | CD4+ pancreas-infiltrating T cells, after activation by insolubilized anti T cell receptor antibody, secrete high levels of interferon gamma and low levels of IL-4. |
| 842 | 7836934 | Therefore, IL-12 administration accelerates IDDM development in genetically susceptible NOD mice, and this correlates with increased Th1 cytokine production by islet-infiltrating cells. |
| 843 | 7840857 | Oral administration of human insulin to NOD mice generates CD4+ T cells that suppress adoptive transfer of diabetes. |
| 844 | 7840857 | When T cell subsets from insulin-fed animals were co-injected with diabetogenic T cells, only purified CD4+ T cells were able to transfer protection since only 3/12 mice became diabetic after 36 days in comparison to 3/6 in the group co-injected with CD4+ T cells from PBS-fed animals, or 5/6 in the group injected with CD8+ T cells. |
| 845 | 7840857 | Oral administration of human insulin to NOD mice generates CD4+ T cells that suppress adoptive transfer of diabetes. |
| 846 | 7840857 | When T cell subsets from insulin-fed animals were co-injected with diabetogenic T cells, only purified CD4+ T cells were able to transfer protection since only 3/12 mice became diabetic after 36 days in comparison to 3/6 in the group co-injected with CD4+ T cells from PBS-fed animals, or 5/6 in the group injected with CD8+ T cells. |
| 847 | 7860729 | The participation of IL-2 in insulin-dependent (type 1) diabetes (IDDM) was analyzed in transgenic (tg) mice expressing the nucleoprotein (NP) of lymphocytic choriomeningitis virus and IL-2 under control of the rat insulin promoter focally in beta cells of the islets of Langerhans. |
| 848 | 7860729 | Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. |
| 849 | 7860729 | Infiltration primarily of CD4 and B lymphocytes and increased expression of MHC class I and II molecules occurred in islets where IL-2 was expressed. |
| 850 | 7860729 | In contrast, viral inoculum to single tg mice expressing either the viral protein or IL-2 failed to enhance the incidence of IDDM over 30% for viral protein or 10% for IL-2 after an 8-mo observation period. |
| 851 | 7860747 | Insulin immunization of nonobese diabetic mice induces a protective insulitis characterized by diminished intraislet interferon-gamma transcription. |
| 852 | 7860747 | Adoptive transfer of splenocytes from B-chain insulin-immunized mice prevented diabetes in recipients co-infused with diabetogenic spleen cells, an effect that was abolished by prior in vivo elimination of either CD4+ or CD8+ cells. |
| 853 | 7860747 | Insulin immunization did not reduce the extent of intraislet inflammation (insulitis); however, it did abolish expression of IFN-gamma mRNA within the insulitis lesions. |
| 854 | 7865456 | To examine the role of IL-2 in the regulation of peripheral tolerance we produced transgenic mice in which the expression of murine IL-2 was directed by the rat insulin II promoter. |
| 855 | 7865456 | The infiltrate consisted primarily of B cells and CD4+ and CD8+ T cells. |
| 856 | 7868915 | Beta-cell-cytotoxic CD8+ T cells from nonobese diabetic mice use highly homologous T cell receptor alpha-chain CDR3 sequences. |
| 857 | 7868915 | Insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a cell-mediated autoimmune process against pancreatic beta-cells. |
| 858 | 7868915 | We have shown that beta-cell-cytotoxic CD8+ T cell clones can transfer IDDM to irradiated NOD mice if co-injected with nondiabetogenic CD4+ spleen T cells. |
| 859 | 7868915 | To determine whether CTLs recruited to pancreatic islets recognize a restricted set of local Ags, we sequenced TCR-alpha and TCR-beta cDNA generated by anchor PCR from CD8+ CTL lines and clones derived from islets of 10 different NOD mice. |
| 860 | 7868915 | By contrast, none of 31 different TCR-alpha rearrangements used by CD8+ spleen T cells encoded motifs 1 or 2, and only one encoded motif 3. |
| 861 | 7868915 | Skewed TCR-alpha-CDR3 usage by islet-derived CTLs was substantiated further by isolation of CTL clones transcribing highly homologous TCR-alpha, but different TCR-beta, rearrangements. |
| 862 | 7888038 | Adoptive transfer of autoimmune diabetes mellitus to athymic rats: synergy of CD4+ and CD8+ T cells and prevention by RT6+ T cells. |
| 863 | 7888038 | We describe the induction and prevention of autoimmune insulin dependent diabetes mellitus (IDDM), and its pathological substrate, insulitis, in congenitally athymic nude rats following injections of major histocompatibility complex (MHC) compatible lymph node T cells. |
| 864 | 7888038 | It was also observed that both CD4+ and CD8+ T cells are required for efficient transfer of autoimmunity. |
| 865 | 7888038 | The data indicate that, as in the NOD mouse, a synergistic interaction between CD4+ and CD8+ T cells is important for beta cell destruction. |
| 866 | 7888038 | Adoptive transfer of autoimmune diabetes mellitus to athymic rats: synergy of CD4+ and CD8+ T cells and prevention by RT6+ T cells. |
| 867 | 7888038 | We describe the induction and prevention of autoimmune insulin dependent diabetes mellitus (IDDM), and its pathological substrate, insulitis, in congenitally athymic nude rats following injections of major histocompatibility complex (MHC) compatible lymph node T cells. |
| 868 | 7888038 | It was also observed that both CD4+ and CD8+ T cells are required for efficient transfer of autoimmunity. |
| 869 | 7888038 | The data indicate that, as in the NOD mouse, a synergistic interaction between CD4+ and CD8+ T cells is important for beta cell destruction. |
| 870 | 7888038 | Adoptive transfer of autoimmune diabetes mellitus to athymic rats: synergy of CD4+ and CD8+ T cells and prevention by RT6+ T cells. |
| 871 | 7888038 | We describe the induction and prevention of autoimmune insulin dependent diabetes mellitus (IDDM), and its pathological substrate, insulitis, in congenitally athymic nude rats following injections of major histocompatibility complex (MHC) compatible lymph node T cells. |
| 872 | 7888038 | It was also observed that both CD4+ and CD8+ T cells are required for efficient transfer of autoimmunity. |
| 873 | 7888038 | The data indicate that, as in the NOD mouse, a synergistic interaction between CD4+ and CD8+ T cells is important for beta cell destruction. |
| 874 | 7889411 | We developed two distinct transgenic mouse models in which virus induced insulin-dependent (type 1) diabetes mellitus (IDDM). |
| 875 | 7889411 | By contrast, induction of an anti-self (anti-viral) CD8+ CTL response to the same virus later in life caused IDDM (incidence < 90%) in both transgenic lines, although the kinetics and requirements for CD4 help, the affinity and avidity of CD8+ CTL differed in each line. |
| 876 | 7889411 | CD4+ T cells played no detectable role, since their depletion failed to alter either the kinetics or incidence of IDDM. |
| 877 | 7889411 | Disease was dependent on T cell help, since deletion of CD4+ cells completely circumvented the IDDM. |
| 878 | 7889411 | We developed two distinct transgenic mouse models in which virus induced insulin-dependent (type 1) diabetes mellitus (IDDM). |
| 879 | 7889411 | By contrast, induction of an anti-self (anti-viral) CD8+ CTL response to the same virus later in life caused IDDM (incidence < 90%) in both transgenic lines, although the kinetics and requirements for CD4 help, the affinity and avidity of CD8+ CTL differed in each line. |
| 880 | 7889411 | CD4+ T cells played no detectable role, since their depletion failed to alter either the kinetics or incidence of IDDM. |
| 881 | 7889411 | Disease was dependent on T cell help, since deletion of CD4+ cells completely circumvented the IDDM. |
| 882 | 7889411 | We developed two distinct transgenic mouse models in which virus induced insulin-dependent (type 1) diabetes mellitus (IDDM). |
| 883 | 7889411 | By contrast, induction of an anti-self (anti-viral) CD8+ CTL response to the same virus later in life caused IDDM (incidence < 90%) in both transgenic lines, although the kinetics and requirements for CD4 help, the affinity and avidity of CD8+ CTL differed in each line. |
| 884 | 7889411 | CD4+ T cells played no detectable role, since their depletion failed to alter either the kinetics or incidence of IDDM. |
| 885 | 7889411 | Disease was dependent on T cell help, since deletion of CD4+ cells completely circumvented the IDDM. |
| 886 | 7902104 | T-cell-T-cell collaboration in allogeneic responses traditionally has been viewed as the requirement for CD4+ T helper cells in the activation of CD8+ cytotoxic T cells. |
| 887 | 7902104 | In this regard, the role of the CD4+ T cell is primarily to provide growth factors, such as interleukin-2, on which the CD8+ T cell is dependent. |
| 888 | 7902104 | T-cell-T-cell collaboration in allogeneic responses traditionally has been viewed as the requirement for CD4+ T helper cells in the activation of CD8+ cytotoxic T cells. |
| 889 | 7902104 | In this regard, the role of the CD4+ T cell is primarily to provide growth factors, such as interleukin-2, on which the CD8+ T cell is dependent. |
| 890 | 7907110 | However, transfer of these clones, together with CD4(+)-rich NOD splenocytes depleted of CD8+ T cells, caused severe insulitis and diabetes. |
| 891 | 7909401 | The circulating autoantibodies to enterocytes in her serum were detected by indirect immunofluorescence technique and the impaired suppressor T (Ts) cell function was proved by plaque forming assay using bead-separated CD4 or CD8 T cells together with CD19 B cells. |
| 892 | 7909401 | The helper functions of adult CD4 T cells to induce Ig-secreting cells from adult and the patient were strikingly suppressed by adult CD8 T cells. |
| 893 | 7909401 | However, the CD8 T cells from the patient lost the ability to inhibit the induction of these Ig-secreting cells when stimulated with adult CD4 T cells. |
| 894 | 7909401 | Moreover, the patient's CD8 T cells stimulated rather than suppressed the induction of Ig-secreting cells from the patient when stimulated with the patient's CD4 T cells. |
| 895 | 7909401 | The circulating autoantibodies to enterocytes in her serum were detected by indirect immunofluorescence technique and the impaired suppressor T (Ts) cell function was proved by plaque forming assay using bead-separated CD4 or CD8 T cells together with CD19 B cells. |
| 896 | 7909401 | The helper functions of adult CD4 T cells to induce Ig-secreting cells from adult and the patient were strikingly suppressed by adult CD8 T cells. |
| 897 | 7909401 | However, the CD8 T cells from the patient lost the ability to inhibit the induction of these Ig-secreting cells when stimulated with adult CD4 T cells. |
| 898 | 7909401 | Moreover, the patient's CD8 T cells stimulated rather than suppressed the induction of Ig-secreting cells from the patient when stimulated with the patient's CD4 T cells. |
| 899 | 7909401 | The circulating autoantibodies to enterocytes in her serum were detected by indirect immunofluorescence technique and the impaired suppressor T (Ts) cell function was proved by plaque forming assay using bead-separated CD4 or CD8 T cells together with CD19 B cells. |
| 900 | 7909401 | The helper functions of adult CD4 T cells to induce Ig-secreting cells from adult and the patient were strikingly suppressed by adult CD8 T cells. |
| 901 | 7909401 | However, the CD8 T cells from the patient lost the ability to inhibit the induction of these Ig-secreting cells when stimulated with adult CD4 T cells. |
| 902 | 7909401 | Moreover, the patient's CD8 T cells stimulated rather than suppressed the induction of Ig-secreting cells from the patient when stimulated with the patient's CD4 T cells. |
| 903 | 7909401 | The circulating autoantibodies to enterocytes in her serum were detected by indirect immunofluorescence technique and the impaired suppressor T (Ts) cell function was proved by plaque forming assay using bead-separated CD4 or CD8 T cells together with CD19 B cells. |
| 904 | 7909401 | The helper functions of adult CD4 T cells to induce Ig-secreting cells from adult and the patient were strikingly suppressed by adult CD8 T cells. |
| 905 | 7909401 | However, the CD8 T cells from the patient lost the ability to inhibit the induction of these Ig-secreting cells when stimulated with adult CD4 T cells. |
| 906 | 7909401 | Moreover, the patient's CD8 T cells stimulated rather than suppressed the induction of Ig-secreting cells from the patient when stimulated with the patient's CD4 T cells. |
| 907 | 7925581 | The accelerating effect of IL-2 was present; but decreased, in NOD mice that lacked CD8+ T cells as well as in NOD SCID mice. |
| 908 | 7925581 | The implications are that in the NOD genetic background, the production of cytokines, such as IL-2, by islet-specific CD4+ T cells can lead to beta cell damage and diabetes and that CD8+ T cells may have a role in accelerating diabetes onset. |
| 909 | 7930594 | Flow cytometric analysis showed that BNY-2 cells were positive for CD4 and CD5 and were negative for CD8 and RT6, indicating that these cells were phenotypically Th cells rather than cytotoxic T cells. mAbs against rat MHC class II Ags (anti-RT1.D) blocked the proliferation response of BNY-2 cells, suggesting that these cells recognize the MHC class II Du molecule. |
| 910 | 7934613 | Both CD4 and CD8 T cells as well as macrophages are required for the development of diabetes in NOD mice. |
| 911 | 8018595 | Analysis of the T cells present in the pancreatic infiltrates of single-copy and homozygous rat insulin promoter IL-2 mice showed a predominance of CD4+ cells which was especially apparent in the very young mice. |
| 912 | 8024653 | Because of anatomical limitations, molecular characterization of islet-inflammatory T-cells in human insulin-dependent diabetes mellitus (IDDM) has remained elusive. |
| 913 | 8024653 | Most of the in vivo-activated isletitis T-cells were CD8+TcR alpha beta+ and CD4-CD8-TcR gamma delta+ in both patients. |
| 914 | 8025213 | Generally, there was an increase in the CD4:CD8 ratio in the peripheral lymphoid organs during the onset of insulitis which was largely due to an increase in the CD4 T cell population while the ratio decreased after the onset of diabetes. |
| 915 | 8025212 | From 3 patients with newly-diagnosed Type 1 diabetes 184 clones were generated, the majority of which (39%) were CD4+TCR alpha beta+, whilst 31% were CD8+TCR alpha beta+. |
| 916 | 8025212 | From 2 healthy control subjects 90 clones were obtained, of which 62% were CD4+TCR alpha beta+ and 33% were CD8+TCR alpha beta+. |
| 917 | 8025212 | From 3 patients with newly-diagnosed Type 1 diabetes 184 clones were generated, the majority of which (39%) were CD4+TCR alpha beta+, whilst 31% were CD8+TCR alpha beta+. |
| 918 | 8025212 | From 2 healthy control subjects 90 clones were obtained, of which 62% were CD4+TCR alpha beta+ and 33% were CD8+TCR alpha beta+. |
| 919 | 8030746 | Interleukin-6 (IL-6) is thought to be involved in the pathogenesis of autoimmune insulin-dependent diabetes mellitus. |
| 920 | 8030746 | In older RIP-IL6 mice, a more florid insulitis was observed which was composed predominantly of B220+ B lymphocytes and, to a lesser extent, Mac-1+ macrophages and CD4+ and CD8+ T lymphocytes. |
| 921 | 8033411 | After administration of CsA to newborn NOD mice, there was a reduction (P < 0.01) of both CD4+CD8- and CD4-CD8+ thymocytes, whereas the number of double positive CD4+CD8+ thymocytes was increased. |
| 922 | 8033411 | Both CD4+ and CD8+ spleen T cells were depleted. |
| 923 | 8033411 | After administration of CsA to newborn NOD mice, there was a reduction (P < 0.01) of both CD4+CD8- and CD4-CD8+ thymocytes, whereas the number of double positive CD4+CD8+ thymocytes was increased. |
| 924 | 8033411 | Both CD4+ and CD8+ spleen T cells were depleted. |
| 925 | 8056185 | In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. |
| 926 | 8056185 | On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. |
| 927 | 8056185 | Since IL-4 did not suppress IL-2 production, it would seem that the IL-2 producing subset in CD4+HLA-DR+ T cells is decreased in IDDM. |
| 928 | 8056185 | These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply. |
| 929 | 8056185 | In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. |
| 930 | 8056185 | On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. |
| 931 | 8056185 | Since IL-4 did not suppress IL-2 production, it would seem that the IL-2 producing subset in CD4+HLA-DR+ T cells is decreased in IDDM. |
| 932 | 8056185 | These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply. |
| 933 | 8056185 | In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. |
| 934 | 8056185 | On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. |
| 935 | 8056185 | Since IL-4 did not suppress IL-2 production, it would seem that the IL-2 producing subset in CD4+HLA-DR+ T cells is decreased in IDDM. |
| 936 | 8056185 | These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply. |
| 937 | 8082309 | Possible association of CD3 and CD4 polymorphisms with insulin-dependent diabetes mellitus (IDDM). |
| 938 | 8082309 | In the present study the association of polymorphisms in the CD4 and the delta subunit of CD3 with IDDM were examined in a Belgian population. |
| 939 | 8082309 | These results therefore suggest that CD4, CD3 or neighbouring genes might contribute to IDDM susceptibility. |
| 940 | 8082309 | Possible association of CD3 and CD4 polymorphisms with insulin-dependent diabetes mellitus (IDDM). |
| 941 | 8082309 | In the present study the association of polymorphisms in the CD4 and the delta subunit of CD3 with IDDM were examined in a Belgian population. |
| 942 | 8082309 | These results therefore suggest that CD4, CD3 or neighbouring genes might contribute to IDDM susceptibility. |
| 943 | 8082309 | Possible association of CD3 and CD4 polymorphisms with insulin-dependent diabetes mellitus (IDDM). |
| 944 | 8082309 | In the present study the association of polymorphisms in the CD4 and the delta subunit of CD3 with IDDM were examined in a Belgian population. |
| 945 | 8082309 | These results therefore suggest that CD4, CD3 or neighbouring genes might contribute to IDDM susceptibility. |
| 946 | 8093606 | Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. |
| 947 | 8093606 | Precise definition of the role of both CD4 and CD8 T-cell subsets from NOD mice in the adoptive transfer of diabetes has been complicated by the possibility that endogenous T-cells may be recruited. |
| 948 | 8093606 | However, the mean time to diabetes onset was doubled when CD4+ lymphocytes were isolated from prediabetic versus diabetic donors, and these transfers were complicated by the generation of small but significant numbers of CD8+ cells over time. |
| 949 | 8093606 | More rigorous exclusion of CD8+ cells by means of anti-CD8 MoAb treatment in vivo of the recipients of enriched CD4+ cells demonstrated a significant difference in the diabetogenic potency of CD4+ lymphocytes from diabetic versus nondiabetic donors. |
| 950 | 8093606 | Evidence is discussed indicating that the age-associated differences in ability of CD4+ T-cells to adoptively transfer diabetes in the absence of the CD8+ T-cells subset is a function of prior, chronic exposure of the CD4+ lymphocytes to beta-cell antigens in the donor. |
| 951 | 8093606 | Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. |
| 952 | 8093606 | Precise definition of the role of both CD4 and CD8 T-cell subsets from NOD mice in the adoptive transfer of diabetes has been complicated by the possibility that endogenous T-cells may be recruited. |
| 953 | 8093606 | However, the mean time to diabetes onset was doubled when CD4+ lymphocytes were isolated from prediabetic versus diabetic donors, and these transfers were complicated by the generation of small but significant numbers of CD8+ cells over time. |
| 954 | 8093606 | More rigorous exclusion of CD8+ cells by means of anti-CD8 MoAb treatment in vivo of the recipients of enriched CD4+ cells demonstrated a significant difference in the diabetogenic potency of CD4+ lymphocytes from diabetic versus nondiabetic donors. |
| 955 | 8093606 | Evidence is discussed indicating that the age-associated differences in ability of CD4+ T-cells to adoptively transfer diabetes in the absence of the CD8+ T-cells subset is a function of prior, chronic exposure of the CD4+ lymphocytes to beta-cell antigens in the donor. |
| 956 | 8093606 | Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. |
| 957 | 8093606 | Precise definition of the role of both CD4 and CD8 T-cell subsets from NOD mice in the adoptive transfer of diabetes has been complicated by the possibility that endogenous T-cells may be recruited. |
| 958 | 8093606 | However, the mean time to diabetes onset was doubled when CD4+ lymphocytes were isolated from prediabetic versus diabetic donors, and these transfers were complicated by the generation of small but significant numbers of CD8+ cells over time. |
| 959 | 8093606 | More rigorous exclusion of CD8+ cells by means of anti-CD8 MoAb treatment in vivo of the recipients of enriched CD4+ cells demonstrated a significant difference in the diabetogenic potency of CD4+ lymphocytes from diabetic versus nondiabetic donors. |
| 960 | 8093606 | Evidence is discussed indicating that the age-associated differences in ability of CD4+ T-cells to adoptively transfer diabetes in the absence of the CD8+ T-cells subset is a function of prior, chronic exposure of the CD4+ lymphocytes to beta-cell antigens in the donor. |
| 961 | 8093606 | Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. |
| 962 | 8093606 | Precise definition of the role of both CD4 and CD8 T-cell subsets from NOD mice in the adoptive transfer of diabetes has been complicated by the possibility that endogenous T-cells may be recruited. |
| 963 | 8093606 | However, the mean time to diabetes onset was doubled when CD4+ lymphocytes were isolated from prediabetic versus diabetic donors, and these transfers were complicated by the generation of small but significant numbers of CD8+ cells over time. |
| 964 | 8093606 | More rigorous exclusion of CD8+ cells by means of anti-CD8 MoAb treatment in vivo of the recipients of enriched CD4+ cells demonstrated a significant difference in the diabetogenic potency of CD4+ lymphocytes from diabetic versus nondiabetic donors. |
| 965 | 8093606 | Evidence is discussed indicating that the age-associated differences in ability of CD4+ T-cells to adoptively transfer diabetes in the absence of the CD8+ T-cells subset is a function of prior, chronic exposure of the CD4+ lymphocytes to beta-cell antigens in the donor. |
| 966 | 8093606 | Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. |
| 967 | 8093606 | Precise definition of the role of both CD4 and CD8 T-cell subsets from NOD mice in the adoptive transfer of diabetes has been complicated by the possibility that endogenous T-cells may be recruited. |
| 968 | 8093606 | However, the mean time to diabetes onset was doubled when CD4+ lymphocytes were isolated from prediabetic versus diabetic donors, and these transfers were complicated by the generation of small but significant numbers of CD8+ cells over time. |
| 969 | 8093606 | More rigorous exclusion of CD8+ cells by means of anti-CD8 MoAb treatment in vivo of the recipients of enriched CD4+ cells demonstrated a significant difference in the diabetogenic potency of CD4+ lymphocytes from diabetic versus nondiabetic donors. |
| 970 | 8093606 | Evidence is discussed indicating that the age-associated differences in ability of CD4+ T-cells to adoptively transfer diabetes in the absence of the CD8+ T-cells subset is a function of prior, chronic exposure of the CD4+ lymphocytes to beta-cell antigens in the donor. |
| 971 | 8094734 | Diabetes in these lymphopoenic rats was associated with extensive insulitis involving CD4+ and CD8+ T cells and macrophages. |
| 972 | 8094734 | The autoimmune diabetes and insulitis were completely prevented by the injection of a particular CD4+ T cell subset, isolated from healthy syngeneic donors, of the phenotype CD45RClow T cell receptor alpha/beta+ RT6+ Thy-1- OX-40-. |
| 973 | 8094734 | Cells of this protective phenotype, which make up about 5% of thoracic duct lymphocytes, were found to provide help for secondary antibody responses and produce interleukin 2 (IL-2) and IL-4, but no interferon gamma, on in vitro activation. |
| 974 | 8094734 | Diabetes in these lymphopoenic rats was associated with extensive insulitis involving CD4+ and CD8+ T cells and macrophages. |
| 975 | 8094734 | The autoimmune diabetes and insulitis were completely prevented by the injection of a particular CD4+ T cell subset, isolated from healthy syngeneic donors, of the phenotype CD45RClow T cell receptor alpha/beta+ RT6+ Thy-1- OX-40-. |
| 976 | 8094734 | Cells of this protective phenotype, which make up about 5% of thoracic duct lymphocytes, were found to provide help for secondary antibody responses and produce interleukin 2 (IL-2) and IL-4, but no interferon gamma, on in vitro activation. |
| 977 | 8095459 | This population, composed of CD4+ and CD8+ T cells, is presumably committed against the relevant beta cell antigens and is the most likely to reveal a bias in V gene usage if such a bias does indeed exist. |
| 978 | 8095459 | In contrast, the depletion of V beta 6-positive T cells results in a severe reduction of transfers, suggesting that V beta 6 gene is used with a relatively high frequency by diabetogenic CD4+ and/or CD8+ T cells. |
| 979 | 8095459 | This population, composed of CD4+ and CD8+ T cells, is presumably committed against the relevant beta cell antigens and is the most likely to reveal a bias in V gene usage if such a bias does indeed exist. |
| 980 | 8095459 | In contrast, the depletion of V beta 6-positive T cells results in a severe reduction of transfers, suggesting that V beta 6 gene is used with a relatively high frequency by diabetogenic CD4+ and/or CD8+ T cells. |
| 981 | 8096128 | A suppressor mechanism involving CD8+ T cells might be involved since in vitro these cells strongly proliferated in response to irradiated CD4+ V beta 8+ T cells that in blocking experiments with specific mAb was found to be class I major histocompatibility complex (MHC)-restricted. |
| 982 | 8096128 | Hence, T cells expressing the CD8 phenotype specifically respond to idiotypic or ergotypic determinants on the inducing activated CD4+V beta 8+ T cells and effectively suppress a diabetogenic disease process by a mechanism that may involve T-T cell interactions. |
| 983 | 8096128 | A suppressor mechanism involving CD8+ T cells might be involved since in vitro these cells strongly proliferated in response to irradiated CD4+ V beta 8+ T cells that in blocking experiments with specific mAb was found to be class I major histocompatibility complex (MHC)-restricted. |
| 984 | 8096128 | Hence, T cells expressing the CD8 phenotype specifically respond to idiotypic or ergotypic determinants on the inducing activated CD4+V beta 8+ T cells and effectively suppress a diabetogenic disease process by a mechanism that may involve T-T cell interactions. |
| 985 | 8098501 | Administration of morphine significantly inhibited the phorbol myristate acetate (PMA)-stimulated increase in interleukin-2 receptor (IL-2R) expression in both CD4+ and CD8+ mouse T cells. |
| 986 | 8098501 | In contrast, morphine treatment had no effect on PMA/calcium ionophore (A23187)-induced increase in IL-2 secretion, suggesting a selective inhibition of IL-2R expression. |
| 987 | 8098501 | Moreover, adrenalectomy abolished this effect of morphine in CD4+ but not CD8+ T cells, suggesting that the inhibitory effect of morphine on IL-2R expression in CD4+ T cells may be mediated through a morphine-induced increase in corticosteroid levels. |
| 988 | 8098501 | Administration of morphine significantly inhibited the phorbol myristate acetate (PMA)-stimulated increase in interleukin-2 receptor (IL-2R) expression in both CD4+ and CD8+ mouse T cells. |
| 989 | 8098501 | In contrast, morphine treatment had no effect on PMA/calcium ionophore (A23187)-induced increase in IL-2 secretion, suggesting a selective inhibition of IL-2R expression. |
| 990 | 8098501 | Moreover, adrenalectomy abolished this effect of morphine in CD4+ but not CD8+ T cells, suggesting that the inhibitory effect of morphine on IL-2R expression in CD4+ T cells may be mediated through a morphine-induced increase in corticosteroid levels. |
| 991 | 8098666 | To analyze of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, we have been doing a series of studies on the induction of insulitis and diabetes in NOD athymic nude mice by means of T cell transfer. |
| 992 | 8098666 | On the other hand, transfer of either CD4+ cell-depleted or CD8+ cell-depleted splenic lymphocytes of diabetic mice did not cause diabetes at least up to 60 days after the cell transfer. |
| 993 | 8098666 | However, insulitis was less potent in this group of mice than in the diabetic recipients given both subsets: only a low insulitis score was obtained and a number of beta-cells remained alive despite the insulitis in mice given the CD8+ T cell-depleted fraction, whereas islet damage was very severe and insulin-secreting beta-cells were no longer detected in the diabetic mice. |
| 994 | 8098666 | Consideration of our results together with earlier findings led to the conclusion that CD4+ T cells are primarily responsible for insulitis and that CD8+ T cells migrate into islets and are differentiated into mature killer cells against beta-cells with the aid of CD4+ T cells in both spontaneous and cyclophosphamide-induced diabetes. |
| 995 | 8098666 | To analyze of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, we have been doing a series of studies on the induction of insulitis and diabetes in NOD athymic nude mice by means of T cell transfer. |
| 996 | 8098666 | On the other hand, transfer of either CD4+ cell-depleted or CD8+ cell-depleted splenic lymphocytes of diabetic mice did not cause diabetes at least up to 60 days after the cell transfer. |
| 997 | 8098666 | However, insulitis was less potent in this group of mice than in the diabetic recipients given both subsets: only a low insulitis score was obtained and a number of beta-cells remained alive despite the insulitis in mice given the CD8+ T cell-depleted fraction, whereas islet damage was very severe and insulin-secreting beta-cells were no longer detected in the diabetic mice. |
| 998 | 8098666 | Consideration of our results together with earlier findings led to the conclusion that CD4+ T cells are primarily responsible for insulitis and that CD8+ T cells migrate into islets and are differentiated into mature killer cells against beta-cells with the aid of CD4+ T cells in both spontaneous and cyclophosphamide-induced diabetes. |
| 999 | 8098666 | To analyze of the roles of CD4+ and CD8+ T cells in the pathogenesis of this mouse, we have been doing a series of studies on the induction of insulitis and diabetes in NOD athymic nude mice by means of T cell transfer. |
| 1000 | 8098666 | On the other hand, transfer of either CD4+ cell-depleted or CD8+ cell-depleted splenic lymphocytes of diabetic mice did not cause diabetes at least up to 60 days after the cell transfer. |
| 1001 | 8098666 | However, insulitis was less potent in this group of mice than in the diabetic recipients given both subsets: only a low insulitis score was obtained and a number of beta-cells remained alive despite the insulitis in mice given the CD8+ T cell-depleted fraction, whereas islet damage was very severe and insulin-secreting beta-cells were no longer detected in the diabetic mice. |
| 1002 | 8098666 | Consideration of our results together with earlier findings led to the conclusion that CD4+ T cells are primarily responsible for insulitis and that CD8+ T cells migrate into islets and are differentiated into mature killer cells against beta-cells with the aid of CD4+ T cells in both spontaneous and cyclophosphamide-induced diabetes. |
| 1003 | 8100268 | A scattered infiltration of macrophages (M pi) precedes localized accumulations of CD4+ and CD8+ T lymphocytes, B lymphocytes, and M pi. |
| 1004 | 8100268 | The endothelium lining small vessels was highly activated in areas of inflammation, as the endothelial cells became cuboidal, and exhibited increased expression of major histocompatibility complex class II (Ia), intercellular adhesion molecule 1, and von Willebrand Factor. |
| 1005 | 8101546 | Presentation of beta-cell antigens to CD4+ and CD8+ T cells of non-obese diabetic mice. |
| 1006 | 8101546 | We isolated CD4+ and CD8+ T cell clones from pancreatic islets of non-obese diabetic (NOD) mice and studied their interactions with pancreatic islets, in culture. |
| 1007 | 8101546 | The two CD8+ T cell clones proliferated and released IFN-gamma upon reaction with islet cells from either NOD or BALB/c but not B6 mice. |
| 1008 | 8101546 | For optimal transfer of disease, the CD4+ T cell clones had to be co-injected with CD8+ T cells from NOD diabetic mice. |
| 1009 | 8101546 | Presentation of beta-cell antigens to CD4+ and CD8+ T cells of non-obese diabetic mice. |
| 1010 | 8101546 | We isolated CD4+ and CD8+ T cell clones from pancreatic islets of non-obese diabetic (NOD) mice and studied their interactions with pancreatic islets, in culture. |
| 1011 | 8101546 | The two CD8+ T cell clones proliferated and released IFN-gamma upon reaction with islet cells from either NOD or BALB/c but not B6 mice. |
| 1012 | 8101546 | For optimal transfer of disease, the CD4+ T cell clones had to be co-injected with CD8+ T cells from NOD diabetic mice. |
| 1013 | 8101546 | Presentation of beta-cell antigens to CD4+ and CD8+ T cells of non-obese diabetic mice. |
| 1014 | 8101546 | We isolated CD4+ and CD8+ T cell clones from pancreatic islets of non-obese diabetic (NOD) mice and studied their interactions with pancreatic islets, in culture. |
| 1015 | 8101546 | The two CD8+ T cell clones proliferated and released IFN-gamma upon reaction with islet cells from either NOD or BALB/c but not B6 mice. |
| 1016 | 8101546 | For optimal transfer of disease, the CD4+ T cell clones had to be co-injected with CD8+ T cells from NOD diabetic mice. |
| 1017 | 8101862 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease marked by hyperglycemia and mononuclear cell infiltration of insulin-producing beta islet cells. |
| 1018 | 8101862 | Predisposition to IDDM in humans has been linked to the class II major histocompatibility complex (MHC), and islet cells often become aberrantly class II positive during the course of the disease. |
| 1019 | 8101862 | These results suggest that in this model of autoimmune diabetes, CD4+ T cells and MHC class II molecules are not required for the development of disease. |
| 1020 | 8102088 | Progressive disease was found to be associated with the presence in the serum of IgA, IgE, and IgG1 Candida-reactive specific antibodies, absent footpad reactions, and elevated production in vitro of the Th2 cytokines IL-4, IL-6, and IL-10 but not the Th1 cytokine IFN-gamma. |
| 1021 | 8102088 | Both the Th2 and Th1 (IL-2 and IFN-gamma) cytokines were produced in vitro by CD4+ lymphocytes from noninfected diabetic mice that, in addition, showed a noticeable footpad reaction to Candida antigens. |
| 1022 | 8105789 | Three were CD8+ and five CD4+. |
| 1023 | 8105789 | The results indicate that practically all the lines (11 out of 12), irrespective of their CD4/CD8 phenotype or V beta expression, can exert cell-mediated cytotoxicity when their TCR/CD3 complex is linked to a target cell. |
| 1024 | 8105789 | Three were CD8+ and five CD4+. |
| 1025 | 8105789 | The results indicate that practically all the lines (11 out of 12), irrespective of their CD4/CD8 phenotype or V beta expression, can exert cell-mediated cytotoxicity when their TCR/CD3 complex is linked to a target cell. |
| 1026 | 8105989 | Results indicate that 1) cytokine mRNA profiles exhibited by islet-infiltrating cells of female and male NOD mice were quite similar with the exception of IL-6 expression and the marked differences in the levels of IL-2 receptor and IL-1 alpha mRNA, 2) CD4+ T lymphocytes expressed IL-4, presumably IL-5, and occasionally IL-10 mRNA but no detectable IL-2 mRNA, 3) CD8+ T lymphocytes exhibited TNF-beta, perforin and high levels of IFN-gamma, and 4) IL-7 was expressed in the islet at very high levels. |
| 1027 | 8119667 | They may be CD4+ or CD8+ and recognize autologous T cells in the presence of autologous PBMC as feeder cells. |
| 1028 | 8163049 | Using two and three colour cytofluorimetry, we studied total and activated (HLA-DR+) CD3+, CD4+, CD8+, lymphocytes and on CD4+ lymphocytes the CD45RA/RO "naive" and "memory" cell phenotypes. |
| 1029 | 8163049 | Amongst the siblings and parents, possession of HLA-DR4 was associated with lower percentages of CD4+ and higher percentages of CD8+ T cells. |
| 1030 | 8163049 | Using two and three colour cytofluorimetry, we studied total and activated (HLA-DR+) CD3+, CD4+, CD8+, lymphocytes and on CD4+ lymphocytes the CD45RA/RO "naive" and "memory" cell phenotypes. |
| 1031 | 8163049 | Amongst the siblings and parents, possession of HLA-DR4 was associated with lower percentages of CD4+ and higher percentages of CD8+ T cells. |
| 1032 | 8178053 | It consists of HLA class I genes and molecules (A, B and C) which control CD8+ cell-mediated antiviral responses, and class II genes and molecules (DR, DQ and DP) which control CD4+ cell responses (anti-bacterial and anti-toxin). |
| 1033 | 8178053 | HLA molecules function by presenting antigenic peptides to CD8+ cells (class I) and CD4+ cells (class II). |
| 1034 | 8178053 | It consists of HLA class I genes and molecules (A, B and C) which control CD8+ cell-mediated antiviral responses, and class II genes and molecules (DR, DQ and DP) which control CD4+ cell responses (anti-bacterial and anti-toxin). |
| 1035 | 8178053 | HLA molecules function by presenting antigenic peptides to CD8+ cells (class I) and CD4+ cells (class II). |
| 1036 | 8201786 | The infiltrating cells were almost all lymphocytes, and the ratio of CD4 to CD8 was 3.8. |
| 1037 | 8207221 | Lymphocytes infiltrating salivary glands expressed LFA-1 and Pgp-1 although Mel-14 Ag was absent. |
| 1038 | 8207221 | With regard to peripheral lymphocytes, the proportion of CD4 and CD8 cells expressing Mel-14 was decreased in the infiltrated islets, whereas the expression of LFA-1, Pgp-1, and LPAM-1/2 was increased. |
| 1039 | 8207221 | Moreover, the proportion of CD4, CD8, and B lymphocytes expressing CD69 was increased in the pancreas. |
| 1040 | 8207221 | Lymphocytes infiltrating salivary glands expressed LFA-1 and Pgp-1 although Mel-14 Ag was absent. |
| 1041 | 8207221 | With regard to peripheral lymphocytes, the proportion of CD4 and CD8 cells expressing Mel-14 was decreased in the infiltrated islets, whereas the expression of LFA-1, Pgp-1, and LPAM-1/2 was increased. |
| 1042 | 8207221 | Moreover, the proportion of CD4, CD8, and B lymphocytes expressing CD69 was increased in the pancreas. |
| 1043 | 8218826 | The thymus of these mice was also found to have an increased proportion of CD3+ thymocytes while CD4/CD8 double positive thymocytes decreased 7 d after CP. |
| 1044 | 8227346 | We examined pancreas biopsy specimens from 18 newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients to elucidate the mechanism underlying beta cell destruction. |
| 1045 | 8227346 | Infiltrating mononuclear cells consisted of CD4+T, CD8+T, B lymphocytes, and macrophages. |
| 1046 | 8227346 | The expression of intercellular adhesion molecule-1 was increased in endothelial cells in two of the nine patients with MHC hyperexpression; in one of them, lymphocyte function-associated antigen-3 expression was also increased. |
| 1047 | 8227346 | In conclusion, we revealed the close relation between CD8+T lymphocyte-predominant insulitis and MHC class I hyperexpression in islet cells. |
| 1048 | 8227346 | This suggests that infiltrating CD8+T lymphocytes recognize islet autoantigens in association with increased MHC class I molecules and act as major effector cells in autoimmune response against islet cells in IDDM pancreases. |
| 1049 | 8240789 | Changes in the plasma concentrations of interleukin-1 beta (IL-1 beta), tumour necrosis factor alpha (TNF alpha), interleukin 2 (IL-2), and lymphocyte subsets were investigated in 19 persons with newly diagnosed (type 1) insulin-dependent diabetes mellitus (IDDM) from admission to hospital prior to insulin treatment and following 1 week and 1 month of treatment. |
| 1050 | 8240789 | The lymphocyte subsets (CD5+, CD8+, CD4+, CD16+, CD20+, HLA-DR+) did not show any significant changes from admission to after the start of insulin treatment. |
| 1051 | 8240789 | It is concluded that the gradual increase in IL-1 beta and TNF alpha plasma levels may reflect an ongoing autoimmune inflammatory reaction at the onset of IDDM. |
| 1052 | 8243828 | The adoptive transfer of diabetes requires the presence of both CD4+ and CD8+ splenic T-cell subsets. |
| 1053 | 8243828 | Although CD8+ lymph node T-cells seemed functionally comparable to CD8+ splenocytes, CD4+ lymph node T-cells failed to cooperate with CD8+ splenocytes to transfer diabetes. |
| 1054 | 8243828 | The adoptive transfer of diabetes requires the presence of both CD4+ and CD8+ splenic T-cell subsets. |
| 1055 | 8243828 | Although CD8+ lymph node T-cells seemed functionally comparable to CD8+ splenocytes, CD4+ lymph node T-cells failed to cooperate with CD8+ splenocytes to transfer diabetes. |
| 1056 | 8245789 | Resting rat and human T cells bound 125I-AGE-albumin with an affinity of 7.8 x 10(7) M-1, whereas, after stimulation with phytohemagglutinin (PHA) for 48 h, binding affinity increased to 5.8 x 10(8) M-1. |
| 1057 | 8245789 | Flow cytometric analysis of resting rat T cells using polyclonal antibodies raised against rat liver AGE-binding proteins (p60 and p90) revealed the constitutive expression of both immunoreactivities. |
| 1058 | 8245789 | The number of resting CD4+ and CD8+ T cells positive for anti-p60 antibody binding (34.2 and 58.5%, respectively) increased to 92 and 90% of cells after 48-h stimulation with PHA. |
| 1059 | 8245789 | Exposure of PHA-activated T lymphocytes to AGE-albumin enhanced expression of interferon gamma (IFN-gamma) mRNA 10-fold and induced greater elaboration of the mature protein than did exposure to unmodified protein or PHA treatment alone. |
| 1060 | 8258349 | The infiltrate contains both CD4+ and CD8+ T cells and both are required for progression to diabetes in non-obese diabetic (NOD) mice. |
| 1061 | 8258349 | It has been thought that the CD4+ lymphocytes are the initiators of the disease, the islet invaders, while CD8+ cells are the effectors, the islet destroyers. |
| 1062 | 8258349 | We question this interpretation because NOD mice lacking MHC class I molecules, hence CD8+ T cells, do not display even insulitis when expected. |
| 1063 | 8258349 | The infiltrate contains both CD4+ and CD8+ T cells and both are required for progression to diabetes in non-obese diabetic (NOD) mice. |
| 1064 | 8258349 | It has been thought that the CD4+ lymphocytes are the initiators of the disease, the islet invaders, while CD8+ cells are the effectors, the islet destroyers. |
| 1065 | 8258349 | We question this interpretation because NOD mice lacking MHC class I molecules, hence CD8+ T cells, do not display even insulitis when expected. |
| 1066 | 8262310 | Lymphocyte antibodies have been described in autoimmune disorders, including insulin-dependent diabetes mellitus (IDDM). |
| 1067 | 8262310 | We demonstrated the binding of the lymphocyte autoantibodies of both CD4+ and CD8+ T-cells. |
| 1068 | 8262316 | In spite of the fact that CD4 plays a critical role in thymocyte development, the abnormal signaling does not appear to influence thymocyte development at the stage when the T-cell receptor is rearranged and the recombinase enzymes RAG-1 and RAG-2 transcripts are downregulated. |
| 1069 | 8270129 | Analyses of T-cell subsets before and after diabetes onset revealed CD4+ T cells as predominant (50-55% of total T cells) with double-negative (CD4-CD8-) T cells (25-30%) and CD8+ T cells (15-20%) also present in significant quantities. |
| 1070 | 8296226 | Critical immunological values were established (CD5+ cells--1200 in 1 microliter, CD4+ cells--35%, expression of CD5 and antigens HLA class II--110 and 75%, respectively) for septic complications which are highly probable in lower indices. |
| 1071 | 8314024 | Although it is widely agreed that class II-restricted CD4+ T-cells are essential for the development of diabetes in the NOD model, some studies have suggested that CD8+ T-cells are not required for beta-cell destruction. |
| 1072 | 8314024 | To assess the contribution of CD8+ T-cells to diabetes, we have developed a class of NOD mouse that lacks expression of beta 2-microglobulin (NOD-B2mnull). |
| 1073 | 8315397 | Beginning at the time of insulitis (7 wk of age), CD4+ and CD8+ mature thymocytes from nonobese diabetic (NOD) mice exhibit a proliferative unresponsiveness in vitro after T cell receptor (TCR) crosslinking. |
| 1074 | 8315397 | However, since equivalent levels of IL-3 were secreted by Con A-activated NOD and BALB/c thymocytes, the unresponsiveness of NOD thymic T cells does not appear to be dependent on reduced IL-2 secretion. |
| 1075 | 8315397 | Exogenous recombinant (r)IL-2 only partially reverses NOD thymocyte proliferative unresponsiveness to anti-CD3, and this is mediated by the inability of IL-2 to stimulate a complete IL-4 secretion response. |
| 1076 | 8315397 | In contrast, exogenous IL-4 reverses the unresponsiveness of both NOD thymic and peripheral T cells completely, and this is associated with the complete restoration of an IL-2 secretion response. |
| 1077 | 8318452 | The non-obese diabetic (NOD) mouse spontaneously develops a T cell-mediated autoimmune disease, sharing many features with human insulin-dependent diabetes mellitus (IDDM), leading to insulin-secreting beta cell destruction. |
| 1078 | 8318452 | First, CD4+ T cells from diabetic animals are required to transfer diabetes to non-diabetic recipients in conjunction with CD8+ effector T cells. |
| 1079 | 8364190 | The neoplastic cells expressed the T-cell receptor (TCR)delta chain detected by TCR delta 1 and delta-TCS1, CD3, CD30, CD45RO, and epithelial membrane antigen, but not the TCR beta chain detected by beta F1, CD1a, CD2, CD4, CD5, CD7, CD8, CD25, HLA-DR, and terminal deoxynucleotidyl transferase. |
| 1080 | 8387218 | Patient response was assessed using changes in CD4+ lymphocyte subset count, HIV p24 antigen, weight, and quality of life. |
| 1081 | 8387218 | Of those positive for p24 antigen at the commencement of the study 67% showed a positive response, and this was most likely in those with CD4+ lymphocyte subset counts above 100 mm3. |
| 1082 | 8387218 | Patient response was assessed using changes in CD4+ lymphocyte subset count, HIV p24 antigen, weight, and quality of life. |
| 1083 | 8387218 | Of those positive for p24 antigen at the commencement of the study 67% showed a positive response, and this was most likely in those with CD4+ lymphocyte subset counts above 100 mm3. |
| 1084 | 8405701 | Tolerance to IDDM induced by CD4 antibodies in nonobese diabetic mice is reversed by cyclophosphamide. |
| 1085 | 8405709 | In IDDM, mononuclear cells accumulate in the islets of Langerhans and destroy insulin-producing beta-cells. |
| 1086 | 8405709 | The cell line was uniformly CD4-positive, TCR V beta 5.1-positive, LFA-1-positive (CD 11a/CD18), VLA-4 alpha-positive (CD 49d), and CD 44-positive but negative for L-selectin (peripheral lymph node homing receptor). |
| 1087 | 8409408 | Several staphylococcal enterotoxins (SE) (SEA, SEC1, SEC2, or SEC3), which are known superantigens, were injected i.v. into female NOD mice at 4 and 10 wk of age. |
| 1088 | 8409408 | Suppressor activity of splenocytes from SE-treated mice was diminished by the depletion of CD4+ T cells, but not by the depletion of CD8+ T cells, indicating that the suppressor cells belonged to the CD4+ T class of lymphocytes. |
| 1089 | 8420039 | Granzyme A is a serine protease expressed by populations of human and mouse natural killer cells and activated CD4+ and CD8+ cytotoxic lymphocytes; its expression marks a subset of inflammatory cells in allografts, autoimmune diabetes, and a number of other inflammatory lesions. |
| 1090 | 8420039 | The grafts were evaluated by palpation for cardiac functions, by immunohistochemistry for CD4/CD8 expression, by hematoxylin-and-eosin staining for inflammatory infiltration, and by in situ hybridization for granzyme A expression. |
| 1091 | 8420039 | Granzyme A is a serine protease expressed by populations of human and mouse natural killer cells and activated CD4+ and CD8+ cytotoxic lymphocytes; its expression marks a subset of inflammatory cells in allografts, autoimmune diabetes, and a number of other inflammatory lesions. |
| 1092 | 8420039 | The grafts were evaluated by palpation for cardiac functions, by immunohistochemistry for CD4/CD8 expression, by hematoxylin-and-eosin staining for inflammatory infiltration, and by in situ hybridization for granzyme A expression. |
| 1093 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1094 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1095 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1096 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1097 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1098 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1099 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1100 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1101 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1102 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1103 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1104 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1105 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1106 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1107 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1108 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1109 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1110 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1111 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1112 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1113 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1114 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1115 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1116 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1117 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1118 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1119 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1120 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1121 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1122 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1123 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1124 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1125 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1126 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1127 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1128 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1129 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1130 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1131 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1132 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1133 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1134 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1135 | 8420810 | The monoclonal antibodies 2H4 (anti-CD45RA) and UCHL1 (anti-CD45RO) were used to subdivide the CD4 and CD8 T-cell subsets into naive and memory cells. |
| 1136 | 8420810 | CD4 and CD8 lymphocytes expressed the CD45 isoforms alone (CD45RA+ or CD45RO+) or in combination CD45RA+RO+). |
| 1137 | 8420810 | Simultaneous coexpression of both CD45RA and CD45RO (CD45RA+RO+) on CD4 and CD8 lymphocytes in patients with recent-onset IDDM was higher than in control subjects (P < 0.001). |
| 1138 | 8420810 | The proportion of CD4 lymphocytes expressing CD45RA alone (CD45RA+RO-) was similar in these groups, but the percentage of CD8 lymphocytes that were CD45RA+RO- was significantly higher in the patients with recent-onset IDDM (P < 0.05). |
| 1139 | 8420810 | The result of these changes is a significant increase in expression of naive phenotypes (CD45RA+ and CD45RA+RO+) on CD4 and CD8 lymphocytes in recent-onset IDDM (P < 0.005 and P < 0.0001). |
| 1140 | 8420810 | In long-standing IDDM, total CD45RA+ expression on CD4 and CD8 lymphocytes was reduced compared with control subjects (P < 0.05) as a result of a tendency of CD45RA+RO- and CD45RA+RO+ subsets to be lower. |
| 1141 | 8420810 | This increase in total naive (CD45RA+) lymphocytes and in coexpression of naive (CD45RA) and memory (CD45RO) markers on CD4 and CD8 lymphocytes subsets in patients with recent-onset IDDM suggests that abnormal regulation of T-cell activation and maturation is important in the pathogenesis of the disease. |
| 1142 | 8472311 | Through CD4, the signal transduction machinery is stimulated via its association with p56lck. |
| 1143 | 8492638 | Aged C57Bl/6 mice showed significant suppression of Con A-stimulated Ca2+ mobilization in both CD4+ and CD8+T cells compared to young mice. |
| 1144 | 8492638 | Similarly, aged mice exhibited a significant increase in spontaneous IL-2R expression in both CD4+ and CD8+ T cells. |
| 1145 | 8492638 | Aged C57Bl/6 mice showed significant suppression of Con A-stimulated Ca2+ mobilization in both CD4+ and CD8+T cells compared to young mice. |
| 1146 | 8492638 | Similarly, aged mice exhibited a significant increase in spontaneous IL-2R expression in both CD4+ and CD8+ T cells. |
| 1147 | 8496610 | To study self reactivity, a transgenic mouse model has been established in which the lymphocytic choriomeningitis virus (LCMV) glycoprotein (gp) is expressed in the beta-islet cells of the pancreas (rat insulin promoter (RIP)-gp). |
| 1148 | 8496610 | In this study, comparative analysis of H-2k RIP-gp-transgenic animals demonstrated that the haplotype influences the incidence and kinetics of diabetes and alters the requirement for the CD4+ T cell subset. |
| 1149 | 8496610 | Transgenic mice expressing both LCMV-gp and TNF-alpha under the control of the RIP were infected with vacc-gp, and 50% of RIP-gp/TNF-alpha-transgenic animals became hyperglycemic. |
| 1150 | 8522063 | CD45RB(low) CD4+ splenocytes from diabetic NOD mice were transferred along with CD8+ splenocytes from diabetic mice into NOD-scid recipients, and all of the recipients became diabetic within 5 weeks posttransfer. |
| 1151 | 8522063 | In contrast, no recipients (0 of 10) of CD45RB(high) CD4+ cells along with CD8+ splenocytes from diabetic mice became diabetic within 5 weeks posttransfer (P < 0.001). |
| 1152 | 8522063 | CD45RB(low) CD4+ cells from diabetic mice showed a significantly higher ratio (approximately fivefold) of gamma-interferon (IFN-gamma) to interleukin (IL)-4 when compared with CD45RB(low) CD4+ cells from nondiabetic mice (P < 0.001). |
| 1153 | 8522063 | CD45RB(low) CD4+ splenocytes from diabetic NOD mice were transferred along with CD8+ splenocytes from diabetic mice into NOD-scid recipients, and all of the recipients became diabetic within 5 weeks posttransfer. |
| 1154 | 8522063 | In contrast, no recipients (0 of 10) of CD45RB(high) CD4+ cells along with CD8+ splenocytes from diabetic mice became diabetic within 5 weeks posttransfer (P < 0.001). |
| 1155 | 8522063 | CD45RB(low) CD4+ cells from diabetic mice showed a significantly higher ratio (approximately fivefold) of gamma-interferon (IFN-gamma) to interleukin (IL)-4 when compared with CD45RB(low) CD4+ cells from nondiabetic mice (P < 0.001). |
| 1156 | 8522063 | CD45RB(low) CD4+ splenocytes from diabetic NOD mice were transferred along with CD8+ splenocytes from diabetic mice into NOD-scid recipients, and all of the recipients became diabetic within 5 weeks posttransfer. |
| 1157 | 8522063 | In contrast, no recipients (0 of 10) of CD45RB(high) CD4+ cells along with CD8+ splenocytes from diabetic mice became diabetic within 5 weeks posttransfer (P < 0.001). |
| 1158 | 8522063 | CD45RB(low) CD4+ cells from diabetic mice showed a significantly higher ratio (approximately fivefold) of gamma-interferon (IFN-gamma) to interleukin (IL)-4 when compared with CD45RB(low) CD4+ cells from nondiabetic mice (P < 0.001). |
| 1159 | 8529494 | A novel function of islet-derived CD8+T cells in initiating and developing autoimmune insulin-dependent diabetes mellitus in non-obese diabetic (NOD) mice. |
| 1160 | 8529494 | Accumulated studies revealed that CD4+T cells were initially required for diabetes in NOD mice, whereas interaction of CD4+T/CD8+T cells is not fully understood. |
| 1161 | 8529494 | To address this question, we established islet-derived CD4+T cells and CD8+T cells from NOD mice. |
| 1162 | 8529494 | One NOD neonate that received CD4+T cells developed diabetes and insulitis with CD8+T cells. |
| 1163 | 8529494 | Similarly, it was observed that neonates that received islet-derived CD8+T cells developed diabetes and obvious insulitis mainly with CD4+T cells. |
| 1164 | 8529494 | These results imply that CD8+T cells function as an initial element to recruit CD4+T cells to islets as well as a final effector. |
| 1165 | 8529494 | A novel function of islet-derived CD8+T cells in initiating and developing autoimmune insulin-dependent diabetes mellitus in non-obese diabetic (NOD) mice. |
| 1166 | 8529494 | Accumulated studies revealed that CD4+T cells were initially required for diabetes in NOD mice, whereas interaction of CD4+T/CD8+T cells is not fully understood. |
| 1167 | 8529494 | To address this question, we established islet-derived CD4+T cells and CD8+T cells from NOD mice. |
| 1168 | 8529494 | One NOD neonate that received CD4+T cells developed diabetes and insulitis with CD8+T cells. |
| 1169 | 8529494 | Similarly, it was observed that neonates that received islet-derived CD8+T cells developed diabetes and obvious insulitis mainly with CD4+T cells. |
| 1170 | 8529494 | These results imply that CD8+T cells function as an initial element to recruit CD4+T cells to islets as well as a final effector. |
| 1171 | 8529494 | A novel function of islet-derived CD8+T cells in initiating and developing autoimmune insulin-dependent diabetes mellitus in non-obese diabetic (NOD) mice. |
| 1172 | 8529494 | Accumulated studies revealed that CD4+T cells were initially required for diabetes in NOD mice, whereas interaction of CD4+T/CD8+T cells is not fully understood. |
| 1173 | 8529494 | To address this question, we established islet-derived CD4+T cells and CD8+T cells from NOD mice. |
| 1174 | 8529494 | One NOD neonate that received CD4+T cells developed diabetes and insulitis with CD8+T cells. |
| 1175 | 8529494 | Similarly, it was observed that neonates that received islet-derived CD8+T cells developed diabetes and obvious insulitis mainly with CD4+T cells. |
| 1176 | 8529494 | These results imply that CD8+T cells function as an initial element to recruit CD4+T cells to islets as well as a final effector. |
| 1177 | 8529494 | A novel function of islet-derived CD8+T cells in initiating and developing autoimmune insulin-dependent diabetes mellitus in non-obese diabetic (NOD) mice. |
| 1178 | 8529494 | Accumulated studies revealed that CD4+T cells were initially required for diabetes in NOD mice, whereas interaction of CD4+T/CD8+T cells is not fully understood. |
| 1179 | 8529494 | To address this question, we established islet-derived CD4+T cells and CD8+T cells from NOD mice. |
| 1180 | 8529494 | One NOD neonate that received CD4+T cells developed diabetes and insulitis with CD8+T cells. |
| 1181 | 8529494 | Similarly, it was observed that neonates that received islet-derived CD8+T cells developed diabetes and obvious insulitis mainly with CD4+T cells. |
| 1182 | 8529494 | These results imply that CD8+T cells function as an initial element to recruit CD4+T cells to islets as well as a final effector. |
| 1183 | 8529494 | A novel function of islet-derived CD8+T cells in initiating and developing autoimmune insulin-dependent diabetes mellitus in non-obese diabetic (NOD) mice. |
| 1184 | 8529494 | Accumulated studies revealed that CD4+T cells were initially required for diabetes in NOD mice, whereas interaction of CD4+T/CD8+T cells is not fully understood. |
| 1185 | 8529494 | To address this question, we established islet-derived CD4+T cells and CD8+T cells from NOD mice. |
| 1186 | 8529494 | One NOD neonate that received CD4+T cells developed diabetes and insulitis with CD8+T cells. |
| 1187 | 8529494 | Similarly, it was observed that neonates that received islet-derived CD8+T cells developed diabetes and obvious insulitis mainly with CD4+T cells. |
| 1188 | 8529494 | These results imply that CD8+T cells function as an initial element to recruit CD4+T cells to islets as well as a final effector. |
| 1189 | 8558007 | Abnormal thymocyte subset distribution and differential reduction of CD4+ and CD8+ T cell subsets during peripheral maturation in diabetes-prone BioBreeding rats. |
| 1190 | 8558007 | In this study we quantified CD8+ and CD4+ T cells in T lymphocytopenic BB rats as compared with control rats at given stages along the maturational pathway from immature thymocytes to mature peripheral T cells. |
| 1191 | 8558007 | Numbers of mature TCRhigh/CD4-8+ thymocytes, and also their TCRhigh/CD4+8+ precursors were decreased, as were levels of CD8 expression on all thymocyte subsets investigated. |
| 1192 | 8558007 | Furthermore, as related to the number of available mature TCRhigh single positive thymocytes, numbers of CD4+ and CD8+ T cells most recently migrated from the thymus were severely decreased in BB blood, indicating either reduced thymic output or rapid cell death after migration. |
| 1193 | 8558007 | Subsequently, in peripheral blood and cervical lymph nodes, a 95% decrease of CD8+ and a 50 to 80% decrease of CD4+ T cells were demonstrated upon maturation from recent thymic migrants to mature peripheral T cells, leaving the BB rat with a severely reduced T cell population, consisting of CD4+ T cells and a minute population of CD8+ T cells. |
| 1194 | 8558007 | Abnormal thymocyte subset distribution and differential reduction of CD4+ and CD8+ T cell subsets during peripheral maturation in diabetes-prone BioBreeding rats. |
| 1195 | 8558007 | In this study we quantified CD8+ and CD4+ T cells in T lymphocytopenic BB rats as compared with control rats at given stages along the maturational pathway from immature thymocytes to mature peripheral T cells. |
| 1196 | 8558007 | Numbers of mature TCRhigh/CD4-8+ thymocytes, and also their TCRhigh/CD4+8+ precursors were decreased, as were levels of CD8 expression on all thymocyte subsets investigated. |
| 1197 | 8558007 | Furthermore, as related to the number of available mature TCRhigh single positive thymocytes, numbers of CD4+ and CD8+ T cells most recently migrated from the thymus were severely decreased in BB blood, indicating either reduced thymic output or rapid cell death after migration. |
| 1198 | 8558007 | Subsequently, in peripheral blood and cervical lymph nodes, a 95% decrease of CD8+ and a 50 to 80% decrease of CD4+ T cells were demonstrated upon maturation from recent thymic migrants to mature peripheral T cells, leaving the BB rat with a severely reduced T cell population, consisting of CD4+ T cells and a minute population of CD8+ T cells. |
| 1199 | 8558007 | Abnormal thymocyte subset distribution and differential reduction of CD4+ and CD8+ T cell subsets during peripheral maturation in diabetes-prone BioBreeding rats. |
| 1200 | 8558007 | In this study we quantified CD8+ and CD4+ T cells in T lymphocytopenic BB rats as compared with control rats at given stages along the maturational pathway from immature thymocytes to mature peripheral T cells. |
| 1201 | 8558007 | Numbers of mature TCRhigh/CD4-8+ thymocytes, and also their TCRhigh/CD4+8+ precursors were decreased, as were levels of CD8 expression on all thymocyte subsets investigated. |
| 1202 | 8558007 | Furthermore, as related to the number of available mature TCRhigh single positive thymocytes, numbers of CD4+ and CD8+ T cells most recently migrated from the thymus were severely decreased in BB blood, indicating either reduced thymic output or rapid cell death after migration. |
| 1203 | 8558007 | Subsequently, in peripheral blood and cervical lymph nodes, a 95% decrease of CD8+ and a 50 to 80% decrease of CD4+ T cells were demonstrated upon maturation from recent thymic migrants to mature peripheral T cells, leaving the BB rat with a severely reduced T cell population, consisting of CD4+ T cells and a minute population of CD8+ T cells. |
| 1204 | 8558007 | Abnormal thymocyte subset distribution and differential reduction of CD4+ and CD8+ T cell subsets during peripheral maturation in diabetes-prone BioBreeding rats. |
| 1205 | 8558007 | In this study we quantified CD8+ and CD4+ T cells in T lymphocytopenic BB rats as compared with control rats at given stages along the maturational pathway from immature thymocytes to mature peripheral T cells. |
| 1206 | 8558007 | Numbers of mature TCRhigh/CD4-8+ thymocytes, and also their TCRhigh/CD4+8+ precursors were decreased, as were levels of CD8 expression on all thymocyte subsets investigated. |
| 1207 | 8558007 | Furthermore, as related to the number of available mature TCRhigh single positive thymocytes, numbers of CD4+ and CD8+ T cells most recently migrated from the thymus were severely decreased in BB blood, indicating either reduced thymic output or rapid cell death after migration. |
| 1208 | 8558007 | Subsequently, in peripheral blood and cervical lymph nodes, a 95% decrease of CD8+ and a 50 to 80% decrease of CD4+ T cells were demonstrated upon maturation from recent thymic migrants to mature peripheral T cells, leaving the BB rat with a severely reduced T cell population, consisting of CD4+ T cells and a minute population of CD8+ T cells. |
| 1209 | 8558007 | Abnormal thymocyte subset distribution and differential reduction of CD4+ and CD8+ T cell subsets during peripheral maturation in diabetes-prone BioBreeding rats. |
| 1210 | 8558007 | In this study we quantified CD8+ and CD4+ T cells in T lymphocytopenic BB rats as compared with control rats at given stages along the maturational pathway from immature thymocytes to mature peripheral T cells. |
| 1211 | 8558007 | Numbers of mature TCRhigh/CD4-8+ thymocytes, and also their TCRhigh/CD4+8+ precursors were decreased, as were levels of CD8 expression on all thymocyte subsets investigated. |
| 1212 | 8558007 | Furthermore, as related to the number of available mature TCRhigh single positive thymocytes, numbers of CD4+ and CD8+ T cells most recently migrated from the thymus were severely decreased in BB blood, indicating either reduced thymic output or rapid cell death after migration. |
| 1213 | 8558007 | Subsequently, in peripheral blood and cervical lymph nodes, a 95% decrease of CD8+ and a 50 to 80% decrease of CD4+ T cells were demonstrated upon maturation from recent thymic migrants to mature peripheral T cells, leaving the BB rat with a severely reduced T cell population, consisting of CD4+ T cells and a minute population of CD8+ T cells. |
| 1214 | 8591703 | Insulitis lesions were examined immunohistochemically for CD4, CD8 and MAC-1 cells. |
| 1215 | 8593938 | Transfer of an interleukin 2/interferon-gamma-secreting islet-specific CD4+ T-cell clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells without help from host B-cells, CD4+ T-cells, or CD8+ T-cells. |
| 1216 | 8593938 | Immunohistochemical staining of pancreatic lesions in young NOD mice receiving either BDC-2.5 or BDC-6.9 showed the presence of CD4+, CD8+, Vbeta4+, and MAC-1+ cells within the infiltrate, similar to infiltrates in lesions of spontaneously diabetic female NOD mice. |
| 1217 | 8593938 | In contrast, NOD- scid mice that received BDC-6.9 showed only the presence of CD4+Vb4+ T-cells and a large population of MAC-1+ cells in islet lesions. |
| 1218 | 8593938 | NOD-scid recipients of cotransferred BDC- 2.5/CD8+ splenic T-cells showed a small population of CD4+ T-cells and a larger population of CD8+ T-cells within the infiltrated islets, whereas no infiltrate was detectable in recipients of CD8+ splenocytes or BDC-2.5 alone. |
| 1219 | 8593938 | Transfer of an interleukin 2/interferon-gamma-secreting islet-specific CD4+ T-cell clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells without help from host B-cells, CD4+ T-cells, or CD8+ T-cells. |
| 1220 | 8593938 | Immunohistochemical staining of pancreatic lesions in young NOD mice receiving either BDC-2.5 or BDC-6.9 showed the presence of CD4+, CD8+, Vbeta4+, and MAC-1+ cells within the infiltrate, similar to infiltrates in lesions of spontaneously diabetic female NOD mice. |
| 1221 | 8593938 | In contrast, NOD- scid mice that received BDC-6.9 showed only the presence of CD4+Vb4+ T-cells and a large population of MAC-1+ cells in islet lesions. |
| 1222 | 8593938 | NOD-scid recipients of cotransferred BDC- 2.5/CD8+ splenic T-cells showed a small population of CD4+ T-cells and a larger population of CD8+ T-cells within the infiltrated islets, whereas no infiltrate was detectable in recipients of CD8+ splenocytes or BDC-2.5 alone. |
| 1223 | 8593938 | Transfer of an interleukin 2/interferon-gamma-secreting islet-specific CD4+ T-cell clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells without help from host B-cells, CD4+ T-cells, or CD8+ T-cells. |
| 1224 | 8593938 | Immunohistochemical staining of pancreatic lesions in young NOD mice receiving either BDC-2.5 or BDC-6.9 showed the presence of CD4+, CD8+, Vbeta4+, and MAC-1+ cells within the infiltrate, similar to infiltrates in lesions of spontaneously diabetic female NOD mice. |
| 1225 | 8593938 | In contrast, NOD- scid mice that received BDC-6.9 showed only the presence of CD4+Vb4+ T-cells and a large population of MAC-1+ cells in islet lesions. |
| 1226 | 8593938 | NOD-scid recipients of cotransferred BDC- 2.5/CD8+ splenic T-cells showed a small population of CD4+ T-cells and a larger population of CD8+ T-cells within the infiltrated islets, whereas no infiltrate was detectable in recipients of CD8+ splenocytes or BDC-2.5 alone. |
| 1227 | 8593938 | Transfer of an interleukin 2/interferon-gamma-secreting islet-specific CD4+ T-cell clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells without help from host B-cells, CD4+ T-cells, or CD8+ T-cells. |
| 1228 | 8593938 | Immunohistochemical staining of pancreatic lesions in young NOD mice receiving either BDC-2.5 or BDC-6.9 showed the presence of CD4+, CD8+, Vbeta4+, and MAC-1+ cells within the infiltrate, similar to infiltrates in lesions of spontaneously diabetic female NOD mice. |
| 1229 | 8593938 | In contrast, NOD- scid mice that received BDC-6.9 showed only the presence of CD4+Vb4+ T-cells and a large population of MAC-1+ cells in islet lesions. |
| 1230 | 8593938 | NOD-scid recipients of cotransferred BDC- 2.5/CD8+ splenic T-cells showed a small population of CD4+ T-cells and a larger population of CD8+ T-cells within the infiltrated islets, whereas no infiltrate was detectable in recipients of CD8+ splenocytes or BDC-2.5 alone. |
| 1231 | 8603576 | The effects of growth hormone and insulin-like growth factor I on the immune system of aged female monkeys. |
| 1232 | 8603576 | The aging process is associated with a significant reduction in circulating GH and insulin-like growth factor I (IGF-I) levels. |
| 1233 | 8603576 | At the end of the 7-week period, the animals were killed. rhGH and rhIGF-I increased serum GH and IGF-I levels, respectively; rhGH and rhIGF-I in combination induced the highest serum IGF-I levels (906 +/- 261 ng/ml vs. control, 185 +/- 36 ng/ml at death). rhGH and rhIGF-I also increased IGFBP-3 levels. rhGH infusion resulted in the most marked changes in lymph node and splenic reactivity, as determined by histological assessment. |
| 1234 | 8603576 | In the peripheral blood, the percent B cells and percent CD8 cell count rose after rhIGF-I therapy, with a fall in the CD4/CD8 ratio. |
| 1235 | 8603576 | In the spleen, on the other hand, the CD4/CD8 ratio nearly doubled (0.33 +/- 0.12 vs. 0.53 +/ 0.12) after rhIGF- I therapy. |
| 1236 | 8603576 | In the spleen, the combination of rhGH and rhIGF- I increased the percent T cells from 26.7 +/- 2.3 to 42.4 +/- 4.4 and the CD4/CD8 ration to 0.71 +/- 0.11. |
| 1237 | 8603576 | The effects of growth hormone and insulin-like growth factor I on the immune system of aged female monkeys. |
| 1238 | 8603576 | The aging process is associated with a significant reduction in circulating GH and insulin-like growth factor I (IGF-I) levels. |
| 1239 | 8603576 | At the end of the 7-week period, the animals were killed. rhGH and rhIGF-I increased serum GH and IGF-I levels, respectively; rhGH and rhIGF-I in combination induced the highest serum IGF-I levels (906 +/- 261 ng/ml vs. control, 185 +/- 36 ng/ml at death). rhGH and rhIGF-I also increased IGFBP-3 levels. rhGH infusion resulted in the most marked changes in lymph node and splenic reactivity, as determined by histological assessment. |
| 1240 | 8603576 | In the peripheral blood, the percent B cells and percent CD8 cell count rose after rhIGF-I therapy, with a fall in the CD4/CD8 ratio. |
| 1241 | 8603576 | In the spleen, on the other hand, the CD4/CD8 ratio nearly doubled (0.33 +/- 0.12 vs. 0.53 +/ 0.12) after rhIGF- I therapy. |
| 1242 | 8603576 | In the spleen, the combination of rhGH and rhIGF- I increased the percent T cells from 26.7 +/- 2.3 to 42.4 +/- 4.4 and the CD4/CD8 ration to 0.71 +/- 0.11. |
| 1243 | 8603576 | The effects of growth hormone and insulin-like growth factor I on the immune system of aged female monkeys. |
| 1244 | 8603576 | The aging process is associated with a significant reduction in circulating GH and insulin-like growth factor I (IGF-I) levels. |
| 1245 | 8603576 | At the end of the 7-week period, the animals were killed. rhGH and rhIGF-I increased serum GH and IGF-I levels, respectively; rhGH and rhIGF-I in combination induced the highest serum IGF-I levels (906 +/- 261 ng/ml vs. control, 185 +/- 36 ng/ml at death). rhGH and rhIGF-I also increased IGFBP-3 levels. rhGH infusion resulted in the most marked changes in lymph node and splenic reactivity, as determined by histological assessment. |
| 1246 | 8603576 | In the peripheral blood, the percent B cells and percent CD8 cell count rose after rhIGF-I therapy, with a fall in the CD4/CD8 ratio. |
| 1247 | 8603576 | In the spleen, on the other hand, the CD4/CD8 ratio nearly doubled (0.33 +/- 0.12 vs. 0.53 +/ 0.12) after rhIGF- I therapy. |
| 1248 | 8603576 | In the spleen, the combination of rhGH and rhIGF- I increased the percent T cells from 26.7 +/- 2.3 to 42.4 +/- 4.4 and the CD4/CD8 ration to 0.71 +/- 0.11. |
| 1249 | 8633371 | Transplantation of human fetal pancreas (HFP) is being considered as a potential treatment for insulin-dependent diabetes mellitus (IDDM). |
| 1250 | 8633371 | Allograft rejection was due to human CD4+ and CD8+ cells, as determined by immunohistochemical analysis of graft-infiltrating cells. |
| 1251 | 8642324 | In addition, adoptive transfer of LCMV-GP-specific TCR transgenic perforin-deficient T cells activated by LCMV-GP recombinant vaccinia virus led to marked insulitis with infiltration of CD4+ and CD8+ T cells without the development of diabetes. |
| 1252 | 8666914 | Nasal administration of glutamate decarboxylase (GAD65) peptides induces Th2 responses and prevents murine insulin-dependent diabetes. |
| 1253 | 8666914 | Induction of passive tolerance to GAD65, through inactivation of reactive T cells before the onset of autoimmunity, prevented determinant spreading and the development of insulin-dependent diabetes mellitus (IDDM). |
| 1254 | 8666914 | Here, we examined whether an alternative strategy, designed to induce active tolerance via the engagement of Th2 immune responses to GAD65, before the spontaneous onset of autoimmunity, could inhibit the cascade of Th1 responses that lead to IDDM. |
| 1255 | 8666914 | GAD65 peptide treated mice displayed greatly reduced IFN gamma responses and increased IL-5 responses to GAD65, confirming the diversion of the spontaneous GAD65 Th1 response toward a Th2 phenotype. |
| 1256 | 8666914 | Consistent with the induction of an active tolerance mechanism, splenic CD4+ (but not CD8+) T cells from GAD65 peptide-treated mice, inhibited the adoptive transfer of IDDM to NOD-scid/scid mice. |
| 1257 | 8666914 | Finally, GAD65 peptide treatment reduced insulitis and long-term IDDM incidence. |
| 1258 | 8690161 | In all of the H-2d islet-grafted (NOD x BALB/c) F1 mice that received the beta-CTL clones, the beta-CTLs homed into the grafts, recruited host Mac-1+ cells and CD4+ and CD8+ T-cells, and caused diabetes within 7 days. |
| 1259 | 8690161 | We conclude that (1) islet-derived beta-CTLs can destroy beta-cells in vivo; (2) infiltration of grafted islets by beta-CTLs is an MHC class I-restricted response; (3) beta-CTLs can recruit naive CD4+ T-cells to the site, leading to further beta-cell damage; and (4) revascularized islet grafts are, like pancreatic islets of irradiated adult NOD mice, "sequestered" from circulating beta-CTLs. |
| 1260 | 8690161 | In all of the H-2d islet-grafted (NOD x BALB/c) F1 mice that received the beta-CTL clones, the beta-CTLs homed into the grafts, recruited host Mac-1+ cells and CD4+ and CD8+ T-cells, and caused diabetes within 7 days. |
| 1261 | 8690161 | We conclude that (1) islet-derived beta-CTLs can destroy beta-cells in vivo; (2) infiltration of grafted islets by beta-CTLs is an MHC class I-restricted response; (3) beta-CTLs can recruit naive CD4+ T-cells to the site, leading to further beta-cell damage; and (4) revascularized islet grafts are, like pancreatic islets of irradiated adult NOD mice, "sequestered" from circulating beta-CTLs. |
| 1262 | 8724837 | Recently, we have shown that CD4+ CD8- thymocytes are a highly potent source of cells that have the ability to control autoimmune diabetes in rats. |
| 1263 | 8734569 | T cells from BB-DP rats show a unique cytokine mRNA profile associated with the IDDM1 susceptibility gene, Lyp. |
| 1264 | 8734569 | One of the most pronounced abnormalities in these animals is a marked T cell lymphopenia which is evident in both CD4+ and CD8+ peripheral T cell subsets. |
| 1265 | 8738958 | According to immunocytochemical analysis, the pancreatic inflammatory infiltrates of streptozotocin-injected transgenic mice contained CD4+ and CD8+ T lymphocytes, B lymphocytes and macrophages. |
| 1266 | 8738973 | We now report that cyclophosphamide constitutes an apoptosis signal to peripheral lymphocytes and we provide evidence that NOD B cells as well as both CD4 and CD8 T cells display resistance to cyclophosphamide-induced apoptosis. |
| 1267 | 8740409 | Immunophenotyping of the inflammatory infiltrate with rat lymphocyte-specific markers showed CD45-, CD8-, and CD4-positive cells. |
| 1268 | 8746558 | Likewise, the NOD-derived NIT-1 beta cell line did not express surface B7 or B7-1 mRNA either constitutively or following exposure to IFN-gamma and TNF-alpha, two cytokines known to be present in the insulitis lesion of NOD mice, or cAMP which can induce B7-1 expression on B cells. |
| 1269 | 8746558 | By immunohistochemistry and flow cytometry, it was determined that the phenotype of B7+ cells in the pancreas of NOD mice 9 days after cyclophosphamide included a mixture of macrophages and both CD4+ and CD8+ T cells. |
| 1270 | 8746558 | RIP-IL-2 transgenic mice, which have extensive islet infiltration but no autoimmune beta cell destruction, also had virtually no B7-1 expression and a minority of B7-2-expressing inflammatory cells. |
| 1271 | 8747721 | Circulating lymphocyte subset imbalance is associated with type-1 insulin-dependent diabetes mellitus (IDDM). |
| 1272 | 8747721 | Total B lymphocytes, CD19+ cells, was increased in IDDM patients (P = 0.001), but was comparable to controls in IDDM patients' first-degree relatives. |
| 1273 | 8747721 | No quantitative abnormality was demonstrated in CD4+ cells in IDDM patients; however, these cells were higher in their first-degree relatives (P = 0.0089). |
| 1274 | 8747721 | Suppressor T lymphocytes, CD8+ cells, in first-degree relatives and controls were not significantly different; however, these cells were significantly reduced in IDDM patients (P = 0.001). |
| 1275 | 8747721 | The ratio of CD4+/CD8+ cells was higher in IDDM patients and their first-degree relatives compared to controls (P = 0.0007 and 0.0103, respectively). |
| 1276 | 8747721 | However, no relationship was found in the levels of CD3+, CD4+ or CD8+ cells in patients possessing either DR3 or DR4. |
| 1277 | 8747721 | Circulating lymphocyte subset imbalance is associated with type-1 insulin-dependent diabetes mellitus (IDDM). |
| 1278 | 8747721 | Total B lymphocytes, CD19+ cells, was increased in IDDM patients (P = 0.001), but was comparable to controls in IDDM patients' first-degree relatives. |
| 1279 | 8747721 | No quantitative abnormality was demonstrated in CD4+ cells in IDDM patients; however, these cells were higher in their first-degree relatives (P = 0.0089). |
| 1280 | 8747721 | Suppressor T lymphocytes, CD8+ cells, in first-degree relatives and controls were not significantly different; however, these cells were significantly reduced in IDDM patients (P = 0.001). |
| 1281 | 8747721 | The ratio of CD4+/CD8+ cells was higher in IDDM patients and their first-degree relatives compared to controls (P = 0.0007 and 0.0103, respectively). |
| 1282 | 8747721 | However, no relationship was found in the levels of CD3+, CD4+ or CD8+ cells in patients possessing either DR3 or DR4. |
| 1283 | 8747721 | Circulating lymphocyte subset imbalance is associated with type-1 insulin-dependent diabetes mellitus (IDDM). |
| 1284 | 8747721 | Total B lymphocytes, CD19+ cells, was increased in IDDM patients (P = 0.001), but was comparable to controls in IDDM patients' first-degree relatives. |
| 1285 | 8747721 | No quantitative abnormality was demonstrated in CD4+ cells in IDDM patients; however, these cells were higher in their first-degree relatives (P = 0.0089). |
| 1286 | 8747721 | Suppressor T lymphocytes, CD8+ cells, in first-degree relatives and controls were not significantly different; however, these cells were significantly reduced in IDDM patients (P = 0.001). |
| 1287 | 8747721 | The ratio of CD4+/CD8+ cells was higher in IDDM patients and their first-degree relatives compared to controls (P = 0.0007 and 0.0103, respectively). |
| 1288 | 8747721 | However, no relationship was found in the levels of CD3+, CD4+ or CD8+ cells in patients possessing either DR3 or DR4. |
| 1289 | 8750571 | CD4 and CD8, gamma/delta TCR bearing T cells and CD45R0 on CD4+ T cells as a marker for memory cells, on TL no differences could be detected between patients with or without anti-TPO. |
| 1290 | 8750571 | Surprisingly, the number of CD3+ TL bearing the IL-2 receptor (CD25) and transferrin receptor (CD71) was not increased. |
| 1291 | 8752897 | IFN-alpha induces autoimmune T cells through the induction of intracellular adhesion molecule-1 and B7.2. |
| 1292 | 8752897 | We demonstrate that the expression of IFN-alpha by the pancreatic beta cells leads to the development of CD4+ T cells that proliferate in the presence of islet Ags. |
| 1293 | 8752897 | We also demonstrate that the pancreatic infiltrating leukocytes in the transgenic mice express increased levels of 87.2 and ICAM-1 and that IFN-alpha can directly induce these two costimulatory molecules on nontransgenic splenic APCs. |
| 1294 | 8752897 | Treatment of the transgenic mice with Abs against these costimulatory molecules demonstrated that B7.2 is essential for the induction of autoreactive T cells, whereas ICAM-1 contributes to but is not essential for the formation of these autoreactive cells. |
| 1295 | 8752897 | As B7.2 and ICAM-1 are able to synergize to provide costimulatory signals to naive T cells under conditions of limiting Ag, we propose that IFN-alpha expression normally contributes to the development of an anti-viral cellular immune response, but that uncontrolled expression of this cytokine will induce autoimmunity. |
| 1296 | 8756680 | The CD4 determinant for downregulation by HIV-1 Nef directly binds to Nef. |
| 1297 | 8756680 | Using heteronuclear NMR spectroscopy, we demonstrate that a 13-residue peptide (MS-QIKRLLSEKKT) from the cytoplasmic tail of CD4 binds to Nef protein. |
| 1298 | 8756680 | This part of CD4 is critical for downregulation of CD4 by HIV-1 Nef [Aiken et al. (1994) Cell 76, 853-864]. |
| 1299 | 8756680 | When Nef is complexed to the SH3 domain of Hck tyrosine protein kinase, the peptide binds to the same site on Nef but with slightly higher affinity (Kd approximately 0.5 mM). |
| 1300 | 8756680 | This indicates that the binding of CD4 and Hck SH3 to Nef are two compatible and slightly cooperative events. |
| 1301 | 8756680 | The CD4 determinant for downregulation by HIV-1 Nef directly binds to Nef. |
| 1302 | 8756680 | Using heteronuclear NMR spectroscopy, we demonstrate that a 13-residue peptide (MS-QIKRLLSEKKT) from the cytoplasmic tail of CD4 binds to Nef protein. |
| 1303 | 8756680 | This part of CD4 is critical for downregulation of CD4 by HIV-1 Nef [Aiken et al. (1994) Cell 76, 853-864]. |
| 1304 | 8756680 | When Nef is complexed to the SH3 domain of Hck tyrosine protein kinase, the peptide binds to the same site on Nef but with slightly higher affinity (Kd approximately 0.5 mM). |
| 1305 | 8756680 | This indicates that the binding of CD4 and Hck SH3 to Nef are two compatible and slightly cooperative events. |
| 1306 | 8756680 | The CD4 determinant for downregulation by HIV-1 Nef directly binds to Nef. |
| 1307 | 8756680 | Using heteronuclear NMR spectroscopy, we demonstrate that a 13-residue peptide (MS-QIKRLLSEKKT) from the cytoplasmic tail of CD4 binds to Nef protein. |
| 1308 | 8756680 | This part of CD4 is critical for downregulation of CD4 by HIV-1 Nef [Aiken et al. (1994) Cell 76, 853-864]. |
| 1309 | 8756680 | When Nef is complexed to the SH3 domain of Hck tyrosine protein kinase, the peptide binds to the same site on Nef but with slightly higher affinity (Kd approximately 0.5 mM). |
| 1310 | 8756680 | This indicates that the binding of CD4 and Hck SH3 to Nef are two compatible and slightly cooperative events. |
| 1311 | 8756680 | The CD4 determinant for downregulation by HIV-1 Nef directly binds to Nef. |
| 1312 | 8756680 | Using heteronuclear NMR spectroscopy, we demonstrate that a 13-residue peptide (MS-QIKRLLSEKKT) from the cytoplasmic tail of CD4 binds to Nef protein. |
| 1313 | 8756680 | This part of CD4 is critical for downregulation of CD4 by HIV-1 Nef [Aiken et al. (1994) Cell 76, 853-864]. |
| 1314 | 8756680 | When Nef is complexed to the SH3 domain of Hck tyrosine protein kinase, the peptide binds to the same site on Nef but with slightly higher affinity (Kd approximately 0.5 mM). |
| 1315 | 8756680 | This indicates that the binding of CD4 and Hck SH3 to Nef are two compatible and slightly cooperative events. |
| 1316 | 8765018 | The role of CD8+ T cells in the initiation of insulin-dependent diabetes mellitus. |
| 1317 | 8765018 | While it is generally accepted that T cells are critical for the development of diabetes in the non-obese diabetic (NOD) mouse, the precise functions of the CD4+ and CD8+ subsets remain ill-defined. |
| 1318 | 8765018 | Transfer experiments have provided evidence that CD4+ cells are the disease initiators, provoking massive mononuclear leukocyte infiltration into the pancreatic islets, while CD8+ cells play an effector role, responsible for the final destruction of islet beta cells. |
| 1319 | 8765018 | It was surprising, then, to find that NOD mice carrying a null mutation at the beta 2-microglobulin (beta 2-mu) locus, and thereby lacking major histocompatibility complex class I molecules and CD8+ T cells, developed neither insulitis nor diabetes. |
| 1320 | 8765018 | Transfer experiments indicate that the lack of CD8+ cells during this period somehow alters the phenotype of CD4+ cells, preventing them from expressing their insulitis potential. |
| 1321 | 8765018 | Given that neither the beta 2-mu mutation nor anti-CD8 treatment affect insulitis in a T cell receptor transgenic (tg) mouse strain with a CD4+ T cell repertoire highly skewed for an anti-islet cell reactivity, the most straight-forward interpretation of these observations is that CD8+ cells are required for effective priming and expansion of autoreactive CD4+ cells. |
| 1322 | 8765018 | The role of CD8+ T cells in the initiation of insulin-dependent diabetes mellitus. |
| 1323 | 8765018 | While it is generally accepted that T cells are critical for the development of diabetes in the non-obese diabetic (NOD) mouse, the precise functions of the CD4+ and CD8+ subsets remain ill-defined. |
| 1324 | 8765018 | Transfer experiments have provided evidence that CD4+ cells are the disease initiators, provoking massive mononuclear leukocyte infiltration into the pancreatic islets, while CD8+ cells play an effector role, responsible for the final destruction of islet beta cells. |
| 1325 | 8765018 | It was surprising, then, to find that NOD mice carrying a null mutation at the beta 2-microglobulin (beta 2-mu) locus, and thereby lacking major histocompatibility complex class I molecules and CD8+ T cells, developed neither insulitis nor diabetes. |
| 1326 | 8765018 | Transfer experiments indicate that the lack of CD8+ cells during this period somehow alters the phenotype of CD4+ cells, preventing them from expressing their insulitis potential. |
| 1327 | 8765018 | Given that neither the beta 2-mu mutation nor anti-CD8 treatment affect insulitis in a T cell receptor transgenic (tg) mouse strain with a CD4+ T cell repertoire highly skewed for an anti-islet cell reactivity, the most straight-forward interpretation of these observations is that CD8+ cells are required for effective priming and expansion of autoreactive CD4+ cells. |
| 1328 | 8765018 | The role of CD8+ T cells in the initiation of insulin-dependent diabetes mellitus. |
| 1329 | 8765018 | While it is generally accepted that T cells are critical for the development of diabetes in the non-obese diabetic (NOD) mouse, the precise functions of the CD4+ and CD8+ subsets remain ill-defined. |
| 1330 | 8765018 | Transfer experiments have provided evidence that CD4+ cells are the disease initiators, provoking massive mononuclear leukocyte infiltration into the pancreatic islets, while CD8+ cells play an effector role, responsible for the final destruction of islet beta cells. |
| 1331 | 8765018 | It was surprising, then, to find that NOD mice carrying a null mutation at the beta 2-microglobulin (beta 2-mu) locus, and thereby lacking major histocompatibility complex class I molecules and CD8+ T cells, developed neither insulitis nor diabetes. |
| 1332 | 8765018 | Transfer experiments indicate that the lack of CD8+ cells during this period somehow alters the phenotype of CD4+ cells, preventing them from expressing their insulitis potential. |
| 1333 | 8765018 | Given that neither the beta 2-mu mutation nor anti-CD8 treatment affect insulitis in a T cell receptor transgenic (tg) mouse strain with a CD4+ T cell repertoire highly skewed for an anti-islet cell reactivity, the most straight-forward interpretation of these observations is that CD8+ cells are required for effective priming and expansion of autoreactive CD4+ cells. |
| 1334 | 8765018 | The role of CD8+ T cells in the initiation of insulin-dependent diabetes mellitus. |
| 1335 | 8765018 | While it is generally accepted that T cells are critical for the development of diabetes in the non-obese diabetic (NOD) mouse, the precise functions of the CD4+ and CD8+ subsets remain ill-defined. |
| 1336 | 8765018 | Transfer experiments have provided evidence that CD4+ cells are the disease initiators, provoking massive mononuclear leukocyte infiltration into the pancreatic islets, while CD8+ cells play an effector role, responsible for the final destruction of islet beta cells. |
| 1337 | 8765018 | It was surprising, then, to find that NOD mice carrying a null mutation at the beta 2-microglobulin (beta 2-mu) locus, and thereby lacking major histocompatibility complex class I molecules and CD8+ T cells, developed neither insulitis nor diabetes. |
| 1338 | 8765018 | Transfer experiments indicate that the lack of CD8+ cells during this period somehow alters the phenotype of CD4+ cells, preventing them from expressing their insulitis potential. |
| 1339 | 8765018 | Given that neither the beta 2-mu mutation nor anti-CD8 treatment affect insulitis in a T cell receptor transgenic (tg) mouse strain with a CD4+ T cell repertoire highly skewed for an anti-islet cell reactivity, the most straight-forward interpretation of these observations is that CD8+ cells are required for effective priming and expansion of autoreactive CD4+ cells. |
| 1340 | 8775551 | Twenty-four patients with moderately controlled insulin dependent diabetes with a duration of diabetes ranging from 2 to 10 years as well as 17 control subjects were vaccinated against hepatitis B virus using Gen Hevac B vaccine. |
| 1341 | 8775551 | In diabetic patients the most striking feature was the reduced CD4/CD8 ratio which was significantly lower (P < 0.001) than that of the control group. |
| 1342 | 8786019 | Defective expression of the apoptosis-inducing CD95 (Fas/APO-1) molecule on T and B cells in IDDM. |
| 1343 | 8786019 | To determine whether a defect involving the CD95 receptor is associated with human insulin-dependent diabetes mellitus (IDDM), we have studied the expression of CD95 on peripheral blood mononuclear cells from IDDM patients at different stages of the disease. |
| 1344 | 8786019 | Three-colour flow cytometry and mean fluorescence analysis showed that T and B lymphocytes from newly diagnosed IDDM and patients with long-standing disease, and subjects at high risk of developing the disease were highly defective in CD95 expression (p < 0.001), whereas monocytes from all the groups studied expressed normal amounts of CD95 molecules on their cell surface. |
| 1345 | 8786019 | T-cell subset analysis showed that the impairment of CD95 expression in IDDM patients and high-risk subjects involved both CD3+ CD4+ (p < 0.001) and CD3+ CD8+ cells (p range: < 0.01-0.001), suggesting that this alteration concerns both helper and cytotoxic T cells. |
| 1346 | 8786019 | Moreover, after activation in vitro with anti-CD3 monoclonal antibody, T cells from newly diagnosed IDDM patients maintained a reduced CD95 expression during the entire cell culture period (24-72 h) in comparison to the control population (p < 0.001). |
| 1347 | 8786019 | In conclusion, we found a reduced expression of the apoptosis-inducing CD95 receptor on T and B lymphocytes of individuals with clinical and preclinical IDDM. |
| 1348 | 8816968 | Insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse results from effector T cell-mediated autoimmune processes directed against pancreatic beta cells. |
| 1349 | 8816968 | The clone was found to produce substantial amounts of transforming growth factor beta (TGF-beta), IL-10, and IFN-gamma, but not IL-2 or IL-4, indicating that this T cell clone is not a member of either the classic Th1 or Th2 cell type. |
| 1350 | 8816968 | On the basis of these observations, we suggest that a new type of CD4+ suppressor T cell, NY4.2, by secreting TGF-beta, can prevent effector T cell-mediated beta cell destruction. |
| 1351 | 8826963 | Derived from NOD mice, diabetogenic T-cell lines and clones have for the most part been CD4+ and T-helper 1 (Th1)-like in their cytokine production. |
| 1352 | 8826963 | Some CD8+ cytotoxic clones have also been reported, although these have generally not transferred diabetes in the absence of CD4+ T-cells. |
| 1353 | 8826963 | While many of the T-cell lines and clones described react with islets, isolated islet cells, or islet membrane preparations, others have known antigen specificities, reacting with defined islet cell proteins such as insulin, GAD, and heat shock proteins. |
| 1354 | 8826963 | Derived from NOD mice, diabetogenic T-cell lines and clones have for the most part been CD4+ and T-helper 1 (Th1)-like in their cytokine production. |
| 1355 | 8826963 | Some CD8+ cytotoxic clones have also been reported, although these have generally not transferred diabetes in the absence of CD4+ T-cells. |
| 1356 | 8826963 | While many of the T-cell lines and clones described react with islets, isolated islet cells, or islet membrane preparations, others have known antigen specificities, reacting with defined islet cell proteins such as insulin, GAD, and heat shock proteins. |
| 1357 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 1358 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 1359 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 1360 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 1361 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 1362 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 1363 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 1364 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 1365 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 1366 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 1367 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 1368 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 1369 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 1370 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 1371 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 1372 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 1373 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 1374 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 1375 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 1376 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 1377 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 1378 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 1379 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 1380 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 1381 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 1382 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 1383 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 1384 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 1385 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 1386 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 1387 | 8845051 | We measured splenocyte and thymocyte subsets by cytofluorometry (CD4+ CD8-, CD4- CD8+, and double-positive thymocytes; Thy1-2+, CD3+, CD4+, and CD8+ spleen cells) and determined splenocyte mitogenesis in response to concanavalin A. |
| 1388 | 8864825 | Most female NOD mice spontaneously develop insulin-dependent diabetes mellitus (IDDM) after the 4th month of age. |
| 1389 | 8864825 | Flow cytometry was used to compare M. avium-infected, HK M. avium inoculated and untreated NOD and NON mice with regard to subpopulations of splenic lymphocytes bearing the surface antigens CD3, CD4, CD8, IgM and B220. |
| 1390 | 8871671 | Expression of a beta2m transgene controlled by the rat insulin promoter (RIP-beta2m) in NODbeta2mnull mice resulted in reconstitution of IFN-gamma-inducible cell surface MHC class I protein on pancreatic beta-cells. |
| 1391 | 8871671 | These studies demonstrate that beta2m and cell surface MHC class I expression on beta-cells are essential for the initiation of diabetes in the NOD mouse and further confirm that efficient progression to diabetes requires both CD4+ and CD8+ T cells. |
| 1392 | 8878395 | RAPA interfered with the maturation of thymocytes to the CD4+CD8+ DP stage, which resulted in a relative increase in TCRalphabeta(-) immature thymocytes, localized in a rim along the outer cortex. |
| 1393 | 8878395 | In the Lewis rat, a normal CD4/CD8 T-cell ratio and an increased Th1/Th2 ratio was observed within the T-cell population. |
| 1394 | 8878395 | The CD4/CD8 T-cell ratio was decreased as a result of a lower number of CD4 T cells; the Th1/Th2 ratio was increased but Th2 remained higher. |
| 1395 | 8878395 | RAPA interfered with the maturation of thymocytes to the CD4+CD8+ DP stage, which resulted in a relative increase in TCRalphabeta(-) immature thymocytes, localized in a rim along the outer cortex. |
| 1396 | 8878395 | In the Lewis rat, a normal CD4/CD8 T-cell ratio and an increased Th1/Th2 ratio was observed within the T-cell population. |
| 1397 | 8878395 | The CD4/CD8 T-cell ratio was decreased as a result of a lower number of CD4 T cells; the Th1/Th2 ratio was increased but Th2 remained higher. |
| 1398 | 8878395 | RAPA interfered with the maturation of thymocytes to the CD4+CD8+ DP stage, which resulted in a relative increase in TCRalphabeta(-) immature thymocytes, localized in a rim along the outer cortex. |
| 1399 | 8878395 | In the Lewis rat, a normal CD4/CD8 T-cell ratio and an increased Th1/Th2 ratio was observed within the T-cell population. |
| 1400 | 8878395 | The CD4/CD8 T-cell ratio was decreased as a result of a lower number of CD4 T cells; the Th1/Th2 ratio was increased but Th2 remained higher. |
| 1401 | 8878437 | Four pancreatic islet-specific CD4+ helper T (Th) 1 (Th1) clones and two Th1 clones transduced with an SRalpha promoter-linked murine IL-10 (mIL-10) cDNA of 2.0-6.0 x 10(6) cells were adoptively transferred to nonobese diabetic (NOD) mice at age 8 d. |
| 1402 | 8878437 | RT-PCR detected the decrease of IFN-gamma mRNA relative to IL-10 mRNA in IL-10-transduced Th1 clones in vitro and also in recipient islets. |
| 1403 | 8878437 | The suppression of diabetes through decreasing IFN-gamma mRNA by the tissue-specific delivery of IL-10 to pancreatic islets with IL-10-transduced Th1 cells affords us the starting basis to develop the gene therapy for autoimmune diabetes. |
| 1404 | 8882417 | Immunoenzyme staining (ABC-technique) and monoclonal antibodies defining CD4, CD8, CD11b, TCR alpha/beta, gamma/delta, V beta 2, V beta 4, V beta 6, V beta 7, V beta 8.1, 2, V beta 10b and V beta 11 were used to examine the infiltrating mononuclear cells (MNC) in salivary glands of NOD mice. |
| 1405 | 8882417 | A predominance of CD4+ T-cells was identified, while a small population of CD8+ cells was found in the salivary gland infiltrates. |
| 1406 | 8882417 | Immunoenzyme staining (ABC-technique) and monoclonal antibodies defining CD4, CD8, CD11b, TCR alpha/beta, gamma/delta, V beta 2, V beta 4, V beta 6, V beta 7, V beta 8.1, 2, V beta 10b and V beta 11 were used to examine the infiltrating mononuclear cells (MNC) in salivary glands of NOD mice. |
| 1407 | 8882417 | A predominance of CD4+ T-cells was identified, while a small population of CD8+ cells was found in the salivary gland infiltrates. |
| 1408 | 8889212 | These findings clearly demonstrate (1) a critical role for CD8 T cells in the acute rejection of pancreatic islet tissue allografts and (2) tissue-specific differences in the participation of CD4 T cells as primary effectors in the rejection reaction. |
| 1409 | 8889212 | Thus, the participation of CD8 and CD4 T cells as primary effectors of graft rejection depends on which class or classes of MHC antigens are constitutively expressed on graft parenchymal cells and are available for recognition. |
| 1410 | 8889212 | These findings clearly demonstrate (1) a critical role for CD8 T cells in the acute rejection of pancreatic islet tissue allografts and (2) tissue-specific differences in the participation of CD4 T cells as primary effectors in the rejection reaction. |
| 1411 | 8889212 | Thus, the participation of CD8 and CD4 T cells as primary effectors of graft rejection depends on which class or classes of MHC antigens are constitutively expressed on graft parenchymal cells and are available for recognition. |
| 1412 | 8906855 | Acceleration of spontaneous diabetes in TCR-beta-transgenic nonobese diabetic mice by beta-cell cytotoxic CD8+ T cells expressing identical endogenous TCR-alpha chains. |
| 1413 | 8906855 | Here we report on the use of single TCR-beta transgenic mice to study the mechanisms that drive the accumulation of pathogenic T cells in the pancreatic islets of nonobese diabetic (NOD) mice, a model for insulin-dependent diabetes mellitus. |
| 1414 | 8906855 | Expression of the V(beta)8.1+ TCR-beta rearrangement of a diabetogenic H-2Kd-restricted beta cell cytotoxic CD8+ T cell (beta-CTL) clone in NOD mice caused a 10-fold increase in the peripheral precursor frequency of beta-CTL and a selective acceleration of the recruitment of CD8+ T cells to the pancreatic islets of prediabetic animals. |
| 1415 | 8906855 | Most islet-derived beta-CTL from diabetic transgenic NOD mice expressed an endogenously-derived TCR-alpha sequence identical to that of the clonotype donating the TCR-beta transgene, and a TCR-alpha-CDR3 sequence homologous to those expressed by most islet-derived beta-CTL from nontransgenic NOD mice. |
| 1416 | 8906855 | TCR-beta transgene expression did not change the peripheral frequency of beta cell-specific CD4+ T cells, the rate at which these cells accumulated in the pancreatic islets, or the incidence of diabetes. |
| 1417 | 8906855 | Taken together, our data indicate that retention of CD8+ and CD4+ T cells in the pancreatic islets of NOD mice is driven by beta cell autoantigens, rather than by local superantigens or non-Ag-specific stimuli, and that beta-CTL are major effectors of beta cell damage in spontaneous insulin-dependent diabetes mellitus. |
| 1418 | 8906855 | Acceleration of spontaneous diabetes in TCR-beta-transgenic nonobese diabetic mice by beta-cell cytotoxic CD8+ T cells expressing identical endogenous TCR-alpha chains. |
| 1419 | 8906855 | Here we report on the use of single TCR-beta transgenic mice to study the mechanisms that drive the accumulation of pathogenic T cells in the pancreatic islets of nonobese diabetic (NOD) mice, a model for insulin-dependent diabetes mellitus. |
| 1420 | 8906855 | Expression of the V(beta)8.1+ TCR-beta rearrangement of a diabetogenic H-2Kd-restricted beta cell cytotoxic CD8+ T cell (beta-CTL) clone in NOD mice caused a 10-fold increase in the peripheral precursor frequency of beta-CTL and a selective acceleration of the recruitment of CD8+ T cells to the pancreatic islets of prediabetic animals. |
| 1421 | 8906855 | Most islet-derived beta-CTL from diabetic transgenic NOD mice expressed an endogenously-derived TCR-alpha sequence identical to that of the clonotype donating the TCR-beta transgene, and a TCR-alpha-CDR3 sequence homologous to those expressed by most islet-derived beta-CTL from nontransgenic NOD mice. |
| 1422 | 8906855 | TCR-beta transgene expression did not change the peripheral frequency of beta cell-specific CD4+ T cells, the rate at which these cells accumulated in the pancreatic islets, or the incidence of diabetes. |
| 1423 | 8906855 | Taken together, our data indicate that retention of CD8+ and CD4+ T cells in the pancreatic islets of NOD mice is driven by beta cell autoantigens, rather than by local superantigens or non-Ag-specific stimuli, and that beta-CTL are major effectors of beta cell damage in spontaneous insulin-dependent diabetes mellitus. |
| 1424 | 8918687 | Mature CD4+ CD8- thymocytes are phenotypically heterogeneous on activation. |
| 1425 | 8918687 | The expression of class II MHC antigens by allogeneically activated thymocytes demonstrated a novel heterogeneity amongst mature CD4+ CD8- thymocytes that could not readily be accounted for in terms of differences in maturity of the cells, in the affinity of the TCR for the stimulating ligands or in the stage in the cell cycle. |
| 1426 | 8918687 | Mature CD4+ CD8- thymocytes are phenotypically heterogeneous on activation. |
| 1427 | 8918687 | The expression of class II MHC antigens by allogeneically activated thymocytes demonstrated a novel heterogeneity amongst mature CD4+ CD8- thymocytes that could not readily be accounted for in terms of differences in maturity of the cells, in the affinity of the TCR for the stimulating ligands or in the stage in the cell cycle. |
| 1428 | 8920883 | To analyze the effects of TNF alpha in insulin-dependent diabetes mellitus (IDDM), we have generated nonobese diabetic (NOD) transgenic mice expressing TNF alpha under the control of the rat insulin II promoter (RIP). |
| 1429 | 8920883 | In transgenic mice, TNF alpha expression on the islets resulted in massive insulitis, composed of CD4+ T cells, CD8+ T cells, and B cells. |
| 1430 | 8920883 | Despite infiltration of considerable number of lymphoid cells in islets, expression of TNF alpha protected NOD mice from IDDM. |
| 1431 | 8920883 | Diabetes was induced however, in the RIP-TNF alpha transgenic mice when CD8+ diabetogenic cloned T cells or splenic cells from diabetic NOD mice were adoptively transferred to these mice. |
| 1432 | 8921958 | CD4+CD8- thymocytes that express L-selectin protect rats from diabetes upon adoptive transfer. |
| 1433 | 8921958 | Further studies have demonstrated that the transfer of CD4+CD8- thymocytes, like that of unfractionated CD4+ peripheral T cells, also protects approximately half of recipients from diabetes suggesting that, as with the peripheral T cells, a functional heterogeneity may exist amongst CD4+CD8- thymocytes. |
| 1434 | 8921958 | In this study, we show that L-selectin is expressed by 50-60% of all CD4+CD8- thymocytes from 6-week-old rats. |
| 1435 | 8921958 | Adoptive transfer of these populations into thymectomized and irradiated rats revealed that the protection from diabetes observed by CD4+CD8- thymocytes was mediated almost entirely by the L-selectin+ subset. |
| 1436 | 8921958 | These data indicate that CD4+CD8- thymocytes must mature to the stage of L-selectin expression, before they can mediate normal T cell function. |
| 1437 | 8921958 | CD4+CD8- thymocytes that express L-selectin protect rats from diabetes upon adoptive transfer. |
| 1438 | 8921958 | Further studies have demonstrated that the transfer of CD4+CD8- thymocytes, like that of unfractionated CD4+ peripheral T cells, also protects approximately half of recipients from diabetes suggesting that, as with the peripheral T cells, a functional heterogeneity may exist amongst CD4+CD8- thymocytes. |
| 1439 | 8921958 | In this study, we show that L-selectin is expressed by 50-60% of all CD4+CD8- thymocytes from 6-week-old rats. |
| 1440 | 8921958 | Adoptive transfer of these populations into thymectomized and irradiated rats revealed that the protection from diabetes observed by CD4+CD8- thymocytes was mediated almost entirely by the L-selectin+ subset. |
| 1441 | 8921958 | These data indicate that CD4+CD8- thymocytes must mature to the stage of L-selectin expression, before they can mediate normal T cell function. |
| 1442 | 8921958 | CD4+CD8- thymocytes that express L-selectin protect rats from diabetes upon adoptive transfer. |
| 1443 | 8921958 | Further studies have demonstrated that the transfer of CD4+CD8- thymocytes, like that of unfractionated CD4+ peripheral T cells, also protects approximately half of recipients from diabetes suggesting that, as with the peripheral T cells, a functional heterogeneity may exist amongst CD4+CD8- thymocytes. |
| 1444 | 8921958 | In this study, we show that L-selectin is expressed by 50-60% of all CD4+CD8- thymocytes from 6-week-old rats. |
| 1445 | 8921958 | Adoptive transfer of these populations into thymectomized and irradiated rats revealed that the protection from diabetes observed by CD4+CD8- thymocytes was mediated almost entirely by the L-selectin+ subset. |
| 1446 | 8921958 | These data indicate that CD4+CD8- thymocytes must mature to the stage of L-selectin expression, before they can mediate normal T cell function. |
| 1447 | 8921958 | CD4+CD8- thymocytes that express L-selectin protect rats from diabetes upon adoptive transfer. |
| 1448 | 8921958 | Further studies have demonstrated that the transfer of CD4+CD8- thymocytes, like that of unfractionated CD4+ peripheral T cells, also protects approximately half of recipients from diabetes suggesting that, as with the peripheral T cells, a functional heterogeneity may exist amongst CD4+CD8- thymocytes. |
| 1449 | 8921958 | In this study, we show that L-selectin is expressed by 50-60% of all CD4+CD8- thymocytes from 6-week-old rats. |
| 1450 | 8921958 | Adoptive transfer of these populations into thymectomized and irradiated rats revealed that the protection from diabetes observed by CD4+CD8- thymocytes was mediated almost entirely by the L-selectin+ subset. |
| 1451 | 8921958 | These data indicate that CD4+CD8- thymocytes must mature to the stage of L-selectin expression, before they can mediate normal T cell function. |
| 1452 | 8921958 | CD4+CD8- thymocytes that express L-selectin protect rats from diabetes upon adoptive transfer. |
| 1453 | 8921958 | Further studies have demonstrated that the transfer of CD4+CD8- thymocytes, like that of unfractionated CD4+ peripheral T cells, also protects approximately half of recipients from diabetes suggesting that, as with the peripheral T cells, a functional heterogeneity may exist amongst CD4+CD8- thymocytes. |
| 1454 | 8921958 | In this study, we show that L-selectin is expressed by 50-60% of all CD4+CD8- thymocytes from 6-week-old rats. |
| 1455 | 8921958 | Adoptive transfer of these populations into thymectomized and irradiated rats revealed that the protection from diabetes observed by CD4+CD8- thymocytes was mediated almost entirely by the L-selectin+ subset. |
| 1456 | 8921958 | These data indicate that CD4+CD8- thymocytes must mature to the stage of L-selectin expression, before they can mediate normal T cell function. |
| 1457 | 8930185 | We tested whether aminoguanidine (AG), a competitive inhibitor of inducible nitric oxide synthase, might block beta cell destruction and prevent insulin-dependent diabetes mellitus in vivo. |
| 1458 | 8930185 | In terms of therapy, life-table analysis indicated the frequency of insulin-dependent diabetes mellitus (6/30 AG-treated vs. 11/31 vehicle-treated, P = .25) and insulitis scores (2.0 +/- 1.1 vs. 2.4 +/- 1.2 in nondiabetic AG- and vehicle-treated mice at 32 wk, respectively, P = .20) were similar in both groups. |
| 1459 | 8930185 | Flow cytometric analysis revealed no quantitative differences in islet infiltrating macrophages, CD4+ or CD8+ T lymphocytes between groups of animals randomly killed at 8, 16 and 32 wk. |
| 1460 | 8934930 | Commonly observed features of these mice include organized lymphocytic foci, composed of CD4+ and CD8+ T-cells, in both the salivary and the lacrimal glands. |
| 1461 | 8937686 | Abnormalities in postthymic T cell development in the BB/W rat model of autoimmune insulin-dependent diabetes mellitus (IDDM) result in part from a lymphopenia (lyp) gene defect. |
| 1462 | 8937686 | These results suggested that, at a minimum, an arrest in maturation of the Thy1+ precursors of RT6+ T cells occurs postthymically in DP rats. |
| 1463 | 8937686 | The results showed that in DP, as compared with DR, rats: 1) 5-fold fewer RTE's are exported from the thymus per 24 hr; 2) more than 80% of the RTE's are CD4+; 3) most of the immediate descendants of RTE's disappear from the peripheral lymphoid tissues within one week after export from the thymus; and 4) few of the descendants of the RTE's that do survive differentiate into RT6+ T cells. |
| 1464 | 8943570 | IL-7 reverses NK1+ T cell-defective IL-4 production in the non-obese diabetic mouse. |
| 1465 | 8943570 | We recently reported that IL-7 preferentially promotes the in vitro expansion of a discrete MHC class I-dependent lymphocyte subset comprising both CD4+ and CD4-CD8- TCR alpha beta + cells bearing several NK cells markers such NK1.1 and Ly-49. |
| 1466 | 8943570 | In the present experiments, the addition of exogenous IL-7 completely restored IL-4 production by anti-TCR alpha beta-stimulated mature (HSA-CD8-) thymocytes in NOD mice. |
| 1467 | 8943570 | A short 2 h preincubation with IL-7 was sufficient to restore both the expression of IL-4 mRNA and IL-4 production capacity. |
| 1468 | 8943570 | This was related to a direct effect on NK1+ thymocytes since: (i) the effect of IL-7 was restricted to the non-mainstream MEL-14- 3G11- TCR alpha beta + subset which mostly concentrates the IL-4-producing capacity and (ii) IL-7 did not restore IL-4 production in class I-deficient mice which lack the NK1+ T cell subset. |
| 1469 | 8943570 | These results were extended in vivo by showing that the IL-7 treatment significantly increased the anti-CD3 triggered IL-4 production by NK1+ T spleen cells. |
| 1470 | 8949575 | A diagnosis of thyroid Langerhans' cell histiocytosis was finally made on the basis of the presence of Birbeck granules and CD1a and CD4 antigen in the thyroid tumour cells. |
| 1471 | 8953520 | The lymphocyte and macrophage profile in the pancreas and spleen of NOD mice: percentage of interleukin-2 and prolactin receptors on immunocompetent cell subsets. |
| 1472 | 8953520 | Using analytical fluorescent cell cytometry we quantitated the percentages of CD4, and CD8 T-cells, B-cells and macrophages and the percentages of these subsets expressing interleukin-2 (IL-2R), prolactin (PRLR) and Hi-intensity PRL (Hi-PRLR) receptors. |
| 1473 | 8953520 | Evaluation of T-splenocytes indicated a 2:1 ratio of CD4 to CD8 T-lymphocytes in the spleen. |
| 1474 | 8953520 | Pancreatic immunocompetent cell subsets expressed lower percentages of IL-2R, PRLR and Hi-PRLR compared to splenocytes. |
| 1475 | 8953520 | The results did not demonstrate any dramatic differences in the immunocompetent cell populations of the spleen or pancreas between male and female animals, however we were able to establish the percentage of immunocompetent cells with IL-2R, PRLR and Hi-PRLR as a reference for future studies. |
| 1476 | 8953520 | The lymphocyte and macrophage profile in the pancreas and spleen of NOD mice: percentage of interleukin-2 and prolactin receptors on immunocompetent cell subsets. |
| 1477 | 8953520 | Using analytical fluorescent cell cytometry we quantitated the percentages of CD4, and CD8 T-cells, B-cells and macrophages and the percentages of these subsets expressing interleukin-2 (IL-2R), prolactin (PRLR) and Hi-intensity PRL (Hi-PRLR) receptors. |
| 1478 | 8953520 | Evaluation of T-splenocytes indicated a 2:1 ratio of CD4 to CD8 T-lymphocytes in the spleen. |
| 1479 | 8953520 | Pancreatic immunocompetent cell subsets expressed lower percentages of IL-2R, PRLR and Hi-PRLR compared to splenocytes. |
| 1480 | 8953520 | The results did not demonstrate any dramatic differences in the immunocompetent cell populations of the spleen or pancreas between male and female animals, however we were able to establish the percentage of immunocompetent cells with IL-2R, PRLR and Hi-PRLR as a reference for future studies. |
| 1481 | 8976193 | Previous studies have shown that the disease is prevented by the intravenous injection of 5 x 10(6) CD4+ CD45RC-TCR alpha beta+ RT6+ peripheral T cells from normal syngeneic donors. |
| 1482 | 8976193 | However, we now report that the CD4+ CD8- population of mature thymocytes is a very potent source of cells, with the capacity to prevent diabetes in our lymphopenic animals. |
| 1483 | 8976193 | Previous studies have shown that the disease is prevented by the intravenous injection of 5 x 10(6) CD4+ CD45RC-TCR alpha beta+ RT6+ peripheral T cells from normal syngeneic donors. |
| 1484 | 8976193 | However, we now report that the CD4+ CD8- population of mature thymocytes is a very potent source of cells, with the capacity to prevent diabetes in our lymphopenic animals. |
| 1485 | 8985314 | The percentage of CD4+ T cells in peripheral blood mononuclear cells was markedly decreased in the 5DHT-treated females compared with those in controls (37.1 +/- 4.8 vs 51.3 +/- 9.3, P < 0.02), whereas no significant differences in the percentage of CD8+ T cells were observed between treated and control female mice. |
| 1486 | 8990188 | This mouse produces CD4+ T cells bearing transgenic T cell receptor but is devoid of CD8+ T cells and B cells. |
| 1487 | 8994867 | The contributions of CD4+ and CD8+ T cells to beta cell destruction are beginning to be understood and this information will probably be of value in the design of intervention strategies for use in human subjects. |
| 1488 | 9012359 | Diabetogenic T-cell clones have been mostly of the CD4+, Th1 phenotype, but CD8+ T cell clones are also capable of transferring disease. |
| 1489 | 9012359 | In some cases, T-cell lines and clones (CD4+ and CD8+) have been found to have protective properties. |
| 1490 | 9012359 | However, there is an increasing number of reports of T cells specific for defined islet proteins, such as insulin and GAD, and some of these lines can induce disease. |
| 1491 | 9012359 | Diabetogenic T-cell clones have been mostly of the CD4+, Th1 phenotype, but CD8+ T cell clones are also capable of transferring disease. |
| 1492 | 9012359 | In some cases, T-cell lines and clones (CD4+ and CD8+) have been found to have protective properties. |
| 1493 | 9012359 | However, there is an increasing number of reports of T cells specific for defined islet proteins, such as insulin and GAD, and some of these lines can induce disease. |
| 1494 | 9013986 | To investigate whether the immunosuppressive neuropeptide calcitonin gene-related peptide (CGRP) was a potential candidate for tissue-specific gene therapy, we engineered nonobese diabetic (NOD) mice to produce CGRP in beta cells by placing the modified calcitonin gene under the control of the rat insulin promoter. |
| 1495 | 9013986 | CGRP inhibits CD4 T cell production of the cytokines that have been implicated in the pathogeny of type I diabetes. |
| 1496 | 9013986 | The production of CGRP by beta cells prevented insulin-dependent diabetes mellitus in male and reduced its incidence by 63% in female mice. |
| 1497 | 9020334 | At the termination of the experiment, recipient peripheral blood lymphocytes (PBL) were characterized by flow cytometry (FACS) for class I, CD4, CD8, RT6.1, and RT6.2, a T cell maturation marker found in WF but not BB rats. |
| 1498 | 9075796 | Association between alphabetaTCR+CD4-CD8- T-cell deficiency and IDDM in NOD/Lt mice. |
| 1499 | 9114036 | Thus, such chimeras regularly show CD4 and CD8 T cell-mediated insulitis and sialitis, in contrast with syngeneic or allogeneic chimeras produced with TE from nonautoimmune strains. |
| 1500 | 9115575 | Lymphocytes from 77 newly diagnosed IDDM patients, 58 IDDM patients with disease duration > 6 months and 30 non-diabetic controls (including patients with several inflammatory conditions) were analyzed for membrane expression of CD4, CD8, CD45RA, CD45RO and CD27 molecules by FACS analysis. |
| 1501 | 9115575 | However, the percentage of CD4+ T cells, and consequently the CD4/CD8 ratio were significantly increased in PBL of recently diagnosed diabetic patients compared to the non-diabetic control group (P < 0.005). |
| 1502 | 9115575 | IDDM patients had a lower percentage of resting memory T cells (CD45RO+ CD27+) than the non-diabetic controls. |
| 1503 | 9115575 | The proportion of CD45RO+ lymphocytes lacking the CD27 molecule ((re)-activated memory cells) was similar in IDDM patients and non-diabetic controls. |
| 1504 | 9115575 | Our findings confirm and extend previous observations that a disturbance in lymphocyte subset distribution is present in patients with IDDM showing an increase in the percentages of circulating CD4 lymphocytes. |
| 1505 | 9115575 | Lymphocytes from 77 newly diagnosed IDDM patients, 58 IDDM patients with disease duration > 6 months and 30 non-diabetic controls (including patients with several inflammatory conditions) were analyzed for membrane expression of CD4, CD8, CD45RA, CD45RO and CD27 molecules by FACS analysis. |
| 1506 | 9115575 | However, the percentage of CD4+ T cells, and consequently the CD4/CD8 ratio were significantly increased in PBL of recently diagnosed diabetic patients compared to the non-diabetic control group (P < 0.005). |
| 1507 | 9115575 | IDDM patients had a lower percentage of resting memory T cells (CD45RO+ CD27+) than the non-diabetic controls. |
| 1508 | 9115575 | The proportion of CD45RO+ lymphocytes lacking the CD27 molecule ((re)-activated memory cells) was similar in IDDM patients and non-diabetic controls. |
| 1509 | 9115575 | Our findings confirm and extend previous observations that a disturbance in lymphocyte subset distribution is present in patients with IDDM showing an increase in the percentages of circulating CD4 lymphocytes. |
| 1510 | 9115575 | Lymphocytes from 77 newly diagnosed IDDM patients, 58 IDDM patients with disease duration > 6 months and 30 non-diabetic controls (including patients with several inflammatory conditions) were analyzed for membrane expression of CD4, CD8, CD45RA, CD45RO and CD27 molecules by FACS analysis. |
| 1511 | 9115575 | However, the percentage of CD4+ T cells, and consequently the CD4/CD8 ratio were significantly increased in PBL of recently diagnosed diabetic patients compared to the non-diabetic control group (P < 0.005). |
| 1512 | 9115575 | IDDM patients had a lower percentage of resting memory T cells (CD45RO+ CD27+) than the non-diabetic controls. |
| 1513 | 9115575 | The proportion of CD45RO+ lymphocytes lacking the CD27 molecule ((re)-activated memory cells) was similar in IDDM patients and non-diabetic controls. |
| 1514 | 9115575 | Our findings confirm and extend previous observations that a disturbance in lymphocyte subset distribution is present in patients with IDDM showing an increase in the percentages of circulating CD4 lymphocytes. |
| 1515 | 9133542 | In both cases, the infiltrate was mainly made of CD4+ cells, with few CD8+ cells. |
| 1516 | 9156823 | An invasion with CD4+ and CD8+ cells started between day 4 and 6 in both groups, progressively increasing until rejection. |
| 1517 | 9184917 | Production of both IFN-gamma and IL-5 by Onchocerca volvulus S1 antigen-specific CD4+ T cells from putatively immune individuals. |
| 1518 | 9184917 | These clones, which are the first generated against a recombinant fllarial antigen, produced both IFN-gamma and IL-5 as well as little IL-4, suggestive of a Th0-like phenotype. |
| 1519 | 9184917 | Induction of both IFN-gamma and IL-5 by S1 suggests that it may trigger macrophage plus eosinophil dependent killing of L3 in vivo. |
| 1520 | 9191168 | Role of CD4+CD8- thymocytes in the prevention of autoimmune diabetes. |
| 1521 | 9200479 | To address this question, we constructed transgenic mice expressing MCP-1 controlled by an insulin promoter. |
| 1522 | 9200479 | These mice developed a chronic insulitic infiltrate composed of F4/80+ monocytes with minor populations of CD4+, CD8+, and B220+ cells. |
| 1523 | 9200487 | Measurement of the macrophage-derived cytokines IL-12, TNF-alpha, and IL-1beta revealed a selective increase of their expression, after KRV infection, in the splenic lymphocytes and the pancreatic islets. |
| 1524 | 9200487 | Measurement of CD4+ T cell-derived cytokines revealed that IL-2 and IFN-gamma cytokine gene expression closely correlates with an elevation of IL-12, but IL-4 and IL-10 do not change. |
| 1525 | 9200646 | Inhibition of diabetes by an insulin-reactive CD4 T-cell clone in the nonobese diabetic mouse. |
| 1526 | 9200922 | Indeed the major epitope for insulin-autoreactive CD4+ T cell was successfully identified by this strategy. |
| 1527 | 9218748 | RIP-LCMV transgenic mice that express the viral glycoprotein (GP) or nucleoprotein (NP) from lymphocytic choriomeningitis virus (LCMV) under control of the rat insulin promoter (RIP) in pancreatic beta-cells develop autoimmune diabetes (IDDM) after infection with LCMV. |
| 1528 | 9218748 | The present study shows that upregulation of MHC class II molecules associated with the attraction/activation of antigen presenting cells (APCs) to the islets occurs as soon as 2 days after LCMV inoculation of transgenic mice, clearly before CD4+ and CD8+ lymphocytes are found entering the islets (days 6 and 7 after LCMV inoculation). |
| 1529 | 9218754 | BCG vaccination prevents insulin-dependent diabetes mellitus (IDDM) in NOD mice after disease acceleration with cyclophosphamide. |
| 1530 | 9218754 | We have previously shown that immunotherapy with complete Freund's adjuvant (CFA) or BCG is highly effective in the prevention of spontaneous insulin-dependent diabetes mellitus (IDDM) and in circumventing the rejection of syngeneic islet grafts in diabetic NOD mice. |
| 1531 | 9218754 | The comprehensive effect of BCG vaccination on cytokine production in Cy-treated mice was to increase IL-4 production and change the IL-4/IFN-gamma ratio in both serum and supernatant of spleen cell cultures. |
| 1532 | 9218754 | We found that BCG-induced protection was associated with increased splenic CD4+CD45 RB(high) T cells. |
| 1533 | 9218758 | Molecular role of TGF-beta, secreted from a new type of CD4+ suppressor T cell, NY4.2, in the prevention of autoimmune IDDM in NOD mice. |
| 1534 | 9218758 | A new type of CD4+ T cell clone (NY4.2) isolated from pancreatic islet-infiltrated lymphocytes of acutely diabetic non-obese diabetic (NOD) mice prevents the development of insulin-dependent diabetes mellitus (IDDM) in NOD mice, as well as the recurrence of autoimmune diabetes in syngeneic islet-transplanted NOD mice. |
| 1535 | 9218758 | This investigation was initiated to determine the molecular role TGF-beta plays in the prevention of autoimmune IDDM by determining its effect on IL-2-induced signal transduction in Con A-activated NOD mouse splenocytes and HT-2 cells. |
| 1536 | 9218758 | Second, we determined whether TGF-beta inhibits the activation of Janus kinases (JAKs), as well as signal transducers and activators of transcription (STAT) proteins, involved in an IL-2-induced signalling pathway that normally leads to the proliferation of T cells. |
| 1537 | 9218758 | We found that TGF-beta inhibited tyrosine phosphorylation of JAK1, JAK3, STAT3 and STAT5 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 1538 | 9218758 | Third, we examined whether TGF-beta inhibits the cooperation between STAT proteins and mitogen-activated protein kinase (MAPK), especially extracellular signal-regulated kinase 2 (ERK2). |
| 1539 | 9218758 | We found that TGF-beta inhibited the association of STAT3 and STAT5 with ERK2 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 1540 | 9218758 | On the basis of these observations, we conclude that TGF-beta may interfere with signal transduction via inhibition of the IL-2-induced JAK/STAT pathway and inhibition of the association of STAT proteins with ERK2 in T cells from NOD splenocytes, resulting in the inhibition of IL-2-dependent T cell proliferation. |
| 1541 | 9218758 | TGF-beta-mediated suppression of T cell activation may be responsible for the prevention of effector T cell-mediated autoimmune IDDM in NOD mice by TGF-beta-producing CD4+ suppressor T cells. |
| 1542 | 9218758 | Molecular role of TGF-beta, secreted from a new type of CD4+ suppressor T cell, NY4.2, in the prevention of autoimmune IDDM in NOD mice. |
| 1543 | 9218758 | A new type of CD4+ T cell clone (NY4.2) isolated from pancreatic islet-infiltrated lymphocytes of acutely diabetic non-obese diabetic (NOD) mice prevents the development of insulin-dependent diabetes mellitus (IDDM) in NOD mice, as well as the recurrence of autoimmune diabetes in syngeneic islet-transplanted NOD mice. |
| 1544 | 9218758 | This investigation was initiated to determine the molecular role TGF-beta plays in the prevention of autoimmune IDDM by determining its effect on IL-2-induced signal transduction in Con A-activated NOD mouse splenocytes and HT-2 cells. |
| 1545 | 9218758 | Second, we determined whether TGF-beta inhibits the activation of Janus kinases (JAKs), as well as signal transducers and activators of transcription (STAT) proteins, involved in an IL-2-induced signalling pathway that normally leads to the proliferation of T cells. |
| 1546 | 9218758 | We found that TGF-beta inhibited tyrosine phosphorylation of JAK1, JAK3, STAT3 and STAT5 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 1547 | 9218758 | Third, we examined whether TGF-beta inhibits the cooperation between STAT proteins and mitogen-activated protein kinase (MAPK), especially extracellular signal-regulated kinase 2 (ERK2). |
| 1548 | 9218758 | We found that TGF-beta inhibited the association of STAT3 and STAT5 with ERK2 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 1549 | 9218758 | On the basis of these observations, we conclude that TGF-beta may interfere with signal transduction via inhibition of the IL-2-induced JAK/STAT pathway and inhibition of the association of STAT proteins with ERK2 in T cells from NOD splenocytes, resulting in the inhibition of IL-2-dependent T cell proliferation. |
| 1550 | 9218758 | TGF-beta-mediated suppression of T cell activation may be responsible for the prevention of effector T cell-mediated autoimmune IDDM in NOD mice by TGF-beta-producing CD4+ suppressor T cells. |
| 1551 | 9218758 | Molecular role of TGF-beta, secreted from a new type of CD4+ suppressor T cell, NY4.2, in the prevention of autoimmune IDDM in NOD mice. |
| 1552 | 9218758 | A new type of CD4+ T cell clone (NY4.2) isolated from pancreatic islet-infiltrated lymphocytes of acutely diabetic non-obese diabetic (NOD) mice prevents the development of insulin-dependent diabetes mellitus (IDDM) in NOD mice, as well as the recurrence of autoimmune diabetes in syngeneic islet-transplanted NOD mice. |
| 1553 | 9218758 | This investigation was initiated to determine the molecular role TGF-beta plays in the prevention of autoimmune IDDM by determining its effect on IL-2-induced signal transduction in Con A-activated NOD mouse splenocytes and HT-2 cells. |
| 1554 | 9218758 | Second, we determined whether TGF-beta inhibits the activation of Janus kinases (JAKs), as well as signal transducers and activators of transcription (STAT) proteins, involved in an IL-2-induced signalling pathway that normally leads to the proliferation of T cells. |
| 1555 | 9218758 | We found that TGF-beta inhibited tyrosine phosphorylation of JAK1, JAK3, STAT3 and STAT5 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 1556 | 9218758 | Third, we examined whether TGF-beta inhibits the cooperation between STAT proteins and mitogen-activated protein kinase (MAPK), especially extracellular signal-regulated kinase 2 (ERK2). |
| 1557 | 9218758 | We found that TGF-beta inhibited the association of STAT3 and STAT5 with ERK2 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 1558 | 9218758 | On the basis of these observations, we conclude that TGF-beta may interfere with signal transduction via inhibition of the IL-2-induced JAK/STAT pathway and inhibition of the association of STAT proteins with ERK2 in T cells from NOD splenocytes, resulting in the inhibition of IL-2-dependent T cell proliferation. |
| 1559 | 9218758 | TGF-beta-mediated suppression of T cell activation may be responsible for the prevention of effector T cell-mediated autoimmune IDDM in NOD mice by TGF-beta-producing CD4+ suppressor T cells. |
| 1560 | 9221759 | Autoimmune diabetes is caused by the CD4(+), T helper 1 (Th1) cell-mediated apoptosis of insulin-producing beta cells. |
| 1561 | 9221759 | Moreover, the Th2-mediated destruction of islet cells was mediated by local interleukin-10 (IL-10) production but not by IL-4. |
| 1562 | 9223318 | Glutamic acid decarboxylase isoform 2 (GAD65; EC 4.1.1.15) has been identified as a key target autoantigen of insulin-dependent diabetes mellitus (IDDM). |
| 1563 | 9223318 | IDDM is genetically associated with the major histocompatibility complex (MHC), and particular alleles from the HLA-DQ and HLA-DR loci contribute to disease. |
| 1564 | 9223318 | We have utilized HLA-DR(alpha1*0101,beta1*0401) (hereafter referred to as DR0401), human CD4, murine class II null triple transgenic mice and recombinant GAD65 to generate T cell hybridomas, and we have used overlapping sets of peptides to map the immunodominant epitopes of this autoantigen. |
| 1565 | 9223318 | Immunodominant GAD65 epitopes defined in transgenic mice correspond to GAD65 regions previously shown to elicit T cell responses specifically in DR0401 IDDM patients, underscoring the validity of this approach. |
| 1566 | 9275116 | After allogeneic co-culture, lymphocyte activation was found by an increased release of the cytokines interferon-gamma, interleukin 2, and macrophage inflammatory protein 2, as well as by an enhanced expression of the interleukin 2 receptor on CD4+ T and CD8+ T cells. |
| 1567 | 9275116 | These changes comprised not only the enhancement of MHC class I and intercellular adhesion molecule 1 but also the induction of MHC class II antigens on pancreatic beta cells. |
| 1568 | 9294207 | With this approach, two peptides were identified that stimulate the beta cell-reactive CD4+ T cell clone 1c10, which was isolated from a newly diagnosed insulin-dependent diabetes mellitus patient. |
| 1569 | 9304048 | PGAI, also called APECED (autoimmune polyendocrinopathy, candidiasis and ectodermal dystrophy), is an autosomal recessive disorder, appearing in childhood and typically characterized by hypoparathyroidism (unusual in PGAII and PGAIII) and adrenal insufficiency. |
| 1570 | 9304048 | In APECED, autoimmune destruction of the pancreatic beta cells with development of insulin-dependent type 1 diabetes is possible, but less frequent than in the other PGAs, especially PGAII. |
| 1571 | 9304048 | In this patient no organo-specific antibodies were detected and the only immunologic disorder was a small decrease of CD3 and CD4/CD8 ratio, both CD4 and CD8 being at the lower normal range. |
| 1572 | 9314549 | Insulitis with infiltration of CD4(+) and CD8(+) T cells occurred similarly in both groups of animals. |
| 1573 | 9324360 | Here we demonstrate that transgenic mice expressing both TNFalpha and the Leishmania major LACK antigen in the pancreas (RIP-TNFalpha/RIP-LACK) exhibit an impaired ability to mount a CD4+ T cell response against LACK. |
| 1574 | 9324360 | In addition, peripheral CD4+ T cells from TCR transgenic mice (TCR-LACK/RIP-TNFalpha/RIP-LACK) produced reduced interleukin-2 but elevated levels of T helper 2 cytokines in response to LACK peptide in vitro. |
| 1575 | 9324360 | Here we demonstrate that transgenic mice expressing both TNFalpha and the Leishmania major LACK antigen in the pancreas (RIP-TNFalpha/RIP-LACK) exhibit an impaired ability to mount a CD4+ T cell response against LACK. |
| 1576 | 9324360 | In addition, peripheral CD4+ T cells from TCR transgenic mice (TCR-LACK/RIP-TNFalpha/RIP-LACK) produced reduced interleukin-2 but elevated levels of T helper 2 cytokines in response to LACK peptide in vitro. |
| 1577 | 9352596 | CD4+ and CD8+ T lymphocytes: clarification of their pathogenic roles in diabetes in the NOD mouse. |
| 1578 | 9352597 | The role of CD4 and CD8 T cells in type I diabetes in the NOD mouse. |
| 1579 | 9362527 | It has been established that insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a CD4+ and CD8+ T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 1580 | 9362527 | The precise roles that beta cell-reactive CD8+ and CD4+ T cells play in the disease process, however, remain ill defined. |
| 1581 | 9362527 | Here we have investigated whether naive beta cell-specific CD8+ and CD4+ T cells can spontaneously accumulate in pancreatic islets, differentiate into effector cells, and destroy beta cells in the absence of other T cell specificities. |
| 1582 | 9362527 | We show that while RAG-2(-/-) 4.1-NOD mice, which only bear beta cell-specific CD4+ T cells, develop diabetes as early and as frequently as RAG-2+ 4.1-NOD mice, RAG-2(-/-) 8.3-NOD mice, which only bear beta cell-specific CD8+ T cells, develop diabetes less frequently and significantly later than RAG-2(+) 8.3-NOD mice. |
| 1583 | 9362527 | The monoclonal CD8+ T cells of RAG-2(-/-) 8.3-NOD mice mature properly, proliferate vigorously in response to antigenic stimulation in vitro, and can differentiate into beta cell-cytotoxic T cells in vivo, but do not efficiently accumulate in islets in the absence of a CD4+ T cell-derived signal, which can be provided by splenic CD4+ T cells from nontransgenic NOD mice. |
| 1584 | 9362527 | These results demonstrate that naive beta cell- specific CD8+ and CD4+ T cells can trigger diabetes in the absence of other T or B cell specificities, but suggest that efficient recruitment of naive diabetogenic beta cell-reactive CD8+ T cells to islets requires the assistance of beta cell-reactive CD4+ T cells. |
| 1585 | 9362527 | It has been established that insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a CD4+ and CD8+ T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 1586 | 9362527 | The precise roles that beta cell-reactive CD8+ and CD4+ T cells play in the disease process, however, remain ill defined. |
| 1587 | 9362527 | Here we have investigated whether naive beta cell-specific CD8+ and CD4+ T cells can spontaneously accumulate in pancreatic islets, differentiate into effector cells, and destroy beta cells in the absence of other T cell specificities. |
| 1588 | 9362527 | We show that while RAG-2(-/-) 4.1-NOD mice, which only bear beta cell-specific CD4+ T cells, develop diabetes as early and as frequently as RAG-2+ 4.1-NOD mice, RAG-2(-/-) 8.3-NOD mice, which only bear beta cell-specific CD8+ T cells, develop diabetes less frequently and significantly later than RAG-2(+) 8.3-NOD mice. |
| 1589 | 9362527 | The monoclonal CD8+ T cells of RAG-2(-/-) 8.3-NOD mice mature properly, proliferate vigorously in response to antigenic stimulation in vitro, and can differentiate into beta cell-cytotoxic T cells in vivo, but do not efficiently accumulate in islets in the absence of a CD4+ T cell-derived signal, which can be provided by splenic CD4+ T cells from nontransgenic NOD mice. |
| 1590 | 9362527 | These results demonstrate that naive beta cell- specific CD8+ and CD4+ T cells can trigger diabetes in the absence of other T or B cell specificities, but suggest that efficient recruitment of naive diabetogenic beta cell-reactive CD8+ T cells to islets requires the assistance of beta cell-reactive CD4+ T cells. |
| 1591 | 9362527 | It has been established that insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a CD4+ and CD8+ T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 1592 | 9362527 | The precise roles that beta cell-reactive CD8+ and CD4+ T cells play in the disease process, however, remain ill defined. |
| 1593 | 9362527 | Here we have investigated whether naive beta cell-specific CD8+ and CD4+ T cells can spontaneously accumulate in pancreatic islets, differentiate into effector cells, and destroy beta cells in the absence of other T cell specificities. |
| 1594 | 9362527 | We show that while RAG-2(-/-) 4.1-NOD mice, which only bear beta cell-specific CD4+ T cells, develop diabetes as early and as frequently as RAG-2+ 4.1-NOD mice, RAG-2(-/-) 8.3-NOD mice, which only bear beta cell-specific CD8+ T cells, develop diabetes less frequently and significantly later than RAG-2(+) 8.3-NOD mice. |
| 1595 | 9362527 | The monoclonal CD8+ T cells of RAG-2(-/-) 8.3-NOD mice mature properly, proliferate vigorously in response to antigenic stimulation in vitro, and can differentiate into beta cell-cytotoxic T cells in vivo, but do not efficiently accumulate in islets in the absence of a CD4+ T cell-derived signal, which can be provided by splenic CD4+ T cells from nontransgenic NOD mice. |
| 1596 | 9362527 | These results demonstrate that naive beta cell- specific CD8+ and CD4+ T cells can trigger diabetes in the absence of other T or B cell specificities, but suggest that efficient recruitment of naive diabetogenic beta cell-reactive CD8+ T cells to islets requires the assistance of beta cell-reactive CD4+ T cells. |
| 1597 | 9362527 | It has been established that insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a CD4+ and CD8+ T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 1598 | 9362527 | The precise roles that beta cell-reactive CD8+ and CD4+ T cells play in the disease process, however, remain ill defined. |
| 1599 | 9362527 | Here we have investigated whether naive beta cell-specific CD8+ and CD4+ T cells can spontaneously accumulate in pancreatic islets, differentiate into effector cells, and destroy beta cells in the absence of other T cell specificities. |
| 1600 | 9362527 | We show that while RAG-2(-/-) 4.1-NOD mice, which only bear beta cell-specific CD4+ T cells, develop diabetes as early and as frequently as RAG-2+ 4.1-NOD mice, RAG-2(-/-) 8.3-NOD mice, which only bear beta cell-specific CD8+ T cells, develop diabetes less frequently and significantly later than RAG-2(+) 8.3-NOD mice. |
| 1601 | 9362527 | The monoclonal CD8+ T cells of RAG-2(-/-) 8.3-NOD mice mature properly, proliferate vigorously in response to antigenic stimulation in vitro, and can differentiate into beta cell-cytotoxic T cells in vivo, but do not efficiently accumulate in islets in the absence of a CD4+ T cell-derived signal, which can be provided by splenic CD4+ T cells from nontransgenic NOD mice. |
| 1602 | 9362527 | These results demonstrate that naive beta cell- specific CD8+ and CD4+ T cells can trigger diabetes in the absence of other T or B cell specificities, but suggest that efficient recruitment of naive diabetogenic beta cell-reactive CD8+ T cells to islets requires the assistance of beta cell-reactive CD4+ T cells. |
| 1603 | 9362527 | It has been established that insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a CD4+ and CD8+ T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 1604 | 9362527 | The precise roles that beta cell-reactive CD8+ and CD4+ T cells play in the disease process, however, remain ill defined. |
| 1605 | 9362527 | Here we have investigated whether naive beta cell-specific CD8+ and CD4+ T cells can spontaneously accumulate in pancreatic islets, differentiate into effector cells, and destroy beta cells in the absence of other T cell specificities. |
| 1606 | 9362527 | We show that while RAG-2(-/-) 4.1-NOD mice, which only bear beta cell-specific CD4+ T cells, develop diabetes as early and as frequently as RAG-2+ 4.1-NOD mice, RAG-2(-/-) 8.3-NOD mice, which only bear beta cell-specific CD8+ T cells, develop diabetes less frequently and significantly later than RAG-2(+) 8.3-NOD mice. |
| 1607 | 9362527 | The monoclonal CD8+ T cells of RAG-2(-/-) 8.3-NOD mice mature properly, proliferate vigorously in response to antigenic stimulation in vitro, and can differentiate into beta cell-cytotoxic T cells in vivo, but do not efficiently accumulate in islets in the absence of a CD4+ T cell-derived signal, which can be provided by splenic CD4+ T cells from nontransgenic NOD mice. |
| 1608 | 9362527 | These results demonstrate that naive beta cell- specific CD8+ and CD4+ T cells can trigger diabetes in the absence of other T or B cell specificities, but suggest that efficient recruitment of naive diabetogenic beta cell-reactive CD8+ T cells to islets requires the assistance of beta cell-reactive CD4+ T cells. |
| 1609 | 9362527 | It has been established that insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a CD4+ and CD8+ T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 1610 | 9362527 | The precise roles that beta cell-reactive CD8+ and CD4+ T cells play in the disease process, however, remain ill defined. |
| 1611 | 9362527 | Here we have investigated whether naive beta cell-specific CD8+ and CD4+ T cells can spontaneously accumulate in pancreatic islets, differentiate into effector cells, and destroy beta cells in the absence of other T cell specificities. |
| 1612 | 9362527 | We show that while RAG-2(-/-) 4.1-NOD mice, which only bear beta cell-specific CD4+ T cells, develop diabetes as early and as frequently as RAG-2+ 4.1-NOD mice, RAG-2(-/-) 8.3-NOD mice, which only bear beta cell-specific CD8+ T cells, develop diabetes less frequently and significantly later than RAG-2(+) 8.3-NOD mice. |
| 1613 | 9362527 | The monoclonal CD8+ T cells of RAG-2(-/-) 8.3-NOD mice mature properly, proliferate vigorously in response to antigenic stimulation in vitro, and can differentiate into beta cell-cytotoxic T cells in vivo, but do not efficiently accumulate in islets in the absence of a CD4+ T cell-derived signal, which can be provided by splenic CD4+ T cells from nontransgenic NOD mice. |
| 1614 | 9362527 | These results demonstrate that naive beta cell- specific CD8+ and CD4+ T cells can trigger diabetes in the absence of other T or B cell specificities, but suggest that efficient recruitment of naive diabetogenic beta cell-reactive CD8+ T cells to islets requires the assistance of beta cell-reactive CD4+ T cells. |
| 1615 | 9366391 | IL-4 prevents insulitis and insulin-dependent diabetes mellitus in nonobese diabetic mice by potentiation of regulatory T helper-2 cell function. |
| 1616 | 9366391 | Beginning at the time of insulitis, nonobese diabetic (NOD) mice demonstrate a thymocyte and peripheral T cell proliferative hyporesponsiveness induced by TCR cross-linking, which is associated with reduced IL-2 and IL-4 secretion. |
| 1617 | 9366391 | We previously reported that NOD CD4+ T cell hyporesponsiveness is reversed completely in vitro by exogenous IL-4, and that administration of IL-4 to NOD mice prevents the onset of insulin-dependent diabetes mellitus (IDDM). |
| 1618 | 9366391 | In the present study, we tested this possibility by analysis of the mechanisms of protection from IDDM afforded by IL-4 treatment in NOD mice. |
| 1619 | 9366391 | We show that IL-4 protects NOD mice from insulitis and IDDM when administered i.p. three times a week for 10 wk beginning at 2 wk of age. |
| 1620 | 9366391 | Thus, IL-4 treatment favors the expansion of regulatory CD4+ Th2 cells in vivo and prevents the onset of insulitis and IDDM mediated by autoreactive Th1 cells. |
| 1621 | 9366391 | IL-4 prevents insulitis and insulin-dependent diabetes mellitus in nonobese diabetic mice by potentiation of regulatory T helper-2 cell function. |
| 1622 | 9366391 | Beginning at the time of insulitis, nonobese diabetic (NOD) mice demonstrate a thymocyte and peripheral T cell proliferative hyporesponsiveness induced by TCR cross-linking, which is associated with reduced IL-2 and IL-4 secretion. |
| 1623 | 9366391 | We previously reported that NOD CD4+ T cell hyporesponsiveness is reversed completely in vitro by exogenous IL-4, and that administration of IL-4 to NOD mice prevents the onset of insulin-dependent diabetes mellitus (IDDM). |
| 1624 | 9366391 | In the present study, we tested this possibility by analysis of the mechanisms of protection from IDDM afforded by IL-4 treatment in NOD mice. |
| 1625 | 9366391 | We show that IL-4 protects NOD mice from insulitis and IDDM when administered i.p. three times a week for 10 wk beginning at 2 wk of age. |
| 1626 | 9366391 | Thus, IL-4 treatment favors the expansion of regulatory CD4+ Th2 cells in vivo and prevents the onset of insulitis and IDDM mediated by autoreactive Th1 cells. |
| 1627 | 9396776 | CD4+ T cell help impairs CD8+ T cell deletion induced by cross-presentation of self-antigens and favors autoimmunity. |
| 1628 | 9396776 | Analysis of the fate of CD8+ T cells indicated that CD4(+) T cell help impaired their deletion. |
| 1629 | 9396776 | CD4+ T cell help impairs CD8+ T cell deletion induced by cross-presentation of self-antigens and favors autoimmunity. |
| 1630 | 9396776 | Analysis of the fate of CD8+ T cells indicated that CD4(+) T cell help impaired their deletion. |
| 1631 | 9421467 | GAD-reactive CD4+ Th1 cells induce diabetes in NOD/SCID mice. |
| 1632 | 9421467 | Although glutamic acid decarboxylase (GAD) has been implicated in IDDM, there is no direct evidence showing GAD-reactive T cells are diabetogenic in vivo. |
| 1633 | 9421467 | Splenocytes from this mouse showed a proliferative response to purified GAD, and were used to generate a CD4+ T cell line, designated 5A, that expresses TCRs encoding Vbeta2 and Vbeta12. 5A T cells exhibit a MHC restricted proliferative response to purified GAD, as well as GAD65 peptide 524-543. |
| 1634 | 9421467 | After antigen-specific stimulation, 5A T cells secrete IFNgamma and TNFalpha/beta, but not IL-4. |
| 1635 | 9421467 | We conclude that GAD injection in young NOD mice may, in some cases, provoke diabetes due to the activation of diabetogenic T cells reactive to GAD65 peptides. |
| 1636 | 9421467 | Our data provide direct evidence that GAD65 autoimmunity may be a critical event in the pathogenesis of IDDM. |
| 1637 | 9421467 | GAD-reactive CD4+ Th1 cells induce diabetes in NOD/SCID mice. |
| 1638 | 9421467 | Although glutamic acid decarboxylase (GAD) has been implicated in IDDM, there is no direct evidence showing GAD-reactive T cells are diabetogenic in vivo. |
| 1639 | 9421467 | Splenocytes from this mouse showed a proliferative response to purified GAD, and were used to generate a CD4+ T cell line, designated 5A, that expresses TCRs encoding Vbeta2 and Vbeta12. 5A T cells exhibit a MHC restricted proliferative response to purified GAD, as well as GAD65 peptide 524-543. |
| 1640 | 9421467 | After antigen-specific stimulation, 5A T cells secrete IFNgamma and TNFalpha/beta, but not IL-4. |
| 1641 | 9421467 | We conclude that GAD injection in young NOD mice may, in some cases, provoke diabetes due to the activation of diabetogenic T cells reactive to GAD65 peptides. |
| 1642 | 9421467 | Our data provide direct evidence that GAD65 autoimmunity may be a critical event in the pathogenesis of IDDM. |
| 1643 | 9423299 | [The relation between diabetes mellitus and IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and monocytes in patients with pulmonary tuberculosis]. |
| 1644 | 9423299 | To elucidate the mechanism of susceptibility to tuberculosis infection in patients with diabetes mellitus, we measured IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and autologous monocytes stimulated with live BCG in patients with pulmonary tuberculosis complicated with DM (TB + DM) or without DM (TB) and healthy controls. |
| 1645 | 9423299 | The levels of IFN-gamma and IL-12 production in TB patients were significantly lower than those in the control. |
| 1646 | 9423299 | [The relation between diabetes mellitus and IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and monocytes in patients with pulmonary tuberculosis]. |
| 1647 | 9423299 | To elucidate the mechanism of susceptibility to tuberculosis infection in patients with diabetes mellitus, we measured IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and autologous monocytes stimulated with live BCG in patients with pulmonary tuberculosis complicated with DM (TB + DM) or without DM (TB) and healthy controls. |
| 1648 | 9423299 | The levels of IFN-gamma and IL-12 production in TB patients were significantly lower than those in the control. |
| 1649 | 9432975 | Continuous antigenic stimulation in vivo can result in the generation of so-called "anergic" CD4(+) or CD8(+) T cells that fail to proliferate upon antigenic stimulation and fail to develop cytolytic effector functions. |
| 1650 | 9432975 | Furthermore, HA-specific T cells anergized in vivo contain higher levels of interleukin (IL)-4 messenger RNA (mRNA) than naive and recently activated T cells with the same specificity and more than a 100-fold higher levels of IL-10 mRNA. |
| 1651 | 9435340 | Human and mouse major histocompatibility complex class II beta chain alleles associated with predisposition to type I diabetes often encode a non-charged residue at position 57 rather than the negatively charged aspartate residue characteristic of non-susceptible haplotypes. |
| 1652 | 9435340 | Direct evidence for the serine to aspartate substitution at position 57 influencing T-cell selection is found by analysis of peripheral T-cell receptor (TCR) usage and the CD4/CD8 T-cell ratio. |
| 1653 | 9498651 | Moreover, in both NOD and B6 mice, CD4+ T cells were more resistant to PCD induced by IL-2 deprivation than CD8+ cells. |
| 1654 | 9498651 | In relation with this increased resistance to apoptosis, expression of the anti-apoptotic Bcl-x protein was upregulated in activated T cells of NOD mice, most notably after 24 h of IL-2 deprivation. |
| 1655 | 9519727 | Linkage and association between a CD4 gene polymorphism and IDDM in Danish IDDM patients. |
| 1656 | 9520453 | Approximately one-half of Caucasians with newly diagnosed insulin-dependent diabetes mellitus (IDDM) have autoantibodies to insulin, and the majority of those express the HLA-DR4 genotype [Ziegler, R., Alper, C. |
| 1657 | 9520453 | However, it has been difficult to demonstrate T cell proliferative responses to human insulin in IDDM patients [Durinovic-Bello, I., Hummel, M. |
| 1658 | 9520453 | We have immunized transgenic mice expressing the susceptible HLA-DR (alpha1*0101,beta1*0401) (hereafter called DRB1*0401) and human CD4 molecules on a murine major histocompatibility complex class II null background, with human preproinsulin (PPI), proinsulin (PI), and insulin and derived large panels of T cell hybridomas to determine the immunogenic epitopes of these proteins. |
| 1659 | 9520453 | These findings may partly explain why susceptibility to type 1 diabetes is associated with HLA-DR4-positive individuals and why T cell responses to the mature insulin protein are rarely detected in IDDM patients. |
| 1660 | 9529321 | alpha/beta-T cell receptor (TCR)+CD4-CD8- (NKT) thymocytes prevent insulin-dependent diabetes mellitus in nonobese diabetic (NOD)/Lt mice by the influence of interleukin (IL)-4 and/or IL-10. |
| 1661 | 9529321 | We have previously shown that nonobese diabetic (NOD) mice are selectively deficient in alpha/beta-T cell receptor (TCR)+CD4-CD8- NKT cells, a defect that may contribute to their susceptibility to the spontaneous development of insulin-dependent diabetes mellitus (IDDM). |
| 1662 | 9529321 | A single intravenous injection of 10(6) CD4-/lowCD8- or CD4-CD8- thymocytes from female (BALB/c x NOD)F1 donors protected intact NOD mice from the spontaneous onset of clinical IDDM. |
| 1663 | 9529321 | When alpha/beta-TCR+ and alpha/beta-TCR- subsets of CD4-CD8- thymocytes were transferred with diabetogenic splenocytes and compared for their ability to prevent the development of IDDM in irradiated adult recipients, only the alpha/beta-TCR+ population was protective, confirming that NKT cells were responsible for this activity. |
| 1664 | 9529321 | The protective effect in the induced model of IDDM was neutralized by anti-IL-4 and anti-IL-10 monoclonal antibodies in vivo, indicating a role for at least one of these cytokines in NKT cell-mediated protection. |
| 1665 | 9529321 | alpha/beta-T cell receptor (TCR)+CD4-CD8- (NKT) thymocytes prevent insulin-dependent diabetes mellitus in nonobese diabetic (NOD)/Lt mice by the influence of interleukin (IL)-4 and/or IL-10. |
| 1666 | 9529321 | We have previously shown that nonobese diabetic (NOD) mice are selectively deficient in alpha/beta-T cell receptor (TCR)+CD4-CD8- NKT cells, a defect that may contribute to their susceptibility to the spontaneous development of insulin-dependent diabetes mellitus (IDDM). |
| 1667 | 9529321 | A single intravenous injection of 10(6) CD4-/lowCD8- or CD4-CD8- thymocytes from female (BALB/c x NOD)F1 donors protected intact NOD mice from the spontaneous onset of clinical IDDM. |
| 1668 | 9529321 | When alpha/beta-TCR+ and alpha/beta-TCR- subsets of CD4-CD8- thymocytes were transferred with diabetogenic splenocytes and compared for their ability to prevent the development of IDDM in irradiated adult recipients, only the alpha/beta-TCR+ population was protective, confirming that NKT cells were responsible for this activity. |
| 1669 | 9529321 | The protective effect in the induced model of IDDM was neutralized by anti-IL-4 and anti-IL-10 monoclonal antibodies in vivo, indicating a role for at least one of these cytokines in NKT cell-mediated protection. |
| 1670 | 9541590 | The concept that naive CD4+ and CD8+ T cells require co-stimulatory signals for activation and proliferation is well documented. |
| 1671 | 9544238 | Individuals from multiplex insulin-dependent diabetes mellitus (IDDM) families express higher levels of TCRBV2S1 than controls. |
| 1672 | 9544238 | The level of TCRBV2S1 expression in the multiplex families was significantly higher than all the control groups for both the CD4+ and CD8+ T lymphocyte subsets. |
| 1673 | 9544238 | The TCRBV3S1 expression in all the diabetic cohorts was significantly lower than the healthy controls, in the CD4 subset only. |
| 1674 | 9544238 | Individuals from multiplex insulin-dependent diabetes mellitus (IDDM) families express higher levels of TCRBV2S1 than controls. |
| 1675 | 9544238 | The level of TCRBV2S1 expression in the multiplex families was significantly higher than all the control groups for both the CD4+ and CD8+ T lymphocyte subsets. |
| 1676 | 9544238 | The TCRBV3S1 expression in all the diabetic cohorts was significantly lower than the healthy controls, in the CD4 subset only. |
| 1677 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 1678 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 1679 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 1680 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 1681 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 1682 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 1683 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 1684 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 1685 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1686 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1687 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1688 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1689 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1690 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1691 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1692 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1693 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1694 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1695 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1696 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1697 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1698 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1699 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1700 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1701 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1702 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1703 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1704 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1705 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1706 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1707 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1708 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1709 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1710 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1711 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1712 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1713 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1714 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1715 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1716 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1717 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1718 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1719 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1720 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1721 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1722 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1723 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1724 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1725 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1726 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1727 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1728 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1729 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1730 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1731 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1732 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1733 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1734 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1735 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1736 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1737 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1738 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1739 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1740 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1741 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1742 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1743 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1744 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1745 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1746 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1747 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1748 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1749 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1750 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1751 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1752 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1753 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1754 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1755 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1756 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1757 | 9570528 | Sequestration of CD4-associated Lck from the TCR complex may elicit T cell hyporesponsiveness in nonobese diabetic mice. |
| 1758 | 9570528 | The Lck protein tyrosine kinase associates noncovalently with the cytoplasmic domain of CD4. |
| 1759 | 9570528 | Upon ligand engagement of the TCR, CD4-associated Lck is rapidly activated and recruited to the TCR complex. |
| 1760 | 9570528 | Here, we investigated whether differential association of Lck with TCR or CD4 mediates the control of NOD thymocyte hyporesponsiveness. |
| 1761 | 9570528 | We demonstrate that less CD4-associated Lck is recruited to the TCR in activated NOD thymocytes than in control thymocytes. |
| 1762 | 9570528 | This CD4-mediated sequestration of Lck from the TCR correlates with the increased binding of CD4-associated Lck through its Src homology 2 domain to free TCRzeta and CD3gamma epsilon chains on the plasma membrane. |
| 1763 | 9570528 | Sequestration of Lck by CD4 does not occur in activated thymocytes from 3-wk-old NOD mice and is only apparent in thymocytes from NOD mice >5 to 6 wk of age. |
| 1764 | 9570528 | This diminished recruitment of CD4-associated Lck to the TCR is not mediated by an increase in the amount of CD8-associated Lck. |
| 1765 | 9570528 | Thus, impaired recruitment of CD4-associated Lck to the TCR complex may represent an early event that results in deficient coupling of the TCR complex to downstream signaling events and gives rise to NOD thymocyte hyporesponsiveness. |
| 1766 | 9576014 | Oral administration of insulin to NOD mice suppresses or delays the onset of diabetes by skewing the response toward CD4+ Th2 cells and TGF-beta producing cells. |
| 1767 | 9576014 | When cytokine profiles were examined, feeding led to a predominance of IL-10 and TGF-beta production. |
| 1768 | 9576014 | Furthermore, feeding SEA in combination with insulin B-chain augmented the level of IL-10 production to insulin. |
| 1769 | 9576014 | T-cell lines established from SEA-fed and -immunized mice secreted IL-4 and IL-10 cytokines whereas the T-cell lines from control-fed mice immunized with SEA secreted predominantly IL-2 and IFN-gamma. |
| 1770 | 9576014 | These results demonstrate that orally administered insulin can induce regulatory T-cells secreting IL-4, IL-10, and TGF-beta and that Th2 responses to oral insulin could be augmented in a synergistic way by feeding SEA and insulin B-chain together. |
| 1771 | 9580038 | We have found that patients with mental anorexia or bulimia present a significant decrease of leucocytes, lymphocytes, CD2 and CD4. |
| 1772 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 1773 | 9583742 | The presentation of beta cell-specific autoantigens by macrophages and/or dendritic cells to CD4+ T helper cells, in association with MHC class II molecules, is considered the initial step in the development of autoimmune IDDM. |
| 1774 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 1775 | 9583742 | IFN-gamma activates other resting macrophages, which, in turn, release cytokines, such as IL-1beta, TNF-alpha, and free radicals, which are toxic to beta cells. |
| 1776 | 9583742 | During this process, IL-2 and other cytokines induce the migration of CD8+ peripheral T cells to the inflamed islets, perhaps by inducing the expression of a specific homing receptor. |
| 1777 | 9583742 | The precytotoxic CD8+ T cells that bear beta cell-specific autoantigen receptors differentiate into cytotoxic effector T cells upon recognition of the beta cell-specific peptide bound to MHC class I molecules in the presence of beta cell-specific CD4+ T helper cells. |
| 1778 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 1779 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 1780 | 9583742 | The presentation of beta cell-specific autoantigens by macrophages and/or dendritic cells to CD4+ T helper cells, in association with MHC class II molecules, is considered the initial step in the development of autoimmune IDDM. |
| 1781 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 1782 | 9583742 | IFN-gamma activates other resting macrophages, which, in turn, release cytokines, such as IL-1beta, TNF-alpha, and free radicals, which are toxic to beta cells. |
| 1783 | 9583742 | During this process, IL-2 and other cytokines induce the migration of CD8+ peripheral T cells to the inflamed islets, perhaps by inducing the expression of a specific homing receptor. |
| 1784 | 9583742 | The precytotoxic CD8+ T cells that bear beta cell-specific autoantigen receptors differentiate into cytotoxic effector T cells upon recognition of the beta cell-specific peptide bound to MHC class I molecules in the presence of beta cell-specific CD4+ T helper cells. |
| 1785 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 1786 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 1787 | 9583742 | The presentation of beta cell-specific autoantigens by macrophages and/or dendritic cells to CD4+ T helper cells, in association with MHC class II molecules, is considered the initial step in the development of autoimmune IDDM. |
| 1788 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 1789 | 9583742 | IFN-gamma activates other resting macrophages, which, in turn, release cytokines, such as IL-1beta, TNF-alpha, and free radicals, which are toxic to beta cells. |
| 1790 | 9583742 | During this process, IL-2 and other cytokines induce the migration of CD8+ peripheral T cells to the inflamed islets, perhaps by inducing the expression of a specific homing receptor. |
| 1791 | 9583742 | The precytotoxic CD8+ T cells that bear beta cell-specific autoantigen receptors differentiate into cytotoxic effector T cells upon recognition of the beta cell-specific peptide bound to MHC class I molecules in the presence of beta cell-specific CD4+ T helper cells. |
| 1792 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 1793 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 1794 | 9583742 | The presentation of beta cell-specific autoantigens by macrophages and/or dendritic cells to CD4+ T helper cells, in association with MHC class II molecules, is considered the initial step in the development of autoimmune IDDM. |
| 1795 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 1796 | 9583742 | IFN-gamma activates other resting macrophages, which, in turn, release cytokines, such as IL-1beta, TNF-alpha, and free radicals, which are toxic to beta cells. |
| 1797 | 9583742 | During this process, IL-2 and other cytokines induce the migration of CD8+ peripheral T cells to the inflamed islets, perhaps by inducing the expression of a specific homing receptor. |
| 1798 | 9583742 | The precytotoxic CD8+ T cells that bear beta cell-specific autoantigen receptors differentiate into cytotoxic effector T cells upon recognition of the beta cell-specific peptide bound to MHC class I molecules in the presence of beta cell-specific CD4+ T helper cells. |
| 1799 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 1800 | 9604865 | IDDM is a T-cell-mediated autoimmune disease in which the insulin-producing beta-cells are destroyed. |
| 1801 | 9604865 | Furthermore, suppression of the diabetogenic response is mediated by the induction of GAD65-specific CD4+ regulatory T-cells. |
| 1802 | 9616216 | Long-term survival of skin allografts induced by donor splenocytes and anti-CD154 antibody in thymectomized mice requires CD4(+) T cells, interferon-gamma, and CTLA4. |
| 1803 | 9616216 | (c) Induction of skin allograft acceptance initially depended on the presence of IFN-gamma, CTLA4, and CD4(+) T cells. |
| 1804 | 9616216 | Addition of anti-CTLA4 or anti-IFN-gamma mAb to the protocol was associated with prompt graft rejection, whereas anti-IL-4 mAb had no effect. |
| 1805 | 9616216 | Long-term survival of skin allografts induced by donor splenocytes and anti-CD154 antibody in thymectomized mice requires CD4(+) T cells, interferon-gamma, and CTLA4. |
| 1806 | 9616216 | (c) Induction of skin allograft acceptance initially depended on the presence of IFN-gamma, CTLA4, and CD4(+) T cells. |
| 1807 | 9616216 | Addition of anti-CTLA4 or anti-IFN-gamma mAb to the protocol was associated with prompt graft rejection, whereas anti-IL-4 mAb had no effect. |
| 1808 | 9619488 | CD4+ T cells may be assigned a functional status (Th1 or Th2) according to the cytokines they produce including IL-2, IFN-gamma and IL-4. |
| 1809 | 9625758 | The pancreatic islet infiltrate in diabetic mice consists of CD8 T cells, CD4 T cells, and B cells, similar to diabetic nontransgenic NOD mice. |
| 1810 | 9625758 | To elucidate the relative importance of each of the subsets of cells, the NOD-rat insulin promoter (RIP)-B7-1 animals were crossed with NOD.beta2microglobulin -/- mice which lack major histocompatibility complex class I molecules and are deficient in peripheral CD8 T cells, NOD.CD4 -/- mice which lack T cells expressing CD4, and NOD.muMT -/- mice which lack B220-positive B cells. |
| 1811 | 9625758 | These experiments showed that both CD4 and CD8 T cells were necessary for the accelerated onset of diabetes, but that B cells, which are needed for diabetes to occur in normal NOD mice, are not required. |
| 1812 | 9625758 | The pancreatic islet infiltrate in diabetic mice consists of CD8 T cells, CD4 T cells, and B cells, similar to diabetic nontransgenic NOD mice. |
| 1813 | 9625758 | To elucidate the relative importance of each of the subsets of cells, the NOD-rat insulin promoter (RIP)-B7-1 animals were crossed with NOD.beta2microglobulin -/- mice which lack major histocompatibility complex class I molecules and are deficient in peripheral CD8 T cells, NOD.CD4 -/- mice which lack T cells expressing CD4, and NOD.muMT -/- mice which lack B220-positive B cells. |
| 1814 | 9625758 | These experiments showed that both CD4 and CD8 T cells were necessary for the accelerated onset of diabetes, but that B cells, which are needed for diabetes to occur in normal NOD mice, are not required. |
| 1815 | 9625758 | The pancreatic islet infiltrate in diabetic mice consists of CD8 T cells, CD4 T cells, and B cells, similar to diabetic nontransgenic NOD mice. |
| 1816 | 9625758 | To elucidate the relative importance of each of the subsets of cells, the NOD-rat insulin promoter (RIP)-B7-1 animals were crossed with NOD.beta2microglobulin -/- mice which lack major histocompatibility complex class I molecules and are deficient in peripheral CD8 T cells, NOD.CD4 -/- mice which lack T cells expressing CD4, and NOD.muMT -/- mice which lack B220-positive B cells. |
| 1817 | 9625758 | These experiments showed that both CD4 and CD8 T cells were necessary for the accelerated onset of diabetes, but that B cells, which are needed for diabetes to occur in normal NOD mice, are not required. |
| 1818 | 9626161 | Increased CD69 and human leukocyte antigen-DR expression on T lymphocytes in insulin-dependent diabetes mellitus of long standing. |
| 1819 | 9626161 | To better define prevailing activation of circulating T cell subsets in insulin-dependent diabetes mellitus (IDDM) of recent onset (DM; n = 31; median age +/- SD, 28 +/- 6.9 yr) and of long standing (DML; n = 27; age, 33 +/- 10.4 yr; median duration of disease, 105 months), CD4+ and CD8+ T cells were analyzed to determine their naive and memory subsets as well as their expression of human leukocyte antigen (HLA)-DR, interleukin-2 receptor alpha-chain (CD25), and CD69 by three-color flow cytometry. |
| 1820 | 9626161 | No deviation was seen in either IDDM group compared to HS in CD25 expression on CD4+ or CD8+ cells or in their CD45RA+ or CD45RA- subsets. |
| 1821 | 9626161 | CD69 expression did not differ between IDDM and HS, but differed between DML (CD4+, CD8+, and CD45RA- CD4+) and DM only. |
| 1822 | 9626161 | In conclusion, our data demonstrate that HLA-DR expression in IDDM is restricted to memory cells (CD45RA-) among CD4+ cells in DML and is more markedly confined to naive (CD45RA+) than to memory CD8+ cells, whereas the early activation antigen CD69 is more readily expressed in DML than in DM. |
| 1823 | 9626161 | Increased CD69 and human leukocyte antigen-DR expression on T lymphocytes in insulin-dependent diabetes mellitus of long standing. |
| 1824 | 9626161 | To better define prevailing activation of circulating T cell subsets in insulin-dependent diabetes mellitus (IDDM) of recent onset (DM; n = 31; median age +/- SD, 28 +/- 6.9 yr) and of long standing (DML; n = 27; age, 33 +/- 10.4 yr; median duration of disease, 105 months), CD4+ and CD8+ T cells were analyzed to determine their naive and memory subsets as well as their expression of human leukocyte antigen (HLA)-DR, interleukin-2 receptor alpha-chain (CD25), and CD69 by three-color flow cytometry. |
| 1825 | 9626161 | No deviation was seen in either IDDM group compared to HS in CD25 expression on CD4+ or CD8+ cells or in their CD45RA+ or CD45RA- subsets. |
| 1826 | 9626161 | CD69 expression did not differ between IDDM and HS, but differed between DML (CD4+, CD8+, and CD45RA- CD4+) and DM only. |
| 1827 | 9626161 | In conclusion, our data demonstrate that HLA-DR expression in IDDM is restricted to memory cells (CD45RA-) among CD4+ cells in DML and is more markedly confined to naive (CD45RA+) than to memory CD8+ cells, whereas the early activation antigen CD69 is more readily expressed in DML than in DM. |
| 1828 | 9626161 | Increased CD69 and human leukocyte antigen-DR expression on T lymphocytes in insulin-dependent diabetes mellitus of long standing. |
| 1829 | 9626161 | To better define prevailing activation of circulating T cell subsets in insulin-dependent diabetes mellitus (IDDM) of recent onset (DM; n = 31; median age +/- SD, 28 +/- 6.9 yr) and of long standing (DML; n = 27; age, 33 +/- 10.4 yr; median duration of disease, 105 months), CD4+ and CD8+ T cells were analyzed to determine their naive and memory subsets as well as their expression of human leukocyte antigen (HLA)-DR, interleukin-2 receptor alpha-chain (CD25), and CD69 by three-color flow cytometry. |
| 1830 | 9626161 | No deviation was seen in either IDDM group compared to HS in CD25 expression on CD4+ or CD8+ cells or in their CD45RA+ or CD45RA- subsets. |
| 1831 | 9626161 | CD69 expression did not differ between IDDM and HS, but differed between DML (CD4+, CD8+, and CD45RA- CD4+) and DM only. |
| 1832 | 9626161 | In conclusion, our data demonstrate that HLA-DR expression in IDDM is restricted to memory cells (CD45RA-) among CD4+ cells in DML and is more markedly confined to naive (CD45RA+) than to memory CD8+ cells, whereas the early activation antigen CD69 is more readily expressed in DML than in DM. |
| 1833 | 9626161 | Increased CD69 and human leukocyte antigen-DR expression on T lymphocytes in insulin-dependent diabetes mellitus of long standing. |
| 1834 | 9626161 | To better define prevailing activation of circulating T cell subsets in insulin-dependent diabetes mellitus (IDDM) of recent onset (DM; n = 31; median age +/- SD, 28 +/- 6.9 yr) and of long standing (DML; n = 27; age, 33 +/- 10.4 yr; median duration of disease, 105 months), CD4+ and CD8+ T cells were analyzed to determine their naive and memory subsets as well as their expression of human leukocyte antigen (HLA)-DR, interleukin-2 receptor alpha-chain (CD25), and CD69 by three-color flow cytometry. |
| 1835 | 9626161 | No deviation was seen in either IDDM group compared to HS in CD25 expression on CD4+ or CD8+ cells or in their CD45RA+ or CD45RA- subsets. |
| 1836 | 9626161 | CD69 expression did not differ between IDDM and HS, but differed between DML (CD4+, CD8+, and CD45RA- CD4+) and DM only. |
| 1837 | 9626161 | In conclusion, our data demonstrate that HLA-DR expression in IDDM is restricted to memory cells (CD45RA-) among CD4+ cells in DML and is more markedly confined to naive (CD45RA+) than to memory CD8+ cells, whereas the early activation antigen CD69 is more readily expressed in DML than in DM. |
| 1838 | 9630837 | Most importantly, treatment induced higher IFN-gamma/IL-4 ratios among CD4 T cells, suggesting a strong shift toward Th1 development, perhaps through direct effects on patterns of gene expression in CD4 T cells. |
| 1839 | 9637485 | Consequently, there is a 10-fold reduction in the number of CD4+ and CD8+ T cells in secondary lymphoid organs. |
| 1840 | 9647438 | Serial frozen sections of grafts and controls were stained by immunoperoxidase for rat MAC-1, class II MHC, CD2, CD4, CD8, B-cells, VLA-4, LFA-1, L-selectin, ICAM-1, and VCAM-1. |
| 1841 | 9647438 | Third, the second wave of lymphocytes arrived from the renal parenchyma to form a dense band at the graft-kidney interface and around grafts by days 4 and 6 (allo >>> iso); CD4+ cells vastly outnumbered CD8+ cells, with CD4+ cells being mobilized first and from interstitial vessels throughout the entire kidney. |
| 1842 | 9647438 | Large numbers of L-selectin+, VLA-4+, and LFA-1+ cells were seen in the infiltrates with the most intensely staining cells being intravascular. |
| 1843 | 9647438 | Endothelial staining for ICAM-1 and VCAM-1 was prominent throughout. |
| 1844 | 9647438 | Both class II MHC and ICAM-1 expression were induced on renal tubular epithelial cells, but neither was found on islet parenchymal cells. |
| 1845 | 9647438 | Serial frozen sections of grafts and controls were stained by immunoperoxidase for rat MAC-1, class II MHC, CD2, CD4, CD8, B-cells, VLA-4, LFA-1, L-selectin, ICAM-1, and VCAM-1. |
| 1846 | 9647438 | Third, the second wave of lymphocytes arrived from the renal parenchyma to form a dense band at the graft-kidney interface and around grafts by days 4 and 6 (allo >>> iso); CD4+ cells vastly outnumbered CD8+ cells, with CD4+ cells being mobilized first and from interstitial vessels throughout the entire kidney. |
| 1847 | 9647438 | Large numbers of L-selectin+, VLA-4+, and LFA-1+ cells were seen in the infiltrates with the most intensely staining cells being intravascular. |
| 1848 | 9647438 | Endothelial staining for ICAM-1 and VCAM-1 was prominent throughout. |
| 1849 | 9647438 | Both class II MHC and ICAM-1 expression were induced on renal tubular epithelial cells, but neither was found on islet parenchymal cells. |
| 1850 | 9648825 | Fluorescence-activated cell sorter analysis of thymocyte subsets revealed marked differences, especially in CD4+CD8+ and CD4+ cells. |
| 1851 | 9650096 | Cloned T cells from a recent onset IDDM patient reactive with insulin B-chain. |
| 1852 | 9650096 | Insulin-dependent diabetes mellitus (IDDM) results from selective autoimmune destruction of insulin producing beta-cells. |
| 1853 | 9650096 | T-cell reactivity and autoantibodies to several islet proteins such as insulin, GAD and IA-2 are associated with IDDM in mice and men. |
| 1854 | 9650096 | We have isolated and characterized a human insulin-specific T-cell clone that was derived from peripheral blood of a newly diagnosed IDDM patient. |
| 1855 | 9650096 | Functionally, the human insulin-specific CD4+ T cells displayed a Th1/0 like cytokine profile and were restricted by HLA-DR. |
| 1856 | 9650096 | Our results indicate that human clonal T cells isolated from a recent onset IDDM patient recognize an epitope overlapping with the insulin B-chain region that is immunodominant and potentially therapeutic in NOD mice. |
| 1857 | 9650096 | This observation may be useful in studying the role of insulin-specific T cells in IDDM, and may eventually help to establish peptide-based immunotherapies in IDDM. |
| 1858 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 1859 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 1860 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 1861 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 1862 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 1863 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 1864 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 1865 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 1866 | 9691086 | Paracrine effect of transforming growth factor-beta1 (TGF-beta1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-beta1 (pTGF-beta1) in pancreatic islet (islet) alpha cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-beta1). |
| 1867 | 9691086 | Based on these, it is concluded that autoimmune diabetes in NOD mice is not a systemic disease and it can be completely prevented by the paracrine TGF-beta1 in the islet compartment through protection against CD4(+) and CD8(+) effector lymphocytes. |
| 1868 | 9703317 | Because this procedure is targeted directly at CD154, a co-activation molecule expressed predominantly by activated CD4+ T-cells, the results suggest that CD4+ cells have a major role in the cellular immune response to xenografts. |
| 1869 | 9725264 | Selection using an L-selectin (CD62L)-specific Ab showed that TCR alpha/beta+CD4+CD62L+ thymocytes, emerging from the mainstream differentiation pathway, concentrate this ability to regulate autoreactive effectors. |
| 1870 | 9725264 | Compared with mature TCR alpha beta+CD8- thymocytes, significantly lower numbers of TCR alpha beta+CD4+CD62L+ were sufficient to achieve an efficient inhibition of disease transfer into NOD-scid recipients. |
| 1871 | 9725264 | Selection using an L-selectin (CD62L)-specific Ab showed that TCR alpha/beta+CD4+CD62L+ thymocytes, emerging from the mainstream differentiation pathway, concentrate this ability to regulate autoreactive effectors. |
| 1872 | 9725264 | Compared with mature TCR alpha beta+CD8- thymocytes, significantly lower numbers of TCR alpha beta+CD4+CD62L+ were sufficient to achieve an efficient inhibition of disease transfer into NOD-scid recipients. |
| 1873 | 9726227 | This clearly demonstrates that transient inactivation of most T-cells with anti-CD4 plus anti-CD8 mAbs effectively controls autoimmune disease in the isograft, despite recovery of CD4 and CD8 T-cells to normal levels. |
| 1874 | 9726227 | Histology showed a predominantly peri-islet T-cell and macrophage infiltrate with ductal expression of the cytokines interleukin (IL)-4, IL-2, and interferon-gamma. |
| 1875 | 9726599 | In mice fed with pig spleen cells, as well as in control mice, the blocking of CD4 + T cells with mAbs led to abolition of proliferation (p < 0.002), while the blocking of CD8 + led to a less marked effect. |
| 1876 | 9726599 | In control mice, the main splenocyte subset involved during proliferation in response to pig islet cells was Thl, since interferon gamma (IFNgamma) production increased significantly (p < 0.01) while that of interleukin-10 (IL-10) increased only slightly. |
| 1877 | 9726599 | The main change observed in mice fed with pig spleen cells was a marked increase in basal IL-10 production (p < 0.01) and the basal IL-10/IFNgamma ratio (p < 0.001). |
| 1878 | 9726599 | It seems likely that feeding with pig spleen cells shifted the Th1/Th2 balance towards a dominance of Th2-type class II-restricted CD4 + T cells, which may have been conducive to activating CD8 + suppressor T cells. |
| 1879 | 9726599 | In mice fed with pig spleen cells, as well as in control mice, the blocking of CD4 + T cells with mAbs led to abolition of proliferation (p < 0.002), while the blocking of CD8 + led to a less marked effect. |
| 1880 | 9726599 | In control mice, the main splenocyte subset involved during proliferation in response to pig islet cells was Thl, since interferon gamma (IFNgamma) production increased significantly (p < 0.01) while that of interleukin-10 (IL-10) increased only slightly. |
| 1881 | 9726599 | The main change observed in mice fed with pig spleen cells was a marked increase in basal IL-10 production (p < 0.01) and the basal IL-10/IFNgamma ratio (p < 0.001). |
| 1882 | 9726599 | It seems likely that feeding with pig spleen cells shifted the Th1/Th2 balance towards a dominance of Th2-type class II-restricted CD4 + T cells, which may have been conducive to activating CD8 + suppressor T cells. |
| 1883 | 9727063 | Insulin-dependent diabetes mellitus in humans is linked with specific HLA class II genes, e.g., HLA-DQA1*0301/ DQB1*0302 (DQ8). |
| 1884 | 9727063 | Two GAD peptide-specific (247-266 and 509-528), DQ8 restricted Th1 CD4(+) T cell lines, were generated from immunized DQ8(+)/I-Abo mice. |
| 1885 | 9727063 | In addition to CD4, islet mRNA from these mice also showed expression of CD8, IFNgamma, TNFalpha, Fas, and Fas ligand. |
| 1886 | 9727063 | Insulin-dependent diabetes mellitus in humans is linked with specific HLA class II genes, e.g., HLA-DQA1*0301/ DQB1*0302 (DQ8). |
| 1887 | 9727063 | Two GAD peptide-specific (247-266 and 509-528), DQ8 restricted Th1 CD4(+) T cell lines, were generated from immunized DQ8(+)/I-Abo mice. |
| 1888 | 9727063 | In addition to CD4, islet mRNA from these mice also showed expression of CD8, IFNgamma, TNFalpha, Fas, and Fas ligand. |
| 1889 | 9757911 | Characterization of self-glutamic acid decarboxylase 65-reactive CD4+ T-cell clones established from Japanese patients with insulin-dependent diabetes mellitus. |
| 1890 | 9757911 | To investigate autoimmunity to glutamic acid decarboxylase (GAD) 65 in Japanese patients with insulin-dependent diabetes mellitus (IDDM, type I diabetes), we established seven CD4+ T-cell clones, by stimulating peripheral blood mononuclear cells (PBMC) of six IDDM patients, using a mixture of overlapping human GAD65 peptides. |
| 1891 | 9757911 | Characterization of self-glutamic acid decarboxylase 65-reactive CD4+ T-cell clones established from Japanese patients with insulin-dependent diabetes mellitus. |
| 1892 | 9757911 | To investigate autoimmunity to glutamic acid decarboxylase (GAD) 65 in Japanese patients with insulin-dependent diabetes mellitus (IDDM, type I diabetes), we established seven CD4+ T-cell clones, by stimulating peripheral blood mononuclear cells (PBMC) of six IDDM patients, using a mixture of overlapping human GAD65 peptides. |
| 1893 | 9770521 | Although both major histocompatibility complex class I-restricted CD8(+) and class II-restricted CD4(+) T cell subsets are required, the specific role each subset plays in the pathogenic process is still unclear. |
| 1894 | 9771979 | Pancreata and grafts were harvested at pre-scheduled time points before onset of diabetes and at onset of diabetes, and stained for insulin, MHC class I, MHC class II, alphabeta-TCR, CD4, CD8 or ED1. |
| 1895 | 9780221 | IL-10 impacts autoimmune diabetes via a CD8+ T cell pathway circumventing the requirement for CD4+ T and B lymphocytes. |
| 1896 | 9780221 | Administration of anti-CD40 ligand (CD40L) mAb did not prevent disease, indicating that CD40/CD40L costimulation is not required for diabetes in IL-10-NOD mice. |
| 1897 | 9780221 | Immunization of IL-10-NOD mice with CFA or heat-shock protein 65, known to block diabetes in NOD mice, had no effect on their diabetes. |
| 1898 | 9780221 | We demonstrate that IL-10 contributes early to the pathology of diabetes via a CD8+ T cell pathway, eliminating the requirement for B lymphocytes and CD40-CD40L costimulation. |
| 1899 | 9794372 | The diabetes-susceptible class II MHC genes (in human and mouse) share unique nonaspartic acid residues at position 57 of the class II beta-chain. |
| 1900 | 9794372 | Here, we demonstrate that immature thymocytes expressing a diabetogenic islet Ag-specific transgenic TCR are positively selected by I-A(g7)PD class II MHC to give rise to mature CD4+ T cells. |
| 1901 | 9794372 | These results indicate that nonaspartic acid residues at position 57 of class II MHC beta-chain is important for diabetogenic CD4+ T cell activation in the periphery but is not essential for the formation of a diabetogenic T cell repertoire in the thymus. |
| 1902 | 9794372 | The diabetes-susceptible class II MHC genes (in human and mouse) share unique nonaspartic acid residues at position 57 of the class II beta-chain. |
| 1903 | 9794372 | Here, we demonstrate that immature thymocytes expressing a diabetogenic islet Ag-specific transgenic TCR are positively selected by I-A(g7)PD class II MHC to give rise to mature CD4+ T cells. |
| 1904 | 9794372 | These results indicate that nonaspartic acid residues at position 57 of class II MHC beta-chain is important for diabetogenic CD4+ T cell activation in the periphery but is not essential for the formation of a diabetogenic T cell repertoire in the thymus. |
| 1905 | 9804349 | Compared with normal wound healing: (i) the CD4/CD8 ratio in chronic wounds was significantly lower (p < 0.0027) due to a relatively lower number of CD4+ T cells; (ii) a significantly higher number of macrophages was present in the edge of both type of chronic ulcers (p < 0.001 versus day 29 p.w.); and (iii) more B cells and plasma cells were detected in both type of chronic wounds compared with any day in the acute wound healing model (p < 0.04 for CD20+ and p < 0.01 for CD79a+ cells). |
| 1906 | 9819564 | The nonobese diabetic (NOD) mouse spontaneously develops an autoimmune diabetes that shares many immunogenetic features with human insulin-dependent diabetes mellitus (IDDM), type 1 diabetes. |
| 1907 | 9819564 | T cells are subdivided into CD4+ helper T cells and CD8+ cytotoxic T cells. |
| 1908 | 9840449 | Peptide from glutamic acid decarboxylase similar to coxsackie B virus stimulates IFN-gamma mRNA expression in Th1-like lymphocytes from children with recent-onset insulin-dependent diabetes mellitus. |
| 1909 | 9840449 | CD4+ or Th-lymphocytes will be activated after stimulation resulting in interferon-gamma (IFN-gamma) production by Th1-like lymphocytes and/or interleukin-4 (IL-4) secretion from Th2-like lymphocytes. |
| 1910 | 9840449 | In this study we have shown that this peptide activates Th1-like lymphocytes which produce increased amounts of IFN-gamma mRNA, but seldom mRNA for IL-4. |
| 1911 | 9840449 | In conclusion, we suggest that GAD65 is involved in the development of type 1 diabetes and that the Th1-response may play a role in the destruction of beta cells. |
| 1912 | 9865833 | Immunohistochemical staining in areas of chronic chorioamnionitis showed CD3+ and CD8+ cells present in moderate numbers, and CD4+ cells in smaller numbers. |
| 1913 | 9865833 | CD20+ and CD56+ cells were rare or absent. |
| 1914 | 9892218 | A mechanism of autoimmune destruction of islet beta-cells in type 1 diabetes has been proposed to be the binding of Fas ligand (FasL) on T-cells to Fas receptors on beta-cells. |
| 1915 | 9892218 | We investigated this proposal by examining the expression of FasL and Fas on islet-infiltrating T-cells and beta-cells in relation to beta-cell destruction in a syngeneic islet transplant model in NOD mice. |
| 1916 | 9892218 | Two-color immunohistochemical assays revealed that FasL was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from both diabetic and normoglycemic mice, and the percentage of each type of cell that expressed FasL was greater in islet grafts from normoglycemic compared with diabetic mice. |
| 1917 | 9892218 | In contrast, Fas was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from diabetic mice, but it was nearly or totally absent on these cells in islet grafts from normoglycemic mice. |
| 1918 | 9892218 | Also, mRNA levels of interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were significantly lower in islet grafts from normoglycemic mice. |
| 1919 | 9892218 | Finally, Fas was induced on NOD islet cells by incubation with IL-1beta, IFN-gamma, and the combination of IL-1beta, TNF-alpha, and IFN-gamma. |
| 1920 | 9892218 | These findings support the concept that cytokine-induced Fas receptor expression on islet beta-cells is a mechanism for their destruction by FasL-expressing CD4+ and CD8+ T-cells and, possibly, by FasL-expressing beta-cells themselves. |
| 1921 | 9892218 | A mechanism of autoimmune destruction of islet beta-cells in type 1 diabetes has been proposed to be the binding of Fas ligand (FasL) on T-cells to Fas receptors on beta-cells. |
| 1922 | 9892218 | We investigated this proposal by examining the expression of FasL and Fas on islet-infiltrating T-cells and beta-cells in relation to beta-cell destruction in a syngeneic islet transplant model in NOD mice. |
| 1923 | 9892218 | Two-color immunohistochemical assays revealed that FasL was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from both diabetic and normoglycemic mice, and the percentage of each type of cell that expressed FasL was greater in islet grafts from normoglycemic compared with diabetic mice. |
| 1924 | 9892218 | In contrast, Fas was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from diabetic mice, but it was nearly or totally absent on these cells in islet grafts from normoglycemic mice. |
| 1925 | 9892218 | Also, mRNA levels of interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were significantly lower in islet grafts from normoglycemic mice. |
| 1926 | 9892218 | Finally, Fas was induced on NOD islet cells by incubation with IL-1beta, IFN-gamma, and the combination of IL-1beta, TNF-alpha, and IFN-gamma. |
| 1927 | 9892218 | These findings support the concept that cytokine-induced Fas receptor expression on islet beta-cells is a mechanism for their destruction by FasL-expressing CD4+ and CD8+ T-cells and, possibly, by FasL-expressing beta-cells themselves. |
| 1928 | 9892218 | A mechanism of autoimmune destruction of islet beta-cells in type 1 diabetes has been proposed to be the binding of Fas ligand (FasL) on T-cells to Fas receptors on beta-cells. |
| 1929 | 9892218 | We investigated this proposal by examining the expression of FasL and Fas on islet-infiltrating T-cells and beta-cells in relation to beta-cell destruction in a syngeneic islet transplant model in NOD mice. |
| 1930 | 9892218 | Two-color immunohistochemical assays revealed that FasL was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from both diabetic and normoglycemic mice, and the percentage of each type of cell that expressed FasL was greater in islet grafts from normoglycemic compared with diabetic mice. |
| 1931 | 9892218 | In contrast, Fas was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from diabetic mice, but it was nearly or totally absent on these cells in islet grafts from normoglycemic mice. |
| 1932 | 9892218 | Also, mRNA levels of interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were significantly lower in islet grafts from normoglycemic mice. |
| 1933 | 9892218 | Finally, Fas was induced on NOD islet cells by incubation with IL-1beta, IFN-gamma, and the combination of IL-1beta, TNF-alpha, and IFN-gamma. |
| 1934 | 9892218 | These findings support the concept that cytokine-induced Fas receptor expression on islet beta-cells is a mechanism for their destruction by FasL-expressing CD4+ and CD8+ T-cells and, possibly, by FasL-expressing beta-cells themselves. |
| 1935 | 9892610 | Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes. |
| 1936 | 9892610 | Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors. |
| 1937 | 9892610 | RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells. |
| 1938 | 9892610 | We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats. |
| 1939 | 9892610 | The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4. |
| 1940 | 9892610 | Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes. |
| 1941 | 9892610 | Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors. |
| 1942 | 9892610 | RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells. |
| 1943 | 9892610 | We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats. |
| 1944 | 9892610 | The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4. |
| 1945 | 9892610 | Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes. |
| 1946 | 9892610 | Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors. |
| 1947 | 9892610 | RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells. |
| 1948 | 9892610 | We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats. |
| 1949 | 9892610 | The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4. |
| 1950 | 9892610 | Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes. |
| 1951 | 9892610 | Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors. |
| 1952 | 9892610 | RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells. |
| 1953 | 9892610 | We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats. |
| 1954 | 9892610 | The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4. |
| 1955 | 9933451 | We analysed the development of insulin-dependent diabetes mellitus (IDDM) produced by adoptive transfer of islet lymphocytes from NOD into NOD.scid mice. |
| 1956 | 9933451 | Here we show that the transfer was most effective when both CD4+ and CD8+ T cells were present in the infiltrate, but CD4+ T cells alone were sufficient to cause the disease. |
| 1957 | 9973444 | An increase in the CD4/CD8 T cell ratio was observed in both the syn- and alloMLR due to a relative weak expansion of CD8+ T cells with DC of the BB-DP rat. |
| 1958 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1959 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 1960 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 1961 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 1962 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 1963 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 1964 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 1965 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 1966 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1967 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 1968 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 1969 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 1970 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 1971 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 1972 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 1973 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 1974 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1975 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 1976 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 1977 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 1978 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 1979 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 1980 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 1981 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 1982 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1983 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 1984 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 1985 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 1986 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 1987 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 1988 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 1989 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 1990 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1991 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 1992 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 1993 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 1994 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 1995 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 1996 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 1997 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 1998 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1999 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 2000 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 2001 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 2002 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 2003 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 2004 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 2005 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 2006 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 2007 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 2008 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 2009 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 2010 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 2011 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 2012 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 2013 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 2014 | 10049952 | Development of disease can be prevented by reconstitution of PVG rats shortly after their final irradiation with either peripheral CD4(+)CD45RC- T cells or CD4(+)CD8(-) thymocytes from syngeneic donors. |
| 2015 | 10049952 | Although the activity of both populations is known to depend on the activities of endogenously produced interleukin 4 and transforming growth factor beta, implying a common mechanism, the issue of antigen specificity of the cells involved has not yet been addressed. |
| 2016 | 10049952 | Significantly, in contrast to the peripheral CD4(+) T cells, CD4(+)CD8(-) thymocytes from 131I-treated PVG donors were still able to prevent thyroiditis upon adoptive transfer. |
| 2017 | 10049952 | Development of disease can be prevented by reconstitution of PVG rats shortly after their final irradiation with either peripheral CD4(+)CD45RC- T cells or CD4(+)CD8(-) thymocytes from syngeneic donors. |
| 2018 | 10049952 | Although the activity of both populations is known to depend on the activities of endogenously produced interleukin 4 and transforming growth factor beta, implying a common mechanism, the issue of antigen specificity of the cells involved has not yet been addressed. |
| 2019 | 10049952 | Significantly, in contrast to the peripheral CD4(+) T cells, CD4(+)CD8(-) thymocytes from 131I-treated PVG donors were still able to prevent thyroiditis upon adoptive transfer. |
| 2020 | 10072489 | Interestingly, despite the fact that the original islet allograft presented only MHC class I alloantigens, CD8+ T cells obtained from tolerant animals readily collaborated with naive CD4+ T cells to reject donor-type islet grafts. |
| 2021 | 10072489 | Conversely, tolerant CD4+ T cells failed to collaborate effectively with naive CD8+ T cells for the rejection of donor-type grafts. |
| 2022 | 10072489 | In conclusion, the MHC class I+, II- islet allograft paradoxically leads to a change in the donor-reactive CD4 T cell subset and not in the CD8 subset. |
| 2023 | 10072489 | We hypothesize that the tolerant state is not due to direct class I alloantigen presentation to CD8 T cells but, rather, occurs via the indirect pathway of donor Ag presentation to CD4 T cells in the context of host MHC class II molecules. |
| 2024 | 10072489 | Interestingly, despite the fact that the original islet allograft presented only MHC class I alloantigens, CD8+ T cells obtained from tolerant animals readily collaborated with naive CD4+ T cells to reject donor-type islet grafts. |
| 2025 | 10072489 | Conversely, tolerant CD4+ T cells failed to collaborate effectively with naive CD8+ T cells for the rejection of donor-type grafts. |
| 2026 | 10072489 | In conclusion, the MHC class I+, II- islet allograft paradoxically leads to a change in the donor-reactive CD4 T cell subset and not in the CD8 subset. |
| 2027 | 10072489 | We hypothesize that the tolerant state is not due to direct class I alloantigen presentation to CD8 T cells but, rather, occurs via the indirect pathway of donor Ag presentation to CD4 T cells in the context of host MHC class II molecules. |
| 2028 | 10072489 | Interestingly, despite the fact that the original islet allograft presented only MHC class I alloantigens, CD8+ T cells obtained from tolerant animals readily collaborated with naive CD4+ T cells to reject donor-type islet grafts. |
| 2029 | 10072489 | Conversely, tolerant CD4+ T cells failed to collaborate effectively with naive CD8+ T cells for the rejection of donor-type grafts. |
| 2030 | 10072489 | In conclusion, the MHC class I+, II- islet allograft paradoxically leads to a change in the donor-reactive CD4 T cell subset and not in the CD8 subset. |
| 2031 | 10072489 | We hypothesize that the tolerant state is not due to direct class I alloantigen presentation to CD8 T cells but, rather, occurs via the indirect pathway of donor Ag presentation to CD4 T cells in the context of host MHC class II molecules. |
| 2032 | 10072489 | Interestingly, despite the fact that the original islet allograft presented only MHC class I alloantigens, CD8+ T cells obtained from tolerant animals readily collaborated with naive CD4+ T cells to reject donor-type islet grafts. |
| 2033 | 10072489 | Conversely, tolerant CD4+ T cells failed to collaborate effectively with naive CD8+ T cells for the rejection of donor-type grafts. |
| 2034 | 10072489 | In conclusion, the MHC class I+, II- islet allograft paradoxically leads to a change in the donor-reactive CD4 T cell subset and not in the CD8 subset. |
| 2035 | 10072489 | We hypothesize that the tolerant state is not due to direct class I alloantigen presentation to CD8 T cells but, rather, occurs via the indirect pathway of donor Ag presentation to CD4 T cells in the context of host MHC class II molecules. |
| 2036 | 10078545 | Major DQ8-restricted T-cell epitopes for human GAD65 mapped using human CD4, DQA1*0301, DQB1*0302 transgenic IA(null) NOD mice. |
| 2037 | 10078545 | To map T-cell epitopes for GAD65 restricted to the diabetes-associated DQ8 heterodimer, we generated transgenic NOD mice expressing HLA-DQ8 and human CD4 while having the mouse class II gene (IA(beta)) deleted. |
| 2038 | 10078545 | Major DQ8-restricted T-cell epitopes for human GAD65 mapped using human CD4, DQA1*0301, DQB1*0302 transgenic IA(null) NOD mice. |
| 2039 | 10078545 | To map T-cell epitopes for GAD65 restricted to the diabetes-associated DQ8 heterodimer, we generated transgenic NOD mice expressing HLA-DQ8 and human CD4 while having the mouse class II gene (IA(beta)) deleted. |
| 2040 | 10087179 | Both CD4(+) T cells and CD8(+) T cells are required for iodine accelerated thyroiditis in NOD mice. |
| 2041 | 10087179 | Furthermore, our studies show for the first time that both CD4(+) and CD8(+) T cells are necessary for the development of this accelerated but essentially spontaneous murine thyroid disease. |
| 2042 | 10087179 | Both CD4(+) T cells and CD8(+) T cells are required for iodine accelerated thyroiditis in NOD mice. |
| 2043 | 10087179 | Furthermore, our studies show for the first time that both CD4(+) and CD8(+) T cells are necessary for the development of this accelerated but essentially spontaneous murine thyroid disease. |
| 2044 | 10096786 | Intensity and mechanisms of in vitro xenorecognition of adult pig pancreatic islet cells by CD4+ and CD8+ lymphocytes from type I diabetic or healthy subjects. |
| 2045 | 10096786 | Proliferation in response to islet cells was strongly decreased (p<0.01) when CD4+ T cells were blocked with monoclonal antibodies, whereas the blocking of CD8+ cells or NK cells gave less pronounced effects. |
| 2046 | 10096786 | Purified CD4+ cells alone did not proliferate in response to islet cells but recovered their proliferative ability when mixed with antigen-presenting cells, whereas CD8+ cells alone proliferated in the presence of interleukin-2 in response to islet cells. |
| 2047 | 10096786 | During proliferation in response to islet cells, interleukin-10 increased 43-fold (p<0.01) but interferon-gamma increased only slightly. |
| 2048 | 10096786 | No statistical differences were detected between diabetic and control subjects with respect to lymphocyte subsets and the recognition mechanisms or to interferon-gamma/interleukin-10 production in response to islet cells. |
| 2049 | 10096786 | This situation involves a dominant CD4 class II-restricted Th2 response, with an indirect recognition pathway, as well as a CD8 T-cell response resulting from direct recognition. |
| 2050 | 10096786 | Intensity and mechanisms of in vitro xenorecognition of adult pig pancreatic islet cells by CD4+ and CD8+ lymphocytes from type I diabetic or healthy subjects. |
| 2051 | 10096786 | Proliferation in response to islet cells was strongly decreased (p<0.01) when CD4+ T cells were blocked with monoclonal antibodies, whereas the blocking of CD8+ cells or NK cells gave less pronounced effects. |
| 2052 | 10096786 | Purified CD4+ cells alone did not proliferate in response to islet cells but recovered their proliferative ability when mixed with antigen-presenting cells, whereas CD8+ cells alone proliferated in the presence of interleukin-2 in response to islet cells. |
| 2053 | 10096786 | During proliferation in response to islet cells, interleukin-10 increased 43-fold (p<0.01) but interferon-gamma increased only slightly. |
| 2054 | 10096786 | No statistical differences were detected between diabetic and control subjects with respect to lymphocyte subsets and the recognition mechanisms or to interferon-gamma/interleukin-10 production in response to islet cells. |
| 2055 | 10096786 | This situation involves a dominant CD4 class II-restricted Th2 response, with an indirect recognition pathway, as well as a CD8 T-cell response resulting from direct recognition. |
| 2056 | 10096786 | Intensity and mechanisms of in vitro xenorecognition of adult pig pancreatic islet cells by CD4+ and CD8+ lymphocytes from type I diabetic or healthy subjects. |
| 2057 | 10096786 | Proliferation in response to islet cells was strongly decreased (p<0.01) when CD4+ T cells were blocked with monoclonal antibodies, whereas the blocking of CD8+ cells or NK cells gave less pronounced effects. |
| 2058 | 10096786 | Purified CD4+ cells alone did not proliferate in response to islet cells but recovered their proliferative ability when mixed with antigen-presenting cells, whereas CD8+ cells alone proliferated in the presence of interleukin-2 in response to islet cells. |
| 2059 | 10096786 | During proliferation in response to islet cells, interleukin-10 increased 43-fold (p<0.01) but interferon-gamma increased only slightly. |
| 2060 | 10096786 | No statistical differences were detected between diabetic and control subjects with respect to lymphocyte subsets and the recognition mechanisms or to interferon-gamma/interleukin-10 production in response to islet cells. |
| 2061 | 10096786 | This situation involves a dominant CD4 class II-restricted Th2 response, with an indirect recognition pathway, as well as a CD8 T-cell response resulting from direct recognition. |
| 2062 | 10096786 | Intensity and mechanisms of in vitro xenorecognition of adult pig pancreatic islet cells by CD4+ and CD8+ lymphocytes from type I diabetic or healthy subjects. |
| 2063 | 10096786 | Proliferation in response to islet cells was strongly decreased (p<0.01) when CD4+ T cells were blocked with monoclonal antibodies, whereas the blocking of CD8+ cells or NK cells gave less pronounced effects. |
| 2064 | 10096786 | Purified CD4+ cells alone did not proliferate in response to islet cells but recovered their proliferative ability when mixed with antigen-presenting cells, whereas CD8+ cells alone proliferated in the presence of interleukin-2 in response to islet cells. |
| 2065 | 10096786 | During proliferation in response to islet cells, interleukin-10 increased 43-fold (p<0.01) but interferon-gamma increased only slightly. |
| 2066 | 10096786 | No statistical differences were detected between diabetic and control subjects with respect to lymphocyte subsets and the recognition mechanisms or to interferon-gamma/interleukin-10 production in response to islet cells. |
| 2067 | 10096786 | This situation involves a dominant CD4 class II-restricted Th2 response, with an indirect recognition pathway, as well as a CD8 T-cell response resulting from direct recognition. |
| 2068 | 10190896 | Of these, interleukin 1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma are perhaps the most important. |
| 2069 | 10190896 | We found that islets deficient in Fas, IFN-gamma receptor, or inducible nitric oxide synthase had normal diabetes development; however, the specific lack of TNF- alpha receptor 1 (p55) afforded islets a profound protection from disease by altering the ability of islet-reactive, CD4(+) T cells to establish insulitis and subsequently destroy islet beta cells. |
| 2070 | 10193314 | We used reverse transcriptase polymerase chain reaction (PCR) and quantitative PCR techniques to examine mRNA expression of interferon (IFN)-gamma (Th1 type cytokine), and interleukin (IL)-4 (Th2 type cytokine) in splenic cells. |
| 2071 | 10193314 | We observed that in Reo-2 infected mice the level of IFN-gamma expression increases with the development of insulitis, whereas expression of message for IL-4 is minimal to detectable with the immuno-inflammatory process 10 days after infection. |
| 2072 | 10193314 | Furthermore altered CD4+/CD8+ cell ratio compared with uninfected mice in the splenic cells by the infection was recovered to the ratio of uninfected mice by the treatment of mAb against mouse IFN-gamma, suggesting normalization of T cell balance in immune system. |
| 2073 | 10201921 | We report that cultured DR- and DP-BB rat thymi generate mature CD4 and CD8 single-positive cells with up-regulated TCRs. |
| 2074 | 10201921 | In contrast, DP-BB rat cultures generate fewer CD4+, CD8+, and RT6+ T cells. |
| 2075 | 10201921 | We report that cultured DR- and DP-BB rat thymi generate mature CD4 and CD8 single-positive cells with up-regulated TCRs. |
| 2076 | 10201921 | In contrast, DP-BB rat cultures generate fewer CD4+, CD8+, and RT6+ T cells. |
| 2077 | 10201997 | Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice. |
| 2078 | 10201997 | Here, we demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient in MHC class II expression and peripheral CD4 T cells, show significant pancreatic infiltration but do not develop diabetes. |
| 2079 | 10201997 | Adoptive transfer studies show that the paucity of CD4 T cells in NOD-CIITA knockout mice is responsible for the absence of diabetes, since the CD8 T cell and B cell compartments are functional. |
| 2080 | 10201997 | An autoaggressive CD8+ T cell clone can, however, transfer diabetes in CIITA knockout recipient mice without CD4 T cell help, albeit with some delay compared with that in CIITA-sufficient recipients. |
| 2081 | 10201997 | This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes. |
| 2082 | 10201997 | Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice. |
| 2083 | 10201997 | Here, we demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient in MHC class II expression and peripheral CD4 T cells, show significant pancreatic infiltration but do not develop diabetes. |
| 2084 | 10201997 | Adoptive transfer studies show that the paucity of CD4 T cells in NOD-CIITA knockout mice is responsible for the absence of diabetes, since the CD8 T cell and B cell compartments are functional. |
| 2085 | 10201997 | An autoaggressive CD8+ T cell clone can, however, transfer diabetes in CIITA knockout recipient mice without CD4 T cell help, albeit with some delay compared with that in CIITA-sufficient recipients. |
| 2086 | 10201997 | This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes. |
| 2087 | 10201997 | Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice. |
| 2088 | 10201997 | Here, we demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient in MHC class II expression and peripheral CD4 T cells, show significant pancreatic infiltration but do not develop diabetes. |
| 2089 | 10201997 | Adoptive transfer studies show that the paucity of CD4 T cells in NOD-CIITA knockout mice is responsible for the absence of diabetes, since the CD8 T cell and B cell compartments are functional. |
| 2090 | 10201997 | An autoaggressive CD8+ T cell clone can, however, transfer diabetes in CIITA knockout recipient mice without CD4 T cell help, albeit with some delay compared with that in CIITA-sufficient recipients. |
| 2091 | 10201997 | This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes. |
| 2092 | 10201997 | Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice. |
| 2093 | 10201997 | Here, we demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient in MHC class II expression and peripheral CD4 T cells, show significant pancreatic infiltration but do not develop diabetes. |
| 2094 | 10201997 | Adoptive transfer studies show that the paucity of CD4 T cells in NOD-CIITA knockout mice is responsible for the absence of diabetes, since the CD8 T cell and B cell compartments are functional. |
| 2095 | 10201997 | An autoaggressive CD8+ T cell clone can, however, transfer diabetes in CIITA knockout recipient mice without CD4 T cell help, albeit with some delay compared with that in CIITA-sufficient recipients. |
| 2096 | 10201997 | This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes. |
| 2097 | 10201997 | Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice. |
| 2098 | 10201997 | Here, we demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient in MHC class II expression and peripheral CD4 T cells, show significant pancreatic infiltration but do not develop diabetes. |
| 2099 | 10201997 | Adoptive transfer studies show that the paucity of CD4 T cells in NOD-CIITA knockout mice is responsible for the absence of diabetes, since the CD8 T cell and B cell compartments are functional. |
| 2100 | 10201997 | An autoaggressive CD8+ T cell clone can, however, transfer diabetes in CIITA knockout recipient mice without CD4 T cell help, albeit with some delay compared with that in CIITA-sufficient recipients. |
| 2101 | 10201997 | This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes. |
| 2102 | 10202001 | One segregates as a recessive trait and is associated with a reduction in the peripheral frequency of diabetogenic CD8+ (but not CD4+) T cells. |
| 2103 | 10202001 | The other segregates as a dominant trait and is mediated by IL-4- and TGF-beta1-independent immune suppressive functions provided by lymphocytes that target diabetogenic CD4+ and CD8+ T cells, without causing their deletion, anergy, immune deviation, or ignorance. |
| 2104 | 10202001 | One segregates as a recessive trait and is associated with a reduction in the peripheral frequency of diabetogenic CD8+ (but not CD4+) T cells. |
| 2105 | 10202001 | The other segregates as a dominant trait and is mediated by IL-4- and TGF-beta1-independent immune suppressive functions provided by lymphocytes that target diabetogenic CD4+ and CD8+ T cells, without causing their deletion, anergy, immune deviation, or ignorance. |
| 2106 | 10201999 | To address the question of whether the cell death-inducing cytokines TNF and lymphotoxin alpha are involved in this process, we generated nonobese diabetic (NOD) mice that are deficient for TNF receptor 1 (TNFR1 or TNFRp55). |
| 2107 | 10201999 | Since this was probably due to the complex immunomodulatory effects of TNF and lymphotoxin alpha signaled via TNFR1 on lymphohemopoietic cells, adoptive transfer experiments with spleen cells from diabetic NOD mice were conducted. |
| 2108 | 10201999 | Together with the described expression patterns of perforin and TNF in the mononuclear islet infiltrates of NOD mice, these results indicate that two diabetogenic effector mechanisms are delivered by distinct cell populations: CD8+ T cells lyse beta cells via perforin-dependent cytotoxicity, whereas CD4+ T cells, macrophages, and dendritic cells contribute to diabetes development via TNFR1-dependent beta cell toxicity. |
| 2109 | 10206487 | The role of CD8+ cells, cell degeneration, and Fas ligand in insulitis after intraperitoneal transfer of NOD splenocytes. |
| 2110 | 10206487 | Cells expressing CD4, CD8, CD18, CD49d/CD29, CD44, CD54, CD80, CD86, CD106, CD11b/CD18 or DNA breaks were stained in the pancreases of female or male scid/ scid mice after adoptive transfer of lymphocytes from older than 12-week female nonobese diabetic (NOD) or Balb/c mice. |
| 2111 | 10206487 | After intraperitoneal adoptive transfer of NOD splenocytes to female severe combined immunodeficiency (scid)/scid mice, in situ end labeling (ISEL)+ as well as CD80+ and CD86+ cell infiltrates appeared first in the blood vessel walls and pancreatic interstitial tissue at 2-3 weeks after transfer. |
| 2112 | 10206487 | CD4+, CD8+, CD18+, CD44+, CD54+, and CD106+ cells then encircled and invaded some islets of the scid/scid mice 2 to 7 weeks after transfer. |
| 2113 | 10206487 | Fas ligand was not present in Western blotting. |
| 2114 | 10206487 | It is proposed that apoptosis commonly occurs in islet-infiltrating lymphocytes and that in the scid/scid adoptive-transfer model, the first islet-infiltrating cells are destroyed by programmed cell death independent of Fas ligand. |
| 2115 | 10206487 | The role of CD8+ cells, cell degeneration, and Fas ligand in insulitis after intraperitoneal transfer of NOD splenocytes. |
| 2116 | 10206487 | Cells expressing CD4, CD8, CD18, CD49d/CD29, CD44, CD54, CD80, CD86, CD106, CD11b/CD18 or DNA breaks were stained in the pancreases of female or male scid/ scid mice after adoptive transfer of lymphocytes from older than 12-week female nonobese diabetic (NOD) or Balb/c mice. |
| 2117 | 10206487 | After intraperitoneal adoptive transfer of NOD splenocytes to female severe combined immunodeficiency (scid)/scid mice, in situ end labeling (ISEL)+ as well as CD80+ and CD86+ cell infiltrates appeared first in the blood vessel walls and pancreatic interstitial tissue at 2-3 weeks after transfer. |
| 2118 | 10206487 | CD4+, CD8+, CD18+, CD44+, CD54+, and CD106+ cells then encircled and invaded some islets of the scid/scid mice 2 to 7 weeks after transfer. |
| 2119 | 10206487 | Fas ligand was not present in Western blotting. |
| 2120 | 10206487 | It is proposed that apoptosis commonly occurs in islet-infiltrating lymphocytes and that in the scid/scid adoptive-transfer model, the first islet-infiltrating cells are destroyed by programmed cell death independent of Fas ligand. |
| 2121 | 10209507 | Jejuna of patients with insulin-dependent diabetes mellitus (IDDM) show signs of immune activation. |
| 2122 | 10209507 | The roles of enteric viruses and food antigens as possible triggers in human insulin-dependent diabetes mellitus and the evidence that mucosal-associated homing receptors are important in both human and experimental diabetes prompted us to undertake an immunohistochemical study of intestinal specimens from patients with IDDM. |
| 2123 | 10209507 | We studied jejunal morphology and immunohistochemistry in 26 patients with IDDM, 13 of whom had the HLA-DQB1*0201 gene and therefore a higher risk of coeliac disease. |
| 2124 | 10209507 | The densities of T cells, CD4+, CD8+, and T cell receptor alpha/beta+ and gamma/delta+ cells in the epithelium and lamina propria were similar in patients and controls, but the patients had significantly more alpha 4/beta 7 integrin+ cells in the lamina propria (P = 0.006). |
| 2125 | 10222028 | In support of this interpretation, we found that the accessory molecules CD4, CD44, and B7-1 (all of which are involved in T cell co-stimulation) were cleaved by Phlogenzym, while CD3 and MHC class II molecules (which are involved in the recognition of antigens by T cells) and LFA-1 were unaffected. |
| 2126 | 10231096 | MHC class I and II molecules play a central role in the immune response against a variety of invading microorganisms and cells that have undergone malignant transformation by shaping the T cell repertoire in the thymus and by presenting peptide antigens from endogenous and exogenous antigens in the periphery to CD8+ cytotoxic T cells and CD4+ helper T cells. |
| 2127 | 10331400 | After activation in vitro with islet cell membrane antigens, the diabetes-inducing cell lines were comprised of both CD4+ CD8- T-cells and 10-30% B-cells. |
| 2128 | 10337011 | Therefore, in order to evaluate cytokine secretion by spleen and islet infiltrating T cells in NOD mice at different stages of the autoimmune process, we developed an ELISPOT assay that detects IL-2, IL-4, and interferon-gamma (IFN-gamma) secretion in vitro at the single-cell level. |
| 2129 | 10337011 | We showed that, whatever the age considered, IFN-gamma is predominantly secreted, and that no IL-4-secreting cells are detected in the islets of male and female NOD mice. |
| 2130 | 10337011 | Spleen cells from 8-week-old female NOD mice, which include regulatory suppressor T cells, do not secrete IL-4, either upon presentation of islet cell antigens in vitro, or after transfer in vivo, but do secrete IFN-gamma. |
| 2131 | 10337011 | IFN-gamma secretion by T cells from diabetic mice results from CD4 but not CD8 T cells in transfer experiments into NOD/severe combined immunodeficient (SCID) recipients. |
| 2132 | 10337011 | These results suggest that (i) detection of regulatory CD4 T cells in NOD mice is not paralleled by a Th2 response; (ii) beta cell destruction does not depend on a switch from a Th2 to a Th1-type response; and (iii) CD8 T cells do not participate in induction of diabetes by secreting IFN-gamma. |
| 2133 | 10337011 | Therefore, in order to evaluate cytokine secretion by spleen and islet infiltrating T cells in NOD mice at different stages of the autoimmune process, we developed an ELISPOT assay that detects IL-2, IL-4, and interferon-gamma (IFN-gamma) secretion in vitro at the single-cell level. |
| 2134 | 10337011 | We showed that, whatever the age considered, IFN-gamma is predominantly secreted, and that no IL-4-secreting cells are detected in the islets of male and female NOD mice. |
| 2135 | 10337011 | Spleen cells from 8-week-old female NOD mice, which include regulatory suppressor T cells, do not secrete IL-4, either upon presentation of islet cell antigens in vitro, or after transfer in vivo, but do secrete IFN-gamma. |
| 2136 | 10337011 | IFN-gamma secretion by T cells from diabetic mice results from CD4 but not CD8 T cells in transfer experiments into NOD/severe combined immunodeficient (SCID) recipients. |
| 2137 | 10337011 | These results suggest that (i) detection of regulatory CD4 T cells in NOD mice is not paralleled by a Th2 response; (ii) beta cell destruction does not depend on a switch from a Th2 to a Th1-type response; and (iii) CD8 T cells do not participate in induction of diabetes by secreting IFN-gamma. |
| 2138 | 10395666 | In addition, the secondary lymphoid organs of these mice harbored phenotypically normal CD4+ and CD8+ T cell compartments. |
| 2139 | 10400139 | Chemokine receptor CCR2 and CCR5 polymorphisms in children with insulin-dependent diabetes mellitus. |
| 2140 | 10400139 | Studies have shown the important roles of several regulatory and proinflammatory cytokines in insulin-dependent diabetes mellitus (IDDM). |
| 2141 | 10400139 | CC-chemokine receptors CCR2 and CCR5 bind chemokines that are involved in the trafficking of leukocytes in both basal and inflammatory states. |
| 2142 | 10400139 | A common 32-bp deletion mutation in the CCR5 gene (CCR5delta32) and a G-to-A nucleotide substitution in the CCR2 at position 190 (CCR2-64I) have recently been described. |
| 2143 | 10400139 | The role of this mutation in IDDM cannot be explained yet, but, because CCR2 mediates the chemotaxis of CD4+ and CD8+ T cells to areas of inflammation and because these cells play important roles in insulitis, a mutation in the CCR2 gene may contribute to the susceptibility to the disease. |
| 2144 | 10400139 | According to these results, the CCR2 gene may be a new candidate for the susceptibility locus of IDDM. |
| 2145 | 10411548 | Mice expressing lymphocytic choriomeningitis virus nucleoprotein (LCMV-NP) as a transgene in their beta cells develop insulin-dependent diabetes mellitus (IDDM) only after LCMV infection. |
| 2146 | 10411548 | Inoculation of plasmid DNA encoding the insulin B chain reduced the incidence of IDDM by 50% in this model. |
| 2147 | 10411548 | The insulin B-chain DNA vaccination was effective through induction of regulatory CD4 lymphocytes that react with the insulin B chain, secrete IL-4, and locally reduce activity of LCMV-NP-autoreactive cytotoxic T lymphocytes in the pancreatic draining lymph node. |
| 2148 | 10426369 | The ability of nonobese diabetic (NOD) mice to mount a cellular immune response to the secretory granule protein tyrosine phosphatase (PTP), phogrin was evaluated by immunization of 8- to 12-week-old animals with recombinant phogrin in complete Freund's adjuvant. |
| 2149 | 10426369 | The results demonstrate the feasibility of generating antigen-specific diabetes-inducing CD4+ cells by direct immunization of NOD mice and their potential use for further studies of the antigenic epitopes in the PTP family members. |
| 2150 | 10430939 | Prevalent CD8(+) T cell response against one peptide/MHC complex in autoimmune diabetes. |
| 2151 | 10430939 | Spontaneous autoimmune diabetes in nonobese diabetic (NOD) mice is the result of a CD4(+) and CD8(+) T cell-dependent autoimmune process directed against the pancreatic beta cells. |
| 2152 | 10430939 | Here, we define the structure of a peptide mimotope that elicits the proliferation, cytokine secretion, differentiation, and cytotoxicity of a diabetogenic H-2K(d)-restricted CD8(+) T cell specificity (NY8.3) that uses a T cell receptor alpha (TCRalpha) rearrangement frequently expressed by CD8(+) T cells propagated from the earliest insulitic lesions of NOD mice (Valpha17-Jalpha42 elements, often joined by the N-region sequence M-R-D/E). |
| 2153 | 10430939 | Stimulation of splenic CD8(+) T cells from single-chain 8. 3-TCRbeta-transgenic NOD mice with this mimotope leads to preferential expansion of T cells bearing an endogenously derived TCRalpha chain identical to the one used by their islet-associated CD8(+) T cells, which is also identical to the 8.3-TCRalpha sequence. |
| 2154 | 10430939 | This work demonstrates that beta cell-reactive CD8(+) T cells mount a prevalent response against a single peptide/MHC complex and provides one peptide ligand for CD8(+) T cells in autoimmune diabetes. |
| 2155 | 10433099 | CD4+ lymphocytes are the most important effector cells in autoimmune diabetes of NOD mice, although some role of CD8+ T cells has been demonstrated. |
| 2156 | 10433099 | However, it is unknown how CD4+ lymphocytes are able to destroy pancreatic beta-cells that do not express MHC (major histocompatibility complex) class II molecules. |
| 2157 | 10433099 | Apoptotic cell death mediated by an interaction of Fas with Fas ligand (FasL) could be a mechanism by which MHC class II-negative pancreatic beta-cells are destroyed by CD4+ T lymphocytes. |
| 2158 | 10433099 | IFN (interferon)-gamma, tumor necrosis factor-alpha, interleukin-1 and their combinations failed to enhance Fas expression. |
| 2159 | 10433099 | Unsorted activated splenocytes from diabetic NOD mice had cytotoxic T lymphocyte activity of a small degree against IFN-gamma-treated MIN6N8 cells with FasL upregulation. |
| 2160 | 10433099 | CD4+ lymphocytes are the most important effector cells in autoimmune diabetes of NOD mice, although some role of CD8+ T cells has been demonstrated. |
| 2161 | 10433099 | However, it is unknown how CD4+ lymphocytes are able to destroy pancreatic beta-cells that do not express MHC (major histocompatibility complex) class II molecules. |
| 2162 | 10433099 | Apoptotic cell death mediated by an interaction of Fas with Fas ligand (FasL) could be a mechanism by which MHC class II-negative pancreatic beta-cells are destroyed by CD4+ T lymphocytes. |
| 2163 | 10433099 | IFN (interferon)-gamma, tumor necrosis factor-alpha, interleukin-1 and their combinations failed to enhance Fas expression. |
| 2164 | 10433099 | Unsorted activated splenocytes from diabetic NOD mice had cytotoxic T lymphocyte activity of a small degree against IFN-gamma-treated MIN6N8 cells with FasL upregulation. |
| 2165 | 10433099 | CD4+ lymphocytes are the most important effector cells in autoimmune diabetes of NOD mice, although some role of CD8+ T cells has been demonstrated. |
| 2166 | 10433099 | However, it is unknown how CD4+ lymphocytes are able to destroy pancreatic beta-cells that do not express MHC (major histocompatibility complex) class II molecules. |
| 2167 | 10433099 | Apoptotic cell death mediated by an interaction of Fas with Fas ligand (FasL) could be a mechanism by which MHC class II-negative pancreatic beta-cells are destroyed by CD4+ T lymphocytes. |
| 2168 | 10433099 | IFN (interferon)-gamma, tumor necrosis factor-alpha, interleukin-1 and their combinations failed to enhance Fas expression. |
| 2169 | 10433099 | Unsorted activated splenocytes from diabetic NOD mice had cytotoxic T lymphocyte activity of a small degree against IFN-gamma-treated MIN6N8 cells with FasL upregulation. |
| 2170 | 10433560 | Substantial benefits are associated with these responses: Initially memory, then naive, CD4 cell counts may rise by 150-200 cells/mm3; CD8 cell numbers also rise sharply but then fall below pretreatment levels, presumably as antigenic stimuli driving the CD8 response decline; cellular activation markers decline; distortions in the T cell repertoire gradually lessen; and increases in proliferative responses to mitogens and recall antigens are more easily elicited. |
| 2171 | 10439311 | CD4+ and CD8+ T-cell clones from congenital rubella syndrome patients with IDDM recognize overlapping GAD65 protein epitopes. |
| 2172 | 10439311 | To fully characterize human glutamic acid decarboxylase (GAD)65 protein T-cell epitopes associated with insulin-dependent diabetes mellitus (IDDM), CTL clones specific to GAD65 protein antigens were isolated from two congenital rubella syndrome (CRS)-associated IDDM patients. |
| 2173 | 10439311 | Overlapping nonamer T-cell epitopes recognized by both CD4+ or CD8+ CTL clones within peptides GAD65(252-266) and GAD65(274-286) were identified as sequences bounded by GAD65(255-266) with 6/9 overlapping residues, and GAD65(276-285) with 8/9 overlapping residues, respectively, using two panels of overlapping peptide analogs in cytotoxicity assays. |
| 2174 | 10439311 | The antigenic GAD65 peptides elicited cytotoxic responses of peptide-specific CD4+ T-cell clones in the context of HLA DRB1*0404. |
| 2175 | 10439311 | The CD8+ T-cell clone specific to GAD65(255-263) was found to be restricted by HLA A3 and A11. |
| 2176 | 10439311 | Similarly, the CD8+ T-cell clone specific to GAD65(277-285) killed peptide-sensitized target cells expressing HLA B35 and B15. |
| 2177 | 10439311 | CD4+ and CD8+ T-cell clones from congenital rubella syndrome patients with IDDM recognize overlapping GAD65 protein epitopes. |
| 2178 | 10439311 | To fully characterize human glutamic acid decarboxylase (GAD)65 protein T-cell epitopes associated with insulin-dependent diabetes mellitus (IDDM), CTL clones specific to GAD65 protein antigens were isolated from two congenital rubella syndrome (CRS)-associated IDDM patients. |
| 2179 | 10439311 | Overlapping nonamer T-cell epitopes recognized by both CD4+ or CD8+ CTL clones within peptides GAD65(252-266) and GAD65(274-286) were identified as sequences bounded by GAD65(255-266) with 6/9 overlapping residues, and GAD65(276-285) with 8/9 overlapping residues, respectively, using two panels of overlapping peptide analogs in cytotoxicity assays. |
| 2180 | 10439311 | The antigenic GAD65 peptides elicited cytotoxic responses of peptide-specific CD4+ T-cell clones in the context of HLA DRB1*0404. |
| 2181 | 10439311 | The CD8+ T-cell clone specific to GAD65(255-263) was found to be restricted by HLA A3 and A11. |
| 2182 | 10439311 | Similarly, the CD8+ T-cell clone specific to GAD65(277-285) killed peptide-sensitized target cells expressing HLA B35 and B15. |
| 2183 | 10439311 | CD4+ and CD8+ T-cell clones from congenital rubella syndrome patients with IDDM recognize overlapping GAD65 protein epitopes. |
| 2184 | 10439311 | To fully characterize human glutamic acid decarboxylase (GAD)65 protein T-cell epitopes associated with insulin-dependent diabetes mellitus (IDDM), CTL clones specific to GAD65 protein antigens were isolated from two congenital rubella syndrome (CRS)-associated IDDM patients. |
| 2185 | 10439311 | Overlapping nonamer T-cell epitopes recognized by both CD4+ or CD8+ CTL clones within peptides GAD65(252-266) and GAD65(274-286) were identified as sequences bounded by GAD65(255-266) with 6/9 overlapping residues, and GAD65(276-285) with 8/9 overlapping residues, respectively, using two panels of overlapping peptide analogs in cytotoxicity assays. |
| 2186 | 10439311 | The antigenic GAD65 peptides elicited cytotoxic responses of peptide-specific CD4+ T-cell clones in the context of HLA DRB1*0404. |
| 2187 | 10439311 | The CD8+ T-cell clone specific to GAD65(255-263) was found to be restricted by HLA A3 and A11. |
| 2188 | 10439311 | Similarly, the CD8+ T-cell clone specific to GAD65(277-285) killed peptide-sensitized target cells expressing HLA B35 and B15. |
| 2189 | 10450504 | In the past decade, a wealth of information has accumulated through studies in non-obese diabetic (NOD) mice regarding the molecular and cellular events that participate in the progression to diabetes in insulin-dependent diabetes mellitus (IDDM). |
| 2190 | 10450504 | Here we describe a new NOD model for analyzing the role of TNF-alpha in IDDM, TNF-alpha-NOD mice. |
| 2191 | 10450504 | Although adoptive transfer studies demonstrated that TNF-alpha can enhance presentation of islet antigen to both effector CD4+ and CD8+ T cells, further investigations in TNF-alpha-NOD mice deficient in either CD4+ or CD8+ T cells demonstrated that diabetes progression is dependent on CD8+ T cells, with CD4+ T cells playing a lesser role. |
| 2192 | 10450504 | The data accumulating from TNF-alpha-NOD mice, described in this review, indicates novel pathways by which inflammatory stimuli can precipitate autoimmunity, and suggests newer approaches in the design of therapeutic treatments that prevent beta-cell destruction in IDDM. |
| 2193 | 10453045 | IL-12 and IL-12 antagonist administration to nonobese diabetic (NOD) mice accelerates and prevents insulin-dependent diabetes mellitus (IDDM), respectively. |
| 2194 | 10453045 | Nevertheless, wild-type and IL-12-deficient NOD mice developed similar insulitis and IDDM. |
| 2195 | 10453045 | Both in wild-type and IL-12-deficient NOD mice, approximately 20% of pancreas-infiltrating CD4+ T cells produced IFN-gamma, whereas very few produced IL-10 or IL-4, indicating that IDDM was associated with a type 1 T cell infiltrate in the target organ. |
| 2196 | 10461865 | Pancreatic sections were also examined for the influx of CD4 and CD8 T cells and macrophages following immunofluorescence staining. |
| 2197 | 10461865 | Immunohistochemical staining showed increasing numbers of CD4 and CD8 T cell subsets and macrophages within the islets and in exocrine, sinusoidal and peri-vascular regions. |
| 2198 | 10461865 | The present results show that cyclophosphamide administration to female NOD mice results in a rapid influx of CD4 and CD8 cells and macrophages. |
| 2199 | 10461865 | The marked up-regulation of inducible nitric oxide synthase in a selective proportion of macrophages, within the islets, immediately preceding and during the onset of diabetes suggests that nitric oxide released by islet macrophages may be an important molecular mediator of beta cell destruction in this accelerated model of insulin-dependent diabetes mellitus. |
| 2200 | 10461865 | Pancreatic sections were also examined for the influx of CD4 and CD8 T cells and macrophages following immunofluorescence staining. |
| 2201 | 10461865 | Immunohistochemical staining showed increasing numbers of CD4 and CD8 T cell subsets and macrophages within the islets and in exocrine, sinusoidal and peri-vascular regions. |
| 2202 | 10461865 | The present results show that cyclophosphamide administration to female NOD mice results in a rapid influx of CD4 and CD8 cells and macrophages. |
| 2203 | 10461865 | The marked up-regulation of inducible nitric oxide synthase in a selective proportion of macrophages, within the islets, immediately preceding and during the onset of diabetes suggests that nitric oxide released by islet macrophages may be an important molecular mediator of beta cell destruction in this accelerated model of insulin-dependent diabetes mellitus. |
| 2204 | 10461865 | Pancreatic sections were also examined for the influx of CD4 and CD8 T cells and macrophages following immunofluorescence staining. |
| 2205 | 10461865 | Immunohistochemical staining showed increasing numbers of CD4 and CD8 T cell subsets and macrophages within the islets and in exocrine, sinusoidal and peri-vascular regions. |
| 2206 | 10461865 | The present results show that cyclophosphamide administration to female NOD mice results in a rapid influx of CD4 and CD8 cells and macrophages. |
| 2207 | 10461865 | The marked up-regulation of inducible nitric oxide synthase in a selective proportion of macrophages, within the islets, immediately preceding and during the onset of diabetes suggests that nitric oxide released by islet macrophages may be an important molecular mediator of beta cell destruction in this accelerated model of insulin-dependent diabetes mellitus. |
| 2208 | 10470079 | Type 1 diabetes is an autoimmune disease in which the insulin-producing pancreatic beta cells are destroyed at an early age by an immune process that involves both CD4 and CD8 T lymphocytes. |
| 2209 | 10470079 | The peptide recognized by the cells is in the same region of the insulin B chain as the epitope recognized by previously isolated pathogenic CD4 T cells. |
| 2210 | 10470079 | Type 1 diabetes is an autoimmune disease in which the insulin-producing pancreatic beta cells are destroyed at an early age by an immune process that involves both CD4 and CD8 T lymphocytes. |
| 2211 | 10470079 | The peptide recognized by the cells is in the same region of the insulin B chain as the epitope recognized by previously isolated pathogenic CD4 T cells. |
| 2212 | 10476932 | Insulin-dependent diabetes mellitus (IDDM) in the nonobese diabetes (NOD) mouse model is thought to be an autoimmune CD4 Th1-like cell-mediated disease. |
| 2213 | 10476932 | We tested the efficacy of oral use of interferon-alpha (IFN-alpha) therapy on IDDM in NOD mice. |
| 2214 | 10476932 | Using urine and blood sugar levels as indicators of IDDM, oral administration of murine IFN-alpha (100 IU/body) to NOD mice significantly delayed the onset of symptomatic diabetes. |
| 2215 | 10476932 | However, oral use of IFN-alpha did not prevent diabetic NOD mice from losing weight once NOD mice were symptomatic, suggesting that orally administered IFN-alpha is a prophylactic rather than therapeutic approach to the management of IDDM. |
| 2216 | 10480599 | Neonatal porcine islet cells induce human CD4+, but not CD8+, lymphocyte proliferation and resist cell-mediated cytolytic injury in vitro. |
| 2217 | 10480600 | Insulin B-chain reactive CD4+ regulatory T-cells induced by oral insulin treatment protect from type 1 diabetes by blocking the cytokine secretion and pancreatic infiltration of diabetogenic effector T-cells. |
| 2218 | 10480600 | We demonstrate that oral insulin feeding of NOD mice induces the function of insulin B-chain reactive CD4+ regulatory T-cells, which compete with diabetogenic effector T-cells for the recognition of insulin in NOD.Scid recipient mice. |
| 2219 | 10480600 | These effector T-cells become deprived of interleukin (IL)-2 and interferon (IFN)-gamma and are unable to expand and migrate to the pancreas. |
| 2220 | 10480600 | Type 1 diabetes-protective splenic regulatory T-cells secrete relatively little transforming growth factor (TGF)-beta1, suggesting that TGF-beta may not contribute to the inactivation of effector T-cells in NOD.Scid recipients. |
| 2221 | 10480600 | Insulin B-chain reactive CD4+ regulatory T-cells induced by oral insulin treatment protect from type 1 diabetes by blocking the cytokine secretion and pancreatic infiltration of diabetogenic effector T-cells. |
| 2222 | 10480600 | We demonstrate that oral insulin feeding of NOD mice induces the function of insulin B-chain reactive CD4+ regulatory T-cells, which compete with diabetogenic effector T-cells for the recognition of insulin in NOD.Scid recipient mice. |
| 2223 | 10480600 | These effector T-cells become deprived of interleukin (IL)-2 and interferon (IFN)-gamma and are unable to expand and migrate to the pancreas. |
| 2224 | 10480600 | Type 1 diabetes-protective splenic regulatory T-cells secrete relatively little transforming growth factor (TGF)-beta1, suggesting that TGF-beta may not contribute to the inactivation of effector T-cells in NOD.Scid recipients. |
| 2225 | 10499191 | Lipid parameters (triglycerides, cholesterol, apolipoproteins A1 and B) were studied as well as nutritional and inflammatory markers (albumin, prealbumin, transferrin, haptoglobin, orosomucoid, C-reactive protein), endocrine and cytokine parameters (thyrotropin, cortisol, leptin, interleukin-6), HIV viral load and CD4-lymphocyte count. |
| 2226 | 10499817 | Both Zn++ and Cu++ show a concentration-dependent inactivation of a protease essential for the proliferation of the AIDS virus HIV-1, while zinc can help prevent diabetes complications through its intracellular activation of the enzyme sorbitol dehydrogenase (SDH). |
| 2227 | 10499817 | AIDS viruses (HIVs) enter immune cells with the aid of the CD4 cell surface receptor in combination with a number of co-receptors which include CCR3, CCR5 and CXCR4. |
| 2228 | 10499817 | Remarkably, the cell surface receptor for LTB4 (BLTR) also seems to act as a co-receptor for CD4, which helps HIVs to infect immune cells. |
| 2229 | 10499817 | The Th2 cytokine II-4 increases the number of CXCR4 and BLTR co-receptors, as a result of which, under Th2, the HIV strains that infect immune cells are precisely those that are best able to accelerate the AIDS disease process. |
| 2230 | 10499817 | Both Zn++ and Cu++ show a concentration-dependent inactivation of a protease essential for the proliferation of the AIDS virus HIV-1, while zinc can help prevent diabetes complications through its intracellular activation of the enzyme sorbitol dehydrogenase (SDH). |
| 2231 | 10499817 | AIDS viruses (HIVs) enter immune cells with the aid of the CD4 cell surface receptor in combination with a number of co-receptors which include CCR3, CCR5 and CXCR4. |
| 2232 | 10499817 | Remarkably, the cell surface receptor for LTB4 (BLTR) also seems to act as a co-receptor for CD4, which helps HIVs to infect immune cells. |
| 2233 | 10499817 | The Th2 cytokine II-4 increases the number of CXCR4 and BLTR co-receptors, as a result of which, under Th2, the HIV strains that infect immune cells are precisely those that are best able to accelerate the AIDS disease process. |
| 2234 | 10512358 | In a number of animal models of spontaneous autoimmune diabetes, pathogenesis has been highly correlated with autoreactive T-cell production of the type 1 cytokine interferon-gamma (IFN-gamma), while protection from disease was associated with type 2 cytokines such as interleukin (IL)-4. |
| 2235 | 10512358 | IL-10 has generally been associated with immunosuppression, including the modulation of class II expression on antigen-presenting cells and the generation of regulatory CD4 T-cells. |
| 2236 | 10524496 | Double transgenic (dTg) mice expressing the hemagglutinin (HA) of influenza virus under the insulin promoter and the TCR specific for the immunodominant CD4 T cell epitope of HA (HA110-120) develop insulin-dependent diabetes mellitus (IDDM). |
| 2237 | 10549569 | Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic beta cells by a progressive beta cell-specific autoimmune process. |
| 2238 | 10549569 | Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of beta cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. |
| 2239 | 10549569 | CD4+ and CD8+ T cells are both believed to be important for the destruction of beta cells. |
| 2240 | 10549569 | In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the beta cells in conjunction with beta cell autoantigens and MHC class I and class II antigens, resulting in the onset of autoimmune type I diabetes. |
| 2241 | 10549569 | Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic beta cells by a progressive beta cell-specific autoimmune process. |
| 2242 | 10549569 | Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of beta cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. |
| 2243 | 10549569 | CD4+ and CD8+ T cells are both believed to be important for the destruction of beta cells. |
| 2244 | 10549569 | In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the beta cells in conjunction with beta cell autoantigens and MHC class I and class II antigens, resulting in the onset of autoimmune type I diabetes. |
| 2245 | 10549569 | Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic beta cells by a progressive beta cell-specific autoimmune process. |
| 2246 | 10549569 | Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of beta cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. |
| 2247 | 10549569 | CD4+ and CD8+ T cells are both believed to be important for the destruction of beta cells. |
| 2248 | 10549569 | In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the beta cells in conjunction with beta cell autoantigens and MHC class I and class II antigens, resulting in the onset of autoimmune type I diabetes. |
| 2249 | 10549628 | Autoreactive CD4+ T cells protect from autoimmune diabetes via bystander suppression using the IL-4/Stat6 pathway. |
| 2250 | 10549628 | Here, we report the generation and characterization of insulin B chain-specific "autoreactive" CD4+ regulatory T cells that locally suppress diabetogenic T cell responses against an unrelated self-antigen (viral transgene) in a virus-induced model for type 1 diabetes. |
| 2251 | 10549628 | Autoreactive CD4+ T cells protect from autoimmune diabetes via bystander suppression using the IL-4/Stat6 pathway. |
| 2252 | 10549628 | Here, we report the generation and characterization of insulin B chain-specific "autoreactive" CD4+ regulatory T cells that locally suppress diabetogenic T cell responses against an unrelated self-antigen (viral transgene) in a virus-induced model for type 1 diabetes. |
| 2253 | 10550215 | The role of CD4 and CD8 T cells in the development of autoimmune diabetes. |
| 2254 | 10553062 | The role of the STAT4 signaling pathway in autoimmune diabetes was investigated using the rat insulin promoter lymphocytic choriomeningitis virus model of virally induced autoimmune diabetes. |
| 2255 | 10553062 | Abrogation of STAT4 signaling significantly reduced the development of CD4+-T cell-dependent but not CD4+-T cell-independent diabetes, illustrating the fine-tuned kinetics involved in the pathogenesis of autoimmunity. |
| 2256 | 10553062 | However, the absence of STAT4 did not prevent the generation of autoreactive Th1/Tc1 T cell responses, as well as protective antiviral immunity. |
| 2257 | 10553062 | Protection from insulin-dependent diabetes mellitus was associated with decreased numbers of autoreactive CTL precursors in the pancreas and the spleen and a general as well as Ag-specific reduction of IFN-gamma secretion by T lymphocytes. |
| 2258 | 10553062 | Selective inhibition of the STAT4 signal transduction pathway might constitute a novel and attractive approach to prevent clinical insulin-dependent diabetes mellitus in prediabetic individuals at risk. |
| 2259 | 10553102 | As few as 500 CD4high islet-infiltrating CD4+ T cells transferred insulin-dependent diabetes mellitus to CD8 reconstituted NOD-SCID mice within 30 days of transfer. |
| 2260 | 10553102 | In contrast, CD4high T cells isolated from either NOD spleen or salivary glands did not transfer insulin-dependent diabetes mellitus into similar CD8-reconstituted NOD-SCID recipients. |
| 2261 | 10556546 | Our group is examining the role that CD4(+) and CD8(+) T cells play in IDDM in the NOD mouse, as it is known that both T cell subsets are required for onset of disease. |
| 2262 | 10556546 | We raised GAD peptide-specific CD8(+) T cells by immunising NOD mice with the GAD peptide alongside an irrelevant peptide that induced a CD4(+) T cell response. |
| 2263 | 10556546 | In order to maintain these peptide specific T cells in vitro and generate clones, it was found that antibodies specific to CD4(+) and MHC class II molecules needed to be included in the culture medium. |
| 2264 | 10556546 | Our group is examining the role that CD4(+) and CD8(+) T cells play in IDDM in the NOD mouse, as it is known that both T cell subsets are required for onset of disease. |
| 2265 | 10556546 | We raised GAD peptide-specific CD8(+) T cells by immunising NOD mice with the GAD peptide alongside an irrelevant peptide that induced a CD4(+) T cell response. |
| 2266 | 10556546 | In order to maintain these peptide specific T cells in vitro and generate clones, it was found that antibodies specific to CD4(+) and MHC class II molecules needed to be included in the culture medium. |
| 2267 | 10556546 | Our group is examining the role that CD4(+) and CD8(+) T cells play in IDDM in the NOD mouse, as it is known that both T cell subsets are required for onset of disease. |
| 2268 | 10556546 | We raised GAD peptide-specific CD8(+) T cells by immunising NOD mice with the GAD peptide alongside an irrelevant peptide that induced a CD4(+) T cell response. |
| 2269 | 10556546 | In order to maintain these peptide specific T cells in vitro and generate clones, it was found that antibodies specific to CD4(+) and MHC class II molecules needed to be included in the culture medium. |
| 2270 | 10580422 | Although CD8+ T-cells are observed within the grafts at later time points, CD4+ T-cells predominate until the graft is destroyed. |
| 2271 | 10580639 | In the past few years, considerable evidence has accumulated to suggest the existence of functionally polarized responses by the CD4+ T helper (Th)--and the CD8+ T cytotoxic (Tc)-cell subsets that depend on the cytokines they produce. |
| 2272 | 10586049 | In vitro studies indicate that the effect of the Ab is independent of CD4 coreceptor function, as Ab treatment also inhibits proliferation and induces a persistent anergy in naive CD4 T cells stimulated by anti-CD3/CD28. |
| 2273 | 10593564 | Both are used to model human insulin-dependent diabetes mellitus (IDDM). |
| 2274 | 10593564 | We now report that the phenotype of NK T cells in the rat is alphabetaTcR+ CD8+ CD4-, comparable to the NK T cell phenotype reported for humans, which is alphabetaTcR+ CD4- Valpha24-JalphaQ, and either CD8- or CD8alphaalpha+. |
| 2275 | 10593564 | Because RT6+ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen. |
| 2276 | 10594693 | The number of CD4- CD8-, CD4+ CD8-, CD4- CD8+ and CD4+ CD8+ subsets was not different between BBDP and BBDR rat thymocytes, whereas spleen and lymph nodes in BBDP rats undergo severe T-cell lymphopenia. |
| 2277 | 10594693 | Notably, mature CD4- CD8+ [T-cell receptor (TCR)-alphabeta+ and CD5+] cells are certainly present in the BBDP rat thymus, unlike some previous reports, suggesting that the differentiation of CD4- CD8+ from CD4+ CD8+ cells occurs normally in the BBDP rat thymus. |
| 2278 | 10594693 | The number of CD4- CD8-, CD4+ CD8-, CD4- CD8+ and CD4+ CD8+ subsets was not different between BBDP and BBDR rat thymocytes, whereas spleen and lymph nodes in BBDP rats undergo severe T-cell lymphopenia. |
| 2279 | 10594693 | Notably, mature CD4- CD8+ [T-cell receptor (TCR)-alphabeta+ and CD5+] cells are certainly present in the BBDP rat thymus, unlike some previous reports, suggesting that the differentiation of CD4- CD8+ from CD4+ CD8+ cells occurs normally in the BBDP rat thymus. |
| 2280 | 10605017 | We now demonstrate that regulatory splenocytes belong to the CD4+ CD62Lhigh T cell subset that comprises a vast majority of naive cells producing low levels of IL-2 and IFN-gamma and no IL-4 and IL-10 upon in vitro stimulation. |
| 2281 | 10605017 | Consistently, the inhibition of diabetes transfer was not mediated by IL-4 and IL-10. |
| 2282 | 10605017 | The phenotypic and functional characteristics of protective CD4+ CD62L+ cells suggest they are different from Th2-, Tr1-, and NK T-type cells, reported to be implicated in the control of diabetes in NOD mice, and may represent a new immunoregulatory population. |
| 2283 | 10605017 | We now demonstrate that regulatory splenocytes belong to the CD4+ CD62Lhigh T cell subset that comprises a vast majority of naive cells producing low levels of IL-2 and IFN-gamma and no IL-4 and IL-10 upon in vitro stimulation. |
| 2284 | 10605017 | Consistently, the inhibition of diabetes transfer was not mediated by IL-4 and IL-10. |
| 2285 | 10605017 | The phenotypic and functional characteristics of protective CD4+ CD62L+ cells suggest they are different from Th2-, Tr1-, and NK T-type cells, reported to be implicated in the control of diabetes in NOD mice, and may represent a new immunoregulatory population. |
| 2286 | 10610182 | In transgenic mice, we have expressed three human components involved in T-cell recognition of an MS-relevant autoantigen presented by the HLA-DR2 molecule: DRA*0101/DRB1*1501 (HLA-DR2), an MHC class II candidate MS susceptibility genes found in individuals of European descent; a T-cell receptor (TCR) from an MS-patient-derived T-cell clone specific for the HLA-DR2 bound immunodominant myelin basic protein (MBP) 4102 peptide; and the human CD4 coreceptor. |
| 2287 | 10610182 | When DR2 and TCR double-transgenic mice were backcrossed twice to Rag2 (for recombination-activating gene 2)-deficient mice, the incidence of spontaneous disease increased, demonstrating that T cells specific for the HLA-DR2 bound MBP peptide are sufficient and necessary for development of disease. |
| 2288 | 10620608 | The diabetes was accompanied by severe insulitis composed of both T cells (CD4(+) and CD8(+)) and B cells. |
| 2289 | 10620608 | T cells from the diabetic mice secreted large amounts of interferon gamma, but not interleukin 4, in response to DQ8(+) islets and the putative islet autoantigens, insulin and glutamic acid decarboxylase (GAD). |
| 2290 | 10620608 | In conclusion, substitution of HLA-DQA1*0301/DQB1*0302, but not HLA-DQA1*0103/DQB1*0601, for murine MHC class II provokes autoimmune diabetes in non-diabetes-prone rat insulin promoter (RIP).B7-1 C57BL/6 mice. |
| 2291 | 10631549 | In the nonobese diabetic mouse model, there is new evidence that insulin plays an important role: not only is it an antigen for pathogenic CD4+ T cells but also it is recognised by highly diabetogenic CD8+ T cells. |
| 2292 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 2293 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 2294 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 2295 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 2296 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 2297 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 2298 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 2299 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 2300 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 2301 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 2302 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 2303 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 2304 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 2305 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 2306 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 2307 | 10668191 | Insulin-dependent diabetes mellitus (IDDM) is caused by autoimmune destruction of pancreatic beta cells with the primary mechanism being cell mediated. |
| 2308 | 10668191 | Since the diabetes-prone BB rat is lymphopenic, with a reduction of both CD4 and CD8 cells, the continuous failure of dCF treated animals to develop diabetes may have been due to generalized immunosuppression. |
| 2309 | 10683375 | IL-1alpha, IL-1beta, and IFN-gamma mark beta cells for Fas-dependent destruction by diabetogenic CD4(+) T lymphocytes. |
| 2310 | 10683375 | Cytokines such as IL-1alpha, IL-1beta, and IFN-gamma have long been implicated in the pathogenesis of autoimmune diabetes, but the mechanisms through which they promote diabetogenesis remain unclear. |
| 2311 | 10683375 | Here we show that CD4(+) T lymphocytes propagated from transgenic nonobese diabetic (NOD) mice expressing the highly diabetogenic, beta cell-specific 4.1-T-cell receptor (4.1-TCR) can kill IL-1alpha-, IL-1beta-, and IFN-gamma-treated beta cells from NOD mice. |
| 2312 | 10683375 | Abrogation of Fas expression in 4.1-TCR-transgenic NOD mice afforded nearly complete protection from diabetes and did not interfere with the development of the transgenic CD4(+) T cells or with their ability to cause insulitis. |
| 2313 | 10683375 | These data demonstrate a novel mechanism of action of IL-1alpha, IL-1beta, and IFN-gamma in autoimmune diabetes, whereby these cytokines mark beta cells for Fas-dependent lysis by autoreactive CD4(+) T cells. |
| 2314 | 10683375 | IL-1alpha, IL-1beta, and IFN-gamma mark beta cells for Fas-dependent destruction by diabetogenic CD4(+) T lymphocytes. |
| 2315 | 10683375 | Cytokines such as IL-1alpha, IL-1beta, and IFN-gamma have long been implicated in the pathogenesis of autoimmune diabetes, but the mechanisms through which they promote diabetogenesis remain unclear. |
| 2316 | 10683375 | Here we show that CD4(+) T lymphocytes propagated from transgenic nonobese diabetic (NOD) mice expressing the highly diabetogenic, beta cell-specific 4.1-T-cell receptor (4.1-TCR) can kill IL-1alpha-, IL-1beta-, and IFN-gamma-treated beta cells from NOD mice. |
| 2317 | 10683375 | Abrogation of Fas expression in 4.1-TCR-transgenic NOD mice afforded nearly complete protection from diabetes and did not interfere with the development of the transgenic CD4(+) T cells or with their ability to cause insulitis. |
| 2318 | 10683375 | These data demonstrate a novel mechanism of action of IL-1alpha, IL-1beta, and IFN-gamma in autoimmune diabetes, whereby these cytokines mark beta cells for Fas-dependent lysis by autoreactive CD4(+) T cells. |
| 2319 | 10683375 | IL-1alpha, IL-1beta, and IFN-gamma mark beta cells for Fas-dependent destruction by diabetogenic CD4(+) T lymphocytes. |
| 2320 | 10683375 | Cytokines such as IL-1alpha, IL-1beta, and IFN-gamma have long been implicated in the pathogenesis of autoimmune diabetes, but the mechanisms through which they promote diabetogenesis remain unclear. |
| 2321 | 10683375 | Here we show that CD4(+) T lymphocytes propagated from transgenic nonobese diabetic (NOD) mice expressing the highly diabetogenic, beta cell-specific 4.1-T-cell receptor (4.1-TCR) can kill IL-1alpha-, IL-1beta-, and IFN-gamma-treated beta cells from NOD mice. |
| 2322 | 10683375 | Abrogation of Fas expression in 4.1-TCR-transgenic NOD mice afforded nearly complete protection from diabetes and did not interfere with the development of the transgenic CD4(+) T cells or with their ability to cause insulitis. |
| 2323 | 10683375 | These data demonstrate a novel mechanism of action of IL-1alpha, IL-1beta, and IFN-gamma in autoimmune diabetes, whereby these cytokines mark beta cells for Fas-dependent lysis by autoreactive CD4(+) T cells. |
| 2324 | 10683375 | IL-1alpha, IL-1beta, and IFN-gamma mark beta cells for Fas-dependent destruction by diabetogenic CD4(+) T lymphocytes. |
| 2325 | 10683375 | Cytokines such as IL-1alpha, IL-1beta, and IFN-gamma have long been implicated in the pathogenesis of autoimmune diabetes, but the mechanisms through which they promote diabetogenesis remain unclear. |
| 2326 | 10683375 | Here we show that CD4(+) T lymphocytes propagated from transgenic nonobese diabetic (NOD) mice expressing the highly diabetogenic, beta cell-specific 4.1-T-cell receptor (4.1-TCR) can kill IL-1alpha-, IL-1beta-, and IFN-gamma-treated beta cells from NOD mice. |
| 2327 | 10683375 | Abrogation of Fas expression in 4.1-TCR-transgenic NOD mice afforded nearly complete protection from diabetes and did not interfere with the development of the transgenic CD4(+) T cells or with their ability to cause insulitis. |
| 2328 | 10683375 | These data demonstrate a novel mechanism of action of IL-1alpha, IL-1beta, and IFN-gamma in autoimmune diabetes, whereby these cytokines mark beta cells for Fas-dependent lysis by autoreactive CD4(+) T cells. |
| 2329 | 10684857 | CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. |
| 2330 | 10684857 | Signals generated through CD28-B7 and CD40 ligand (CD40L)-CD40 interactions have been shown to be crucial for the induction of long-term allograft survivability. |
| 2331 | 10684857 | To investigate potential mechanisms of CD40L-induced allograft acceptance, we coimmobilized hu5C8 with suboptimal amounts of anti-CD3 to stimulate CD4(+) T cells. |
| 2332 | 10684857 | We now report that anti-CD3/CD40L costimulation results in CD28-independent activation and subsequent deletion of resting T cells. |
| 2333 | 10684857 | Coligation of CD3 and CD40L increased expression of CD69, CD25, and CD54 on CD4(+) T cells. |
| 2334 | 10684857 | We also found that costimulation with anti-CD3/CD40L resulted in enhanced production of interleukin (IL)-10, interferon gamma, and tumor necrosis factor alpha but not IL-2 or IL-6. |
| 2335 | 10684857 | Consistent with that observation, anti-CD3/CD40L did not enhance the antiapoptotic proteins Bcl-2 and Bcl-xL. |
| 2336 | 10684857 | Further, the addition of CD28 at 24 h failed to rescue those cells induced to die after costimulation with anti-CD3/CD40L. |
| 2337 | 10684857 | CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. |
| 2338 | 10684857 | Signals generated through CD28-B7 and CD40 ligand (CD40L)-CD40 interactions have been shown to be crucial for the induction of long-term allograft survivability. |
| 2339 | 10684857 | To investigate potential mechanisms of CD40L-induced allograft acceptance, we coimmobilized hu5C8 with suboptimal amounts of anti-CD3 to stimulate CD4(+) T cells. |
| 2340 | 10684857 | We now report that anti-CD3/CD40L costimulation results in CD28-independent activation and subsequent deletion of resting T cells. |
| 2341 | 10684857 | Coligation of CD3 and CD40L increased expression of CD69, CD25, and CD54 on CD4(+) T cells. |
| 2342 | 10684857 | We also found that costimulation with anti-CD3/CD40L resulted in enhanced production of interleukin (IL)-10, interferon gamma, and tumor necrosis factor alpha but not IL-2 or IL-6. |
| 2343 | 10684857 | Consistent with that observation, anti-CD3/CD40L did not enhance the antiapoptotic proteins Bcl-2 and Bcl-xL. |
| 2344 | 10684857 | Further, the addition of CD28 at 24 h failed to rescue those cells induced to die after costimulation with anti-CD3/CD40L. |
| 2345 | 10684857 | CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. |
| 2346 | 10684857 | Signals generated through CD28-B7 and CD40 ligand (CD40L)-CD40 interactions have been shown to be crucial for the induction of long-term allograft survivability. |
| 2347 | 10684857 | To investigate potential mechanisms of CD40L-induced allograft acceptance, we coimmobilized hu5C8 with suboptimal amounts of anti-CD3 to stimulate CD4(+) T cells. |
| 2348 | 10684857 | We now report that anti-CD3/CD40L costimulation results in CD28-independent activation and subsequent deletion of resting T cells. |
| 2349 | 10684857 | Coligation of CD3 and CD40L increased expression of CD69, CD25, and CD54 on CD4(+) T cells. |
| 2350 | 10684857 | We also found that costimulation with anti-CD3/CD40L resulted in enhanced production of interleukin (IL)-10, interferon gamma, and tumor necrosis factor alpha but not IL-2 or IL-6. |
| 2351 | 10684857 | Consistent with that observation, anti-CD3/CD40L did not enhance the antiapoptotic proteins Bcl-2 and Bcl-xL. |
| 2352 | 10684857 | Further, the addition of CD28 at 24 h failed to rescue those cells induced to die after costimulation with anti-CD3/CD40L. |
| 2353 | 10697437 | The number of CD4+ T lymphocytes co-expressing CD45RA and CD45RO antigens were statistically higher in the patients with recently diagnosed insulin-dependent diabetes mellitus. |
| 2354 | 10706679 | Inhibition of autoimmune diabetes by Fas ligand: the paradox is solved. |
| 2355 | 10706679 | Pretreatment of lymphocytes with soluble FasL (sFasL) also inhibited diabetes transfer. sFasL treatment decreased the number of CD4+CD45RBlow cells and increased the number of propidium iodide-stained cells among CD4+CD45RBlow cells, suggesting that sFasL induces apoptosis on CD4+CD45RBlow "memory" cells. |
| 2356 | 10706696 | Furthermore, the mechanism by which diabetes is transferred by a Tg Th2 T cell clone differs from that of the original CD4+ Th1 BDC-2.5 T cell clone made in this laboratory. |
| 2357 | 10719672 | Treatment of prediabetic mice with the pancreatic islet autoantigen insulin, by aerosol or intranasal delivery, reduces the incidence of diabetes and is associated with induction of CD8 (alpha alpha) gamma delta T cells, small numbers of which prevent adoptive transfer of diabetes. |
| 2358 | 10719672 | We examine the evidence for gamma delta T cells in mucosal tolerance and discuss possible mechanisms underlying the induction and action of insulin-induced CD8 gamma delta regulatory T cells. |
| 2359 | 10719672 | In contrast, intranasal (pro)insulin peptide, or oral insulin which is degraded in the gut, induces CD4 regulatory cells. |
| 2360 | 10725754 | Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions. |
| 2361 | 10725754 | Previous work has indicated that an important component for the initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta cell Ags. |
| 2362 | 10725754 | However, unless previously activated in vitro, such CD8 T cells have previously been thought to require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. |
| 2363 | 10725754 | In this study, we show that IDDM development is greatly accelerated in a stock of NOD mice expressing TCR transgenes derived from a MHC class I-restricted CD8 T cell clone (designated AI4) previously found to contribute to the earliest preclinical stages of pancreatic beta cell destruction. |
| 2364 | 10725754 | Importantly, these TCR transgenic NOD mice (designated NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 helper T cells were eliminated by introduction of the scid mutation or a functionally inactivated CD4 allele. |
| 2365 | 10725754 | In a previously described stock of NOD mice expressing TCR transgenes derived from another MHC class I-restricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual CD4 T cells. |
| 2366 | 10725754 | Hence, there is variability in the helper dependence of CD8 T cells contributing to the development of autoimmune IDDM. |
| 2367 | 10725754 | The AI4 clonotype represents the first CD8 T cell with a demonstrated ability to progress from a naive to functionally activated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell helper functions. |
| 2368 | 10725754 | Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions. |
| 2369 | 10725754 | Previous work has indicated that an important component for the initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta cell Ags. |
| 2370 | 10725754 | However, unless previously activated in vitro, such CD8 T cells have previously been thought to require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. |
| 2371 | 10725754 | In this study, we show that IDDM development is greatly accelerated in a stock of NOD mice expressing TCR transgenes derived from a MHC class I-restricted CD8 T cell clone (designated AI4) previously found to contribute to the earliest preclinical stages of pancreatic beta cell destruction. |
| 2372 | 10725754 | Importantly, these TCR transgenic NOD mice (designated NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 helper T cells were eliminated by introduction of the scid mutation or a functionally inactivated CD4 allele. |
| 2373 | 10725754 | In a previously described stock of NOD mice expressing TCR transgenes derived from another MHC class I-restricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual CD4 T cells. |
| 2374 | 10725754 | Hence, there is variability in the helper dependence of CD8 T cells contributing to the development of autoimmune IDDM. |
| 2375 | 10725754 | The AI4 clonotype represents the first CD8 T cell with a demonstrated ability to progress from a naive to functionally activated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell helper functions. |
| 2376 | 10725754 | Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions. |
| 2377 | 10725754 | Previous work has indicated that an important component for the initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta cell Ags. |
| 2378 | 10725754 | However, unless previously activated in vitro, such CD8 T cells have previously been thought to require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. |
| 2379 | 10725754 | In this study, we show that IDDM development is greatly accelerated in a stock of NOD mice expressing TCR transgenes derived from a MHC class I-restricted CD8 T cell clone (designated AI4) previously found to contribute to the earliest preclinical stages of pancreatic beta cell destruction. |
| 2380 | 10725754 | Importantly, these TCR transgenic NOD mice (designated NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 helper T cells were eliminated by introduction of the scid mutation or a functionally inactivated CD4 allele. |
| 2381 | 10725754 | In a previously described stock of NOD mice expressing TCR transgenes derived from another MHC class I-restricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual CD4 T cells. |
| 2382 | 10725754 | Hence, there is variability in the helper dependence of CD8 T cells contributing to the development of autoimmune IDDM. |
| 2383 | 10725754 | The AI4 clonotype represents the first CD8 T cell with a demonstrated ability to progress from a naive to functionally activated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell helper functions. |
| 2384 | 10725754 | Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions. |
| 2385 | 10725754 | Previous work has indicated that an important component for the initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta cell Ags. |
| 2386 | 10725754 | However, unless previously activated in vitro, such CD8 T cells have previously been thought to require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. |
| 2387 | 10725754 | In this study, we show that IDDM development is greatly accelerated in a stock of NOD mice expressing TCR transgenes derived from a MHC class I-restricted CD8 T cell clone (designated AI4) previously found to contribute to the earliest preclinical stages of pancreatic beta cell destruction. |
| 2388 | 10725754 | Importantly, these TCR transgenic NOD mice (designated NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 helper T cells were eliminated by introduction of the scid mutation or a functionally inactivated CD4 allele. |
| 2389 | 10725754 | In a previously described stock of NOD mice expressing TCR transgenes derived from another MHC class I-restricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual CD4 T cells. |
| 2390 | 10725754 | Hence, there is variability in the helper dependence of CD8 T cells contributing to the development of autoimmune IDDM. |
| 2391 | 10725754 | The AI4 clonotype represents the first CD8 T cell with a demonstrated ability to progress from a naive to functionally activated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell helper functions. |
| 2392 | 10725754 | Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions. |
| 2393 | 10725754 | Previous work has indicated that an important component for the initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta cell Ags. |
| 2394 | 10725754 | However, unless previously activated in vitro, such CD8 T cells have previously been thought to require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. |
| 2395 | 10725754 | In this study, we show that IDDM development is greatly accelerated in a stock of NOD mice expressing TCR transgenes derived from a MHC class I-restricted CD8 T cell clone (designated AI4) previously found to contribute to the earliest preclinical stages of pancreatic beta cell destruction. |
| 2396 | 10725754 | Importantly, these TCR transgenic NOD mice (designated NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 helper T cells were eliminated by introduction of the scid mutation or a functionally inactivated CD4 allele. |
| 2397 | 10725754 | In a previously described stock of NOD mice expressing TCR transgenes derived from another MHC class I-restricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual CD4 T cells. |
| 2398 | 10725754 | Hence, there is variability in the helper dependence of CD8 T cells contributing to the development of autoimmune IDDM. |
| 2399 | 10725754 | The AI4 clonotype represents the first CD8 T cell with a demonstrated ability to progress from a naive to functionally activated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell helper functions. |
| 2400 | 10770268 | One of the primary mechanisms of active cellular suppression is via secretion of suppressive cytokines such as TGF-beta, IL-4, and IL-10 following antigen-specific triggering. |
| 2401 | 10770268 | TGF-beta is produced both by CD4+ and CD8+ GALT-derived T cells and is an important mediator of the active suppression component of oral tolerance. |
| 2402 | 10773364 | The popliteal lymph node response to streptozotocin is under type 1, MHC class-I restricted, CD8(+) T-cell control. |
| 2403 | 10773364 | In order to determine whether PLN responses involve CD4(+) or CD8(+) T-cells, the effects of streptozotocin (STZ), a prototypic immunotoxic compound, were analyzed after injection into the hind footpad of C57 BL/6 mice and major histocompatibility complex (MHC) class I or II deficient mice. |
| 2404 | 10773364 | The involvement of type 1 or type 2 cell control on the production of cytokine mRNAs was analyzed in lymph node cells by quantitative RT-PCR, together with the analysis of a wide range of cytokine mRNAs after STZ injection (IL-1alpha, IL-1beta, TNF-alpha, IFN-gamma, IL-2, IL-2 receptor, IL-4, IL-5, IL-6, IL-10 and IL-12). |
| 2405 | 10773364 | We have found that mice depleted in CD8(+) T-cells did not respond to STZ, whereas mice depleted in CD4(+) T-cells exhibited the expected positive PLN responses, with increased weight and cellularity indices. |
| 2406 | 10773364 | STZ induced a low production of interleukin (IL)-2 mRNAs, a mild increase in IL-1alpha and IL-6 mRNAs production, and a dramatic increase in IFN-gamma, IL-1beta, TNF-alpha, IL-12 and IL-2 receptor mRNAs, which correlated with positive PLN responses. |
| 2407 | 10773364 | No effects on IL-4, IL-5 and IL-10 mRNAs synthesis were noted. |
| 2408 | 10773364 | In CD8(+) T-cell deficient mice, there was no production of IFN-gamma or IL-6 mRNAs. |
| 2409 | 10773364 | These results suggest that PLN responses to STZ are under the control of type 1, MHC class-I-restricted, CD8(+) T-cells. |
| 2410 | 10773364 | The popliteal lymph node response to streptozotocin is under type 1, MHC class-I restricted, CD8(+) T-cell control. |
| 2411 | 10773364 | In order to determine whether PLN responses involve CD4(+) or CD8(+) T-cells, the effects of streptozotocin (STZ), a prototypic immunotoxic compound, were analyzed after injection into the hind footpad of C57 BL/6 mice and major histocompatibility complex (MHC) class I or II deficient mice. |
| 2412 | 10773364 | The involvement of type 1 or type 2 cell control on the production of cytokine mRNAs was analyzed in lymph node cells by quantitative RT-PCR, together with the analysis of a wide range of cytokine mRNAs after STZ injection (IL-1alpha, IL-1beta, TNF-alpha, IFN-gamma, IL-2, IL-2 receptor, IL-4, IL-5, IL-6, IL-10 and IL-12). |
| 2413 | 10773364 | We have found that mice depleted in CD8(+) T-cells did not respond to STZ, whereas mice depleted in CD4(+) T-cells exhibited the expected positive PLN responses, with increased weight and cellularity indices. |
| 2414 | 10773364 | STZ induced a low production of interleukin (IL)-2 mRNAs, a mild increase in IL-1alpha and IL-6 mRNAs production, and a dramatic increase in IFN-gamma, IL-1beta, TNF-alpha, IL-12 and IL-2 receptor mRNAs, which correlated with positive PLN responses. |
| 2415 | 10773364 | No effects on IL-4, IL-5 and IL-10 mRNAs synthesis were noted. |
| 2416 | 10773364 | In CD8(+) T-cell deficient mice, there was no production of IFN-gamma or IL-6 mRNAs. |
| 2417 | 10773364 | These results suggest that PLN responses to STZ are under the control of type 1, MHC class-I-restricted, CD8(+) T-cells. |
| 2418 | 10779402 | Flow cytometric analysis then revealed that LPS-stimulation in vitro induced the expression of an IL-2 receptor (CD25) on CD4 T cells; this indicates that the activation of islet-specific T cells is a prerequisite to eliciting diabetes in this situation. |
| 2419 | 10795741 | B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes. |
| 2420 | 10795741 | In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. |
| 2421 | 10795741 | These mice present a profound decrease of the immunoregulatory CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice. |
| 2422 | 10795741 | B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes. |
| 2423 | 10795741 | In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. |
| 2424 | 10795741 | These mice present a profound decrease of the immunoregulatory CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice. |
| 2425 | 10799914 | Natural development of diabetes in nonobese diabetic (NOD) mice requires both CD4 and CD8 T cells. |
| 2426 | 10806782 | The results showed that before treatment the level of serum zinc and red cell C3b receptor rosette(RBCK-C3b RR), T-lymphocyte subgroup CD3, CD4, and CD4/CD8 were decreased(P < 0.01), while CD8, red cell immune complex rosette(RBC-ICR) were increased. |
| 2427 | 10806782 | After treatment with zinc gluconate for 1 month the serum zinc level, RBC-C3b RR, RBC-ICR, CD3 and CD4/CD8 became normal, CD8 also approached to normal. |
| 2428 | 10806782 | The results showed that before treatment the level of serum zinc and red cell C3b receptor rosette(RBCK-C3b RR), T-lymphocyte subgroup CD3, CD4, and CD4/CD8 were decreased(P < 0.01), while CD8, red cell immune complex rosette(RBC-ICR) were increased. |
| 2429 | 10806782 | After treatment with zinc gluconate for 1 month the serum zinc level, RBC-C3b RR, RBC-ICR, CD3 and CD4/CD8 became normal, CD8 also approached to normal. |
| 2430 | 10861053 | Although therapeutic injection of protein and synthetic peptides corresponding to CD4+ T cell epitopes has been shown to prevent or block autoimmune disease in several models, down-regulation of an ongoing CD8+ T cell-mediated autoimmune response using this approach has not yet been reported. |
| 2431 | 10861053 | Thus, in addition to autoreactive CD4+ T cells, CD8+ T cells may constitute targets for Ag-specific therapy in autoimmune diseases. |
| 2432 | 10861053 | Although therapeutic injection of protein and synthetic peptides corresponding to CD4+ T cell epitopes has been shown to prevent or block autoimmune disease in several models, down-regulation of an ongoing CD8+ T cell-mediated autoimmune response using this approach has not yet been reported. |
| 2433 | 10861053 | Thus, in addition to autoreactive CD4+ T cells, CD8+ T cells may constitute targets for Ag-specific therapy in autoimmune diseases. |
| 2434 | 10873305 | The identification of factors that regulate the proliferation and differentiation of double-positive (DP) into CD4(+) and CD8(+) single-positive (SP) thymocytes has proven difficult due to the inability of DP thymocytes to proliferate, expand, and differentiate into SP thymocytes in available cell culture media. |
| 2435 | 10873305 | During a 5-day culture in XLCM in the absence of thymic stromal cells, DP thymocytes from normal mice and MHC double knockout mice (lack SP thymocytes) proliferate, expand, and differentiate into several (alphabetaTCR(+), NK1.1(+)alphabetaTCR(+), and gammadeltaTCR(+)) subsets of CD4(+) and predominantly CD8(+) SP thymocytes. |
| 2436 | 10873305 | The identification of factors that regulate the proliferation and differentiation of double-positive (DP) into CD4(+) and CD8(+) single-positive (SP) thymocytes has proven difficult due to the inability of DP thymocytes to proliferate, expand, and differentiate into SP thymocytes in available cell culture media. |
| 2437 | 10873305 | During a 5-day culture in XLCM in the absence of thymic stromal cells, DP thymocytes from normal mice and MHC double knockout mice (lack SP thymocytes) proliferate, expand, and differentiate into several (alphabetaTCR(+), NK1.1(+)alphabetaTCR(+), and gammadeltaTCR(+)) subsets of CD4(+) and predominantly CD8(+) SP thymocytes. |
| 2438 | 10925277 | We show that the Ab inhibits transfer of insulin-dependent diabetes mellitus by the CD4+ Th1 clone BDC2.5 to nonobese diabetic mice. |
| 2439 | 10946320 | We found that both Th1-like CD45RC+CD4+ and cytotoxic CD8+ T cells were up-regulated, whereas Th2-like CD45RC-CD4+ T cells were down-regulated, and that isolated and activated CD45RC+CD4+ and CD8+ T cells from KRV-infected DR-BB rats induced autoimmune diabetes in young diabetes-prone BioBreeding (DP-BB) rats. |
| 2440 | 10946320 | We conclude that KRV-induced autoimmune diabetes in DR-BB rats is not due to molecular mimicry, but is due to a breakdown of the finely tuned immune balance of Th1-like CD45RC+CD4+ and Th2-like CD45RC-CD4+ T cells, resulting in the selective activation of beta cell-cytotoxic effector T cells. |
| 2441 | 10946320 | We found that both Th1-like CD45RC+CD4+ and cytotoxic CD8+ T cells were up-regulated, whereas Th2-like CD45RC-CD4+ T cells were down-regulated, and that isolated and activated CD45RC+CD4+ and CD8+ T cells from KRV-infected DR-BB rats induced autoimmune diabetes in young diabetes-prone BioBreeding (DP-BB) rats. |
| 2442 | 10946320 | We conclude that KRV-induced autoimmune diabetes in DR-BB rats is not due to molecular mimicry, but is due to a breakdown of the finely tuned immune balance of Th1-like CD45RC+CD4+ and Th2-like CD45RC-CD4+ T cells, resulting in the selective activation of beta cell-cytotoxic effector T cells. |
| 2443 | 10952038 | Both CD4+ and CD8+ cells were detected in the IR(High) T cell population, but IR(High) expression was detected predominantly on CD4+ cells. |
| 2444 | 10952038 | The lack of IL-2 receptor and transferrin receptor expression as seen previously, together with the CD62L(Low)/- CD44(High) phenotype suggests that IR(High) T cells are memory cells. |
| 2445 | 10975477 | Intracellular cytokine staining and flow cytometry were used to investigate whether immunoadsorption (IA) of immunoglobulins alters intracytoplasmic cytokine production in CD4+ and CD8+ T cells from the blood of patients with refractory rheumatoid arthritis (n = 7), membrane proliferative glomerulonephritis (n = 1), and Goodpasture's syndrome (n = 1). |
| 2446 | 10975477 | Four patients (Group 1) showed severely depressed production of TNF-alpha, IL-2, IFN-gamma, and IL-4 by CD4+ and CD8+ T cells and responded to 3 IA sessions with significant increases in CD4+TNF-alpha+, CD4+IL-2+, and CD8+IL-2+ T cells. |
| 2447 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 2448 | 10975477 | Group 2 (n = 5) showed unimpaired intracellular cytokine levels and responded to IA with a heterogeneous pattern of changes in TNF-alpha, IL-2, IFN-gamma, and IL-4 production, but these alterations were smaller than those in Group 1. |
| 2449 | 10975477 | Intracellular cytokine staining and flow cytometry were used to investigate whether immunoadsorption (IA) of immunoglobulins alters intracytoplasmic cytokine production in CD4+ and CD8+ T cells from the blood of patients with refractory rheumatoid arthritis (n = 7), membrane proliferative glomerulonephritis (n = 1), and Goodpasture's syndrome (n = 1). |
| 2450 | 10975477 | Four patients (Group 1) showed severely depressed production of TNF-alpha, IL-2, IFN-gamma, and IL-4 by CD4+ and CD8+ T cells and responded to 3 IA sessions with significant increases in CD4+TNF-alpha+, CD4+IL-2+, and CD8+IL-2+ T cells. |
| 2451 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 2452 | 10975477 | Group 2 (n = 5) showed unimpaired intracellular cytokine levels and responded to IA with a heterogeneous pattern of changes in TNF-alpha, IL-2, IFN-gamma, and IL-4 production, but these alterations were smaller than those in Group 1. |
| 2453 | 10975477 | Intracellular cytokine staining and flow cytometry were used to investigate whether immunoadsorption (IA) of immunoglobulins alters intracytoplasmic cytokine production in CD4+ and CD8+ T cells from the blood of patients with refractory rheumatoid arthritis (n = 7), membrane proliferative glomerulonephritis (n = 1), and Goodpasture's syndrome (n = 1). |
| 2454 | 10975477 | Four patients (Group 1) showed severely depressed production of TNF-alpha, IL-2, IFN-gamma, and IL-4 by CD4+ and CD8+ T cells and responded to 3 IA sessions with significant increases in CD4+TNF-alpha+, CD4+IL-2+, and CD8+IL-2+ T cells. |
| 2455 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 2456 | 10975477 | Group 2 (n = 5) showed unimpaired intracellular cytokine levels and responded to IA with a heterogeneous pattern of changes in TNF-alpha, IL-2, IFN-gamma, and IL-4 production, but these alterations were smaller than those in Group 1. |
| 2457 | 10975480 | We treated the patient by lymphocytapheresis (LCP), which resulted in an improvement of his symptoms, a reduction in the CD4 lymphocyte population, a reduction of the CD4/CD8 ratio, and a reduced thickening of the dura mater that lasted for more than 14 months. |
| 2458 | 10975823 | CD25 is a marker for CD4+ thymocytes that prevent autoimmune diabetes in rats, but peripheral T cells with this function are found in both CD25+ and CD25- subpopulations. |
| 2459 | 10975823 | Previously we have shown that autoimmune diabetes, induced in rats by a protocol of adult thymectomy and split-dose gamma irradiation, can be prevented by the transfer of a subset of CD4+ T cells with a memory phenotype (CD45RC-), as well as by CD4+CD8- thymocytes, from syngeneic donors. |
| 2460 | 10975823 | In thoracic duct lymph, cells that could prevent diabetes were found in both CD25- and CD25+ subsets of CD4+CD45RC- cells. |
| 2461 | 10975823 | CD25 is a marker for CD4+ thymocytes that prevent autoimmune diabetes in rats, but peripheral T cells with this function are found in both CD25+ and CD25- subpopulations. |
| 2462 | 10975823 | Previously we have shown that autoimmune diabetes, induced in rats by a protocol of adult thymectomy and split-dose gamma irradiation, can be prevented by the transfer of a subset of CD4+ T cells with a memory phenotype (CD45RC-), as well as by CD4+CD8- thymocytes, from syngeneic donors. |
| 2463 | 10975823 | In thoracic duct lymph, cells that could prevent diabetes were found in both CD25- and CD25+ subsets of CD4+CD45RC- cells. |
| 2464 | 10975823 | CD25 is a marker for CD4+ thymocytes that prevent autoimmune diabetes in rats, but peripheral T cells with this function are found in both CD25+ and CD25- subpopulations. |
| 2465 | 10975823 | Previously we have shown that autoimmune diabetes, induced in rats by a protocol of adult thymectomy and split-dose gamma irradiation, can be prevented by the transfer of a subset of CD4+ T cells with a memory phenotype (CD45RC-), as well as by CD4+CD8- thymocytes, from syngeneic donors. |
| 2466 | 10975823 | In thoracic duct lymph, cells that could prevent diabetes were found in both CD25- and CD25+ subsets of CD4+CD45RC- cells. |
| 2467 | 10984555 | We thus determined the cortisol response to an intravenous bolus of 1 microg ACTH in 21 controls, 18 HIV-positive (BMI 19.5+/-0.9 kg/m(2), albumin 24+/-1.4 g/l, CD4 count 192+/-47/mm(3)) and 22 HIV-negative (BMI 19.3+/-0.8 kg/m(2), albumin 29+/-1 g/l, CD4 count 652+/-76/mm(3)) patients with active PTB. |
| 2468 | 11035112 | Costimulation delivered by nonautoimmune strain APCs normalized NOD CD4 T cell division and the extent of activation-induced death. |
| 2469 | 11045760 | In vitro treatment of splenocytes with GT revealed relative decreases in CD4+ and increases in CD8+ T-cell subsets, whereas in vivo treatment with GT did not result in detectable alterations in relative CD4+ and CD8+ cell subsets. |
| 2470 | 11079813 | There were also significant decreases in CD4+ and CD8+ thymocytes and the proliferative response of splenocytes. |
| 2471 | 11079813 | Our results suggest that the number and function of T cells in WF may be reduced, which may be related at least in part to elevated TNF-alpha levels, although the role of the other factors such as glucose, insulin, cholesterol, and triglycerides on T-cell immunity should be further investigated. |
| 2472 | 11106373 | Furthermore, I-A(g7)/GAD peptide tetramer can detect most if not all of the antigen-specific CD4(+) T cells from immunized NOD mice. |
| 2473 | 11106373 | Antigen-specific T cells detected by the tetramers can up-regulate their CD4 expression on the cell surface after being restimulated with the GAD peptides in vitro. |
| 2474 | 11106373 | Furthermore, I-A(g7)/GAD peptide tetramer can detect most if not all of the antigen-specific CD4(+) T cells from immunized NOD mice. |
| 2475 | 11106373 | Antigen-specific T cells detected by the tetramers can up-regulate their CD4 expression on the cell surface after being restimulated with the GAD peptides in vitro. |
| 2476 | 11120794 | The insulinoma-associated protein 2 (IA-2) is a phosphatase-like autoantigen inducing T and B cell responses associated with human insulin-dependent diabetes mellitus (IDDM). |
| 2477 | 11120794 | We now report that T cell responses to IA-2 can also be detected in the nonobese diabetic (NOD) mouse, a model of human IDDM. |
| 2478 | 11120794 | Cytokine secretion in response to purified mouse rIA-2, characterized by high IFN-gamma and relatively low IL-10 and IL-6 secretion, was elicited in spleen cells from unprimed NOD mice. |
| 2479 | 11120794 | Conversely, no response to IA-2 was induced in spleen cells from BALB/c, C57BL/6, or Biozzi AB/H mice that express, like NOD, the I-A(g7) class II molecule, but are not susceptible to spontaneous IDDM. |
| 2480 | 11120794 | The IA-2-induced IFN-gamma response in NOD spleen cells could already be detected at 3 wk and peaked at 8 wk of age, whereas the IL-10 secretion was maximal at 4 wk of age and then waned. |
| 2481 | 11120794 | IA-2-dependent IFN-gamma secretion was induced in CD4(+) cells from spleen as well as pancreatic and mesenteric lymph nodes. |
| 2482 | 11120794 | The biological relevance of the response to IA-2 is indicated by the enhanced IDDM following a single injection of the recombinant protein emulsified in IFA into 18-day-old NOD mice. |
| 2483 | 11120794 | In addition, IFN-gamma production in response to IA-2 and IDDM acceleration could be induced by IL-12 administration to 12-day-old NOD mice. |
| 2484 | 11120794 | These results identify IA-2 as an early T cell-inducing autoantigen in the NOD mouse and indicate a role for the IA-2-induced Th1 cell response in IDDM pathogenesis. |
| 2485 | 11129119 | These include increased expression of proteasome processing proteins (LMP2), transporters of antigen peptides (TAP), invariant chain (Ii), HLA-DM, and the co-stimulatory molecule, B7, as well as STAT and NF-kappaB activation. |
| 2486 | 11129119 | A critical factor in these changes is the loss of normal negative regulation of MHC class I, class II, and thyrotropin receptor (TSHR) gene expression, which is necessary to maintain self-tolerance during the normal changes in gene expression involved in hormonally-increased growth and function of the cell. |
| 2487 | 11129119 | Self-tolerance to the TSHR is maintained in normals because there is a population of CD8- cells which normally suppresses a population of CD4+ cells that can interact with the TSHR if thyrocytes become APCs. |
| 2488 | 11147792 | In a second transgenic model in which islet cells express the lymphocytic choriomeningitis virus nucleoprotein, the virus infection triggers autoimmune diabetes within a few weeks involving both CD4 and CD8 T-cells; here too transgenic c-Maf provided significant protection. |
| 2489 | 11172025 | We identified a naturally presented autoantigen from the human islet antigen glutamic acid decarboxylase, 65-kDa isoform (GAD65), by using a combination of chromatography and mass spectrometry of peptides bound by the type I diabetes (insulin-dependent diabetes mellitus, IDDM)-associated HLA-DR4 molecule. |
| 2490 | 11172025 | Peptides encompassing this epitope-stimulated GAD65-specific T cells from diabetic patients and a DR4-positive individual at high risk for developing IDDM. |
| 2491 | 11172025 | This direct identification and manipulation of GAD65 epitope recognition provides an approach toward dissection of the complex CD4(+) T cell response in IDDM. |
| 2492 | 11179337 | CD40 is constitutively expressed on marrow-derived cells such as dendritic cells and B lymphocytes and is induced by gamma interferon (IFN-gamma) on most somatic cells. |
| 2493 | 11179337 | There was no difference between the acquisition of CD69 and CD154 by mesenteric lymph node T cells of C. parvum-infected animals with intact or disrupted CD40-CD154 pathways. |
| 2494 | 11179337 | CD4 T cells entered the intestinal laminae propriae of C. parvum-infected animals whether or not the CD40 genes of these recipients were intact. |
| 2495 | 11207247 | CD4(+) T cells arise spontaneously in young NOD mice to an apparently dominant determinant found within the GAD65 peptide 530--543 (p530); however, T cells to the overlapping determinant 524-538 (p524) dominate the response only after immunization with GAD65(524--543). |
| 2496 | 11207247 | T cell clones and hybridomas from both of these T cell groups were responsive to APC pulsed with GAD65(524--543) or whole rGAD65. p524-reactive cells appeared to be regulatory upon adoptive transfer into young NOD mice and could inhibit insulin-dependent diabetes mellitus development, although they were unable to produce IL-4, IL-10, or TGF beta upon antigenic challenge. |
| 2497 | 11244033 | Autoreactive T cells specific to these autoantigens are present in most normal individuals but are kept under control by a number of peripheral tolerance mechanisms, among which CD4(+) CD25(+) CD62L(+) T cell-mediated regulation probably plays a central role. |
| 2498 | 11244036 | Complexities of CD28/B7: CTLA-4 costimulatory pathways in autoimmunity and transplantation. |
| 2499 | 11244036 | In this review, we summarize the current understanding of these complex costimulatory pathways including the individual roles of the CD28, CTLA-4, B7-1 (CD80), and B7-2 (CD86) molecules. |
| 2500 | 11244036 | This is most apparent in regulation of the CD4(+)CD25(+)CTLA-4(+) immunoregulatory T cells that control multiple autoimmune diseases. |
| 2501 | 11247635 | Accumulating evidence suggests that CD4(+)T helper type 1 (Th1) cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse model. |
| 2502 | 11247635 | To investigate the role of IL-12 that is locally produced by islet-infiltrating cells in the development of IDDM, we generated transgenic NOD mice in which the IL-12 p40 homodimer, a natural antagonist of IL-12, was produced exclusively in islets without affecting the levels of IL-12 p40 in the systemic circulation. |
| 2503 | 11247635 | These results clearly demonstrate that IL-12 locally produced by islet-infiltrating cells plays a critical role in the development of IDDM. |
| 2504 | 11274421 | We screened synthetic peptide libraries dedicated to bind to HLA-DR3, which predisposes to both diseases, using clonal CD4(+) T cells reactive to GAD65 isolated from a prediabetic stiff-man syndrome patient. |
| 2505 | 11278441 | Structural similarity (molecular mimicry) between viral epitopes and self-peptides can lead to the induction of autoaggressive CD4(+) as well as CD8(+) T cell responses. |
| 2506 | 11278441 | One of these self-peptides, derived from tumor necrosis factor receptor I (FGPSNWHFM, amino acids 302-310), maintained LCMV-specific CD8(+) T cells in an active state as observed both in vitro in cytotoxic assays and in vivo in a model of virus-induced autoimmune diabetes, the rat insulin promoter-LCMV NP transgenic mouse. |
| 2507 | 11312256 | IL-12p40 and IFN-gamma mRNA levels were decreased in pancreata of the vIL-10 Tg mice, although CD4 mRNA level was markedly increased. |
| 2508 | 11317656 | The Src kinases, particularly hck, play an important part in the activation of macrophages and the subsequent production of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and nitric oxide (NO), leading to the destruction of beta cells which results in the development of diabetes. |
| 2509 | 11317656 | The infection of DR-BB rats with KRV results in the disruption of the finely tuned immune balance of Th1-like CD45RC+CD4+ and Th2-like CD45RC-CD4+ T cells, leading to the selective activation of beta-cell-cytotoxic effector T cells. |
| 2510 | 11324686 | The non-obese diabetic (NOD) mouse is an animal model of human insulin-dependent diabetes mellitus (IDDM). |
| 2511 | 11324686 | Cumulative evidence suggests that Thl CD4+ T cells play a critical role in the autoimmune process leading to beta cell destruction. |
| 2512 | 11324686 | In addition to CD4+ T cells, CD8+ cells and B cells also participate in the pathogenesis. |
| 2513 | 11324686 | There are several candidate antigens recognized by autoreactive T cells such as glutamic acid decarboxylase (GAD), insulin and heat shock protein (HSP) 60. |
| 2514 | 11324686 | The non-obese diabetic (NOD) mouse is an animal model of human insulin-dependent diabetes mellitus (IDDM). |
| 2515 | 11324686 | Cumulative evidence suggests that Thl CD4+ T cells play a critical role in the autoimmune process leading to beta cell destruction. |
| 2516 | 11324686 | In addition to CD4+ T cells, CD8+ cells and B cells also participate in the pathogenesis. |
| 2517 | 11324686 | There are several candidate antigens recognized by autoreactive T cells such as glutamic acid decarboxylase (GAD), insulin and heat shock protein (HSP) 60. |
| 2518 | 11358432 | We used autologous blood monocyte-derived dendritic cells to elicit HLA-A2-restricted CTL to a peptide, MVWESGCTV (aa 797-805), that is contiguous with a dominant CD4 T-cell epitope in the islet antigen tyrosine phosphatase IA-2. |
| 2519 | 11376339 | T cell receptor (TCR)-transgenic CD4+ T cells were primed under controlled conditions in vitro before being adoptively transferred into transgenic recipients expressing membrane ovalbumin under the control of the rat insulin promoter (RIP-mOVA). |
| 2520 | 11376339 | Pathogenicity was associated with T cell production of the macrophage-attracting chemokines CCL3 and CCL4. |
| 2521 | 11376339 | Thus, interactions of lymphocyte function-associated antigen 1 with ICAM-1 during priming induce both qualitative and quantitative alterations in T effector function and induce potentially autodestructive responses. |
| 2522 | 11418698 | We previously demonstrated that administration of plasmid DNAs (pDNAs) encoding IL-4 and a fragment of glutamic acid decarboxylase 65 (GAD65) fused to IgGFc induces GAD65-specific Th2 cells and prevents insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice. |
| 2523 | 11418698 | Insulin was chosen based on studies demonstrating that administration of insulin or insulin B chain by a variety of strategies prevents IDDM in NOD mice. |
| 2524 | 11418698 | Surprisingly, young NOD mice receiving i.m. injections of pDNA encoding insulin B chain-IgGFc with or without IL-4 exhibited an accelerated progression of insulitis and developed early diabetes. |
| 2525 | 11418698 | Exacerbation of IDDM correlated with an increased frequency of IFN-gamma-secreting CD4(+) and CD8(+) T cells in response to insulin B chain-specific peptides compared with untreated mice. |
| 2526 | 11418698 | In contrast, treatment with pDNAs encoding insulin A chain-IgGFc and IL-4 elicited a low frequency of IL-4-secreting Th cells and had no effect on the progression of IDDM. |
| 2527 | 11418698 | Vaccination with pDNAs encoding GAD65-IgGFc and IL-4, however, prevented IDDM. |
| 2528 | 11418698 | These results demonstrate that insulin- and GAD65-specific T cell reactivity induced by pDNA vaccination has distinct effects on the progression of IDDM. |
| 2529 | 11441123 | Nonobese diabetic (NOD) mice develop spontaneous autoimmune diabetes that involves participation of both CD4+ and CD8+ T cells. |
| 2530 | 11441916 | At rest and at two hours, counts of white blood cells (WBC), mixed lymphocytes, mature T-cells (CD3), T-helper cells (CD4), T-suppressor/ cytotoxic cells (CD8), B-cells (CD19), natural killer cells (CD16/CD56), and interleukin-2 receptor bearing peripheral blood mononuclear cells (CD25) were measured by flow cytometry. |
| 2531 | 11450149 | The aim of the present study was to evaluate the presence of T helper lymphocyte subpopulations: naive (CD4+CD45RA+), memory cells (CD4+CDRO+) and lymphocytes coexpressing both studied phenotypes (CD4+CD45RA+CD45RO+) in subjects at risk of type 1 diabetes (first degree relatives of IDDM patients with autoantibodies) in comparison to age and sex matched controls. |
| 2532 | 11450149 | It could be suggested that CD4+CD45RA+/CD4+CD45RO+ ratio could serve as surrogate marker of diabetes type 1 risk development and presumably for estimation of the efficacy of the preventive procedures in subjects at high risk of IDDM, but further prospective studies are needed. |
| 2533 | 11450149 | The aim of the present study was to evaluate the presence of T helper lymphocyte subpopulations: naive (CD4+CD45RA+), memory cells (CD4+CDRO+) and lymphocytes coexpressing both studied phenotypes (CD4+CD45RA+CD45RO+) in subjects at risk of type 1 diabetes (first degree relatives of IDDM patients with autoantibodies) in comparison to age and sex matched controls. |
| 2534 | 11450149 | It could be suggested that CD4+CD45RA+/CD4+CD45RO+ ratio could serve as surrogate marker of diabetes type 1 risk development and presumably for estimation of the efficacy of the preventive procedures in subjects at high risk of IDDM, but further prospective studies are needed. |
| 2535 | 11465949 | Both CD4 and CD8 T cells have been shown to be independently capable of beta cell destruction. |
| 2536 | 11465949 | It has previously been shown that the absence of TNF-alpha receptor 1 (p55) on the islets protected islets from CD4 T-cell-mediated destruction as long as the T cells did not have access to wild-type islets in vivo. |
| 2537 | 11465949 | In this study, we demonstrate that islet TNF-alpha receptor 1 (p55) influences the expression of LIGHT (TNFSF-14), a TNF family member with both cytolytic and costimulatory properties, on BDC2.5 T cells and the expression of its receptor HVEM (TNFRSF-14) by islets, indicating a role for LIGHT-HVEM interactions in autoimmune diabetes. |
| 2538 | 11465949 | Both CD4 and CD8 T cells have been shown to be independently capable of beta cell destruction. |
| 2539 | 11465949 | It has previously been shown that the absence of TNF-alpha receptor 1 (p55) on the islets protected islets from CD4 T-cell-mediated destruction as long as the T cells did not have access to wild-type islets in vivo. |
| 2540 | 11465949 | In this study, we demonstrate that islet TNF-alpha receptor 1 (p55) influences the expression of LIGHT (TNFSF-14), a TNF family member with both cytolytic and costimulatory properties, on BDC2.5 T cells and the expression of its receptor HVEM (TNFRSF-14) by islets, indicating a role for LIGHT-HVEM interactions in autoimmune diabetes. |
| 2541 | 11466393 | Increased entry into the IFN-gamma effector pathway by CD4+ T cells selected by I-Ag7 on a nonobese diabetic versus C57BL/6 genetic background. |
| 2542 | 11466393 | IFN-gamma-mediated Th1 effects play a major role in the pathogenesis of autoimmune diabetes in nonobese diabetic (NOD) mice. |
| 2543 | 11466393 | We analyzed functional responses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but differ in their non-MHC genetic background. |
| 2544 | 11466393 | Despite comparable proliferative responses, NOD CD4(+) T cells had significantly increased IFN-gamma intracellular/extracellular protein and mRNA responses compared with B6.G7 T cells as measured by intracellular cytokine analysis, time resolved fluorometry, and RNase protection assays. |
| 2545 | 11466393 | The increased IFN-gamma production was not due to an increase in the amount of IFN-gamma produced per cell but to an increase in the number of NOD CD4(+) T cells entering the IFN-gamma-producing pathway. |
| 2546 | 11466393 | B6.G7 lymphoid cells demonstrated an absolute decrease in IFN-gamma mRNA, an increase in IL-4 mRNA production, and a significantly decreased IFN-gamma:IL-4 mRNA transcript ratio compared with NOD cells. |
| 2547 | 11466393 | CD4(+) T cells from C57BL6 mice also showed significantly decreased IFN-gamma production compared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgressed onto an NOD non-MHC background). |
| 2548 | 11466393 | Therefore, the NOD non-MHC background predisposes to a quantitatively increased IFN-gamma response, independent of MHC class II-mediated T cell repertoire selection, even when compared with a prototypical Th1 strain. |
| 2549 | 11466393 | Increased entry into the IFN-gamma effector pathway by CD4+ T cells selected by I-Ag7 on a nonobese diabetic versus C57BL/6 genetic background. |
| 2550 | 11466393 | IFN-gamma-mediated Th1 effects play a major role in the pathogenesis of autoimmune diabetes in nonobese diabetic (NOD) mice. |
| 2551 | 11466393 | We analyzed functional responses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but differ in their non-MHC genetic background. |
| 2552 | 11466393 | Despite comparable proliferative responses, NOD CD4(+) T cells had significantly increased IFN-gamma intracellular/extracellular protein and mRNA responses compared with B6.G7 T cells as measured by intracellular cytokine analysis, time resolved fluorometry, and RNase protection assays. |
| 2553 | 11466393 | The increased IFN-gamma production was not due to an increase in the amount of IFN-gamma produced per cell but to an increase in the number of NOD CD4(+) T cells entering the IFN-gamma-producing pathway. |
| 2554 | 11466393 | B6.G7 lymphoid cells demonstrated an absolute decrease in IFN-gamma mRNA, an increase in IL-4 mRNA production, and a significantly decreased IFN-gamma:IL-4 mRNA transcript ratio compared with NOD cells. |
| 2555 | 11466393 | CD4(+) T cells from C57BL6 mice also showed significantly decreased IFN-gamma production compared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgressed onto an NOD non-MHC background). |
| 2556 | 11466393 | Therefore, the NOD non-MHC background predisposes to a quantitatively increased IFN-gamma response, independent of MHC class II-mediated T cell repertoire selection, even when compared with a prototypical Th1 strain. |
| 2557 | 11466393 | Increased entry into the IFN-gamma effector pathway by CD4+ T cells selected by I-Ag7 on a nonobese diabetic versus C57BL/6 genetic background. |
| 2558 | 11466393 | IFN-gamma-mediated Th1 effects play a major role in the pathogenesis of autoimmune diabetes in nonobese diabetic (NOD) mice. |
| 2559 | 11466393 | We analyzed functional responses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but differ in their non-MHC genetic background. |
| 2560 | 11466393 | Despite comparable proliferative responses, NOD CD4(+) T cells had significantly increased IFN-gamma intracellular/extracellular protein and mRNA responses compared with B6.G7 T cells as measured by intracellular cytokine analysis, time resolved fluorometry, and RNase protection assays. |
| 2561 | 11466393 | The increased IFN-gamma production was not due to an increase in the amount of IFN-gamma produced per cell but to an increase in the number of NOD CD4(+) T cells entering the IFN-gamma-producing pathway. |
| 2562 | 11466393 | B6.G7 lymphoid cells demonstrated an absolute decrease in IFN-gamma mRNA, an increase in IL-4 mRNA production, and a significantly decreased IFN-gamma:IL-4 mRNA transcript ratio compared with NOD cells. |
| 2563 | 11466393 | CD4(+) T cells from C57BL6 mice also showed significantly decreased IFN-gamma production compared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgressed onto an NOD non-MHC background). |
| 2564 | 11466393 | Therefore, the NOD non-MHC background predisposes to a quantitatively increased IFN-gamma response, independent of MHC class II-mediated T cell repertoire selection, even when compared with a prototypical Th1 strain. |
| 2565 | 11466393 | Increased entry into the IFN-gamma effector pathway by CD4+ T cells selected by I-Ag7 on a nonobese diabetic versus C57BL/6 genetic background. |
| 2566 | 11466393 | IFN-gamma-mediated Th1 effects play a major role in the pathogenesis of autoimmune diabetes in nonobese diabetic (NOD) mice. |
| 2567 | 11466393 | We analyzed functional responses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but differ in their non-MHC genetic background. |
| 2568 | 11466393 | Despite comparable proliferative responses, NOD CD4(+) T cells had significantly increased IFN-gamma intracellular/extracellular protein and mRNA responses compared with B6.G7 T cells as measured by intracellular cytokine analysis, time resolved fluorometry, and RNase protection assays. |
| 2569 | 11466393 | The increased IFN-gamma production was not due to an increase in the amount of IFN-gamma produced per cell but to an increase in the number of NOD CD4(+) T cells entering the IFN-gamma-producing pathway. |
| 2570 | 11466393 | B6.G7 lymphoid cells demonstrated an absolute decrease in IFN-gamma mRNA, an increase in IL-4 mRNA production, and a significantly decreased IFN-gamma:IL-4 mRNA transcript ratio compared with NOD cells. |
| 2571 | 11466393 | CD4(+) T cells from C57BL6 mice also showed significantly decreased IFN-gamma production compared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgressed onto an NOD non-MHC background). |
| 2572 | 11466393 | Therefore, the NOD non-MHC background predisposes to a quantitatively increased IFN-gamma response, independent of MHC class II-mediated T cell repertoire selection, even when compared with a prototypical Th1 strain. |
| 2573 | 11466393 | Increased entry into the IFN-gamma effector pathway by CD4+ T cells selected by I-Ag7 on a nonobese diabetic versus C57BL/6 genetic background. |
| 2574 | 11466393 | IFN-gamma-mediated Th1 effects play a major role in the pathogenesis of autoimmune diabetes in nonobese diabetic (NOD) mice. |
| 2575 | 11466393 | We analyzed functional responses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but differ in their non-MHC genetic background. |
| 2576 | 11466393 | Despite comparable proliferative responses, NOD CD4(+) T cells had significantly increased IFN-gamma intracellular/extracellular protein and mRNA responses compared with B6.G7 T cells as measured by intracellular cytokine analysis, time resolved fluorometry, and RNase protection assays. |
| 2577 | 11466393 | The increased IFN-gamma production was not due to an increase in the amount of IFN-gamma produced per cell but to an increase in the number of NOD CD4(+) T cells entering the IFN-gamma-producing pathway. |
| 2578 | 11466393 | B6.G7 lymphoid cells demonstrated an absolute decrease in IFN-gamma mRNA, an increase in IL-4 mRNA production, and a significantly decreased IFN-gamma:IL-4 mRNA transcript ratio compared with NOD cells. |
| 2579 | 11466393 | CD4(+) T cells from C57BL6 mice also showed significantly decreased IFN-gamma production compared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgressed onto an NOD non-MHC background). |
| 2580 | 11466393 | Therefore, the NOD non-MHC background predisposes to a quantitatively increased IFN-gamma response, independent of MHC class II-mediated T cell repertoire selection, even when compared with a prototypical Th1 strain. |
| 2581 | 11466400 | CD4(+) T cell responses to glutamic acid decarboxylase (GAD65) spontaneously arise in nonobese diabetic (NOD) mice before the onset of insulin-dependent diabetes mellitus (IDDM) and may be critical to the pathogenic process. |
| 2582 | 11466400 | However, since both CD4(+) and CD8(+) T cells are involved in autoimmune diabetes, we sought to determine whether GAD65-specific CD8(+) T cells were also present in prediabetic NOD mice and contribute to IDDM. |
| 2583 | 11466400 | Naive NOD spleen cells stimulated with GAD65 peptides 206-214 (p206) and 546-554 (p546) produced IFN-gamma and showed Ag-specific CTL responses against targets pulsed with homologous peptide. |
| 2584 | 11466400 | Spontaneous CTL responses to p206 and p546 were mediated by CD8(+) T cells that are capable of lysing GAD65-expressing target cells, and p546-specific T cells transferred insulitis to NOD.scid mice. |
| 2585 | 11466400 | This report reveals a potential therapeutic role for MHC class I-restricted peptides in treating autoimmune disease and revisits the notion that the CD4- and CD8-inducing determinants on some molecules may benefit from a proximal relationship. |
| 2586 | 11466400 | CD4(+) T cell responses to glutamic acid decarboxylase (GAD65) spontaneously arise in nonobese diabetic (NOD) mice before the onset of insulin-dependent diabetes mellitus (IDDM) and may be critical to the pathogenic process. |
| 2587 | 11466400 | However, since both CD4(+) and CD8(+) T cells are involved in autoimmune diabetes, we sought to determine whether GAD65-specific CD8(+) T cells were also present in prediabetic NOD mice and contribute to IDDM. |
| 2588 | 11466400 | Naive NOD spleen cells stimulated with GAD65 peptides 206-214 (p206) and 546-554 (p546) produced IFN-gamma and showed Ag-specific CTL responses against targets pulsed with homologous peptide. |
| 2589 | 11466400 | Spontaneous CTL responses to p206 and p546 were mediated by CD8(+) T cells that are capable of lysing GAD65-expressing target cells, and p546-specific T cells transferred insulitis to NOD.scid mice. |
| 2590 | 11466400 | This report reveals a potential therapeutic role for MHC class I-restricted peptides in treating autoimmune disease and revisits the notion that the CD4- and CD8-inducing determinants on some molecules may benefit from a proximal relationship. |
| 2591 | 11466400 | CD4(+) T cell responses to glutamic acid decarboxylase (GAD65) spontaneously arise in nonobese diabetic (NOD) mice before the onset of insulin-dependent diabetes mellitus (IDDM) and may be critical to the pathogenic process. |
| 2592 | 11466400 | However, since both CD4(+) and CD8(+) T cells are involved in autoimmune diabetes, we sought to determine whether GAD65-specific CD8(+) T cells were also present in prediabetic NOD mice and contribute to IDDM. |
| 2593 | 11466400 | Naive NOD spleen cells stimulated with GAD65 peptides 206-214 (p206) and 546-554 (p546) produced IFN-gamma and showed Ag-specific CTL responses against targets pulsed with homologous peptide. |
| 2594 | 11466400 | Spontaneous CTL responses to p206 and p546 were mediated by CD8(+) T cells that are capable of lysing GAD65-expressing target cells, and p546-specific T cells transferred insulitis to NOD.scid mice. |
| 2595 | 11466400 | This report reveals a potential therapeutic role for MHC class I-restricted peptides in treating autoimmune disease and revisits the notion that the CD4- and CD8-inducing determinants on some molecules may benefit from a proximal relationship. |
| 2596 | 11467420 | Intra-islet CD4 and CD8 cells and macrophages were also enumerated at day 11. |
| 2597 | 11467420 | In the latter group, CD4 and CD8 cells and macrophages were also higher at day 11 than all other 4 groups (CD4: p < 0.05; CD8: p< 0.05; macrophages: p<0.0001). |
| 2598 | 11467420 | Intra-islet CD4 and CD8 cells and macrophages were also enumerated at day 11. |
| 2599 | 11467420 | In the latter group, CD4 and CD8 cells and macrophages were also higher at day 11 than all other 4 groups (CD4: p < 0.05; CD8: p< 0.05; macrophages: p<0.0001). |
| 2600 | 11472422 | The increase of murine interleukin-1 beta when mouse plastic-adherent spleen cells were cultured with PIC (P < 0.04) was indicative of macrophage activation. |
| 2601 | 11472422 | Another mechanism was apparent, since co-incubation of PIC with purified mouse T cells or CD4+ T cells, re-mixed with antigen-presenting cells, led to a decrease (P < 0.01) of insulin release. |
| 2602 | 11535635 | The peripheral nerve tissue was infiltrated with dendritic cells, CD4(+), and CD8(+) T cells. |
| 2603 | 11535635 | This model demonstrates that NOD mice have "cryptic" autoimmune defects that can polarize toward the nervous tissue after the selective disruption of CD28/B7-2 costimulatory pathway. |
| 2604 | 11544341 | IL-15 is a powerful T cell growth factor (TCGF) with particular importance for the maintenance of CD8(+) T cells. |
| 2605 | 11544341 | Because costimulation blockade does not result in universal tolerance, we hypothesized that "escape" from costimulation blockade might represent a CD8(+) and IL-15/IL-15R(+)-dependent process. |
| 2606 | 11544341 | For this analysis, we have used an IL-15 mutant/Fcgamma2a protein, a potentially cytolytic protein that is also a high-affinity receptor site specific antagonist for the IL-15Ralpha receptor protein, as a therapeutic agent. |
| 2607 | 11544341 | The IL-15-related fusion protein was used as monotherapy or in combination with CTLA4/Fc in murine islet allograft models. |
| 2608 | 11544341 | As monotherapies, CTLA4/Fc and an IL-15 mutant/Fcgamma2a were comparably effective in a semiallogeneic model system, and combined treatment with IL-15 mutant/Fcgamma2a plus CTLA4/Fc produced universal permanent engraftment. |
| 2609 | 11544341 | The analysis revealed that the IL-15 mutant/Fc treatment confers partial protection from both CD4(+) and CD8(+) T cell graft infiltration. |
| 2610 | 11544341 | In rejections occurring despite CTLA4/Fc treatment, concomitant treatment with the IL-15 mutant/Fcgamma2a protein blocked a CD8(+) T cell-dominated rejection processes. |
| 2611 | 11544341 | Hence, we have demonstrated that targeting the IL-15/IL-15R pathway represents a new and potent strategy to prevent costimulation blockade-resistant CD8(+) T cell-driven rejection. |
| 2612 | 11544345 | To examine these issues, we analyzed TCR Vbeta chain-specific up-regulation of the early T cell activation marker, CD69, on CD4 T cells after incubation with Coxsackievirus B4 (CVB4) Ags. |
| 2613 | 11544345 | Up-regulation of CD69 by different TCR families was significantly more frequent in new onset type 1 DM patients (p = 0.04), 100% of whom (n = 8) showed activation of CD4 T cells bearing Vbeta8, compared with 50% of control subjects (n = 8; p = 0.04). |
| 2614 | 11544345 | To examine these issues, we analyzed TCR Vbeta chain-specific up-regulation of the early T cell activation marker, CD69, on CD4 T cells after incubation with Coxsackievirus B4 (CVB4) Ags. |
| 2615 | 11544345 | Up-regulation of CD69 by different TCR families was significantly more frequent in new onset type 1 DM patients (p = 0.04), 100% of whom (n = 8) showed activation of CD4 T cells bearing Vbeta8, compared with 50% of control subjects (n = 8; p = 0.04). |
| 2616 | 11590186 | Here, we completely blocked adoptive transfer of diabetes and reduced spontaneous disease incidence from 71% to 17% by simultaneously administering a combination of antibodies directed against alpha4, beta2, and beta7 integrins and their ligands VCAM-1, MAdCAM-1, and ICAM-1 for 52 and 28 days, respectively. |
| 2617 | 11590186 | CD4 and CD8 T cells and macrophages were excluded from islets and remained entrapped in a peri-islet location as inactive exiles, no longer expressing normal levels of interferon-gamma, interleukin-4, and iNOS. |
| 2618 | 11591120 | In comparison with IRF-1(+/+), the percentage of CD4(+) and Mac-1(+) splenic cells significantly increased, whereas CD3(+), CD8(+) and B220(+) cells decreased in IRF-1(-/-). |
| 2619 | 11591120 | Furthermore, spleen cell proliferation in response to Con A or murine GAD65 peptide, a major autoantigen of the pancreatic beta-cell, significantly increased, and the IFN-gamma/IL-10 ratio in the culture supernatant significantly decreased in IRF-1(-/-), suggesting Th2 deviation in cytokine balance. |
| 2620 | 11591759 | In this regard, in vitro anti-CD3-mediated stimulation demonstrates impaired activation of lymph node CD4 T cells in muMT(-/-) NOD mice as compared with that of wild-type counterparts, a deficiency that is correlated with an exaggerated CD4 T cell:APC ratio in lymph nodes of muMT(-/-) NOD mice. |
| 2621 | 11600216 | The disease is characterized by loss of tolerance to auto-antigens such as GAD, insulin, and the protein tyrosine phosphatase-like molecule, IA-2. |
| 2622 | 11600216 | We identified T cell epitopes on the intracytoplasmic region of IA-2 by immunizing DQ8/NOD, DQ8/B10, and NOD mice with overlapping 18 mer peptides in CFA. |
| 2623 | 11600216 | We demonstrated MHC class II and CD4 restriction of proliferative responses using appropriate blocking antibodies. |
| 2624 | 11722631 | These cells, which express CD4, CD25, and CD62L, develop in the thymus and survive in a CD28-dependent manner in the periphery to maintain the homeostatic equilibrium of immunity and tolerance. |
| 2625 | 11723052 | Importantly, numbers and effector functions of autoaggressive CD4 and CD8 lymphocytes were not decreased in the protected mice, and CTLs were still able to kill syngeneic islet cells in vitro with equal efficacy compared with CTLs from the original RIP-LCMV strain. |
| 2626 | 11723051 | When thymic precursor cells of beta2-microglobulin gene-deficient AKR mice, which have a deficient NKT population, were introduced into NOD.scid recipients, both CD4(+) and CD8(+) T-cell populations developed and the recipient mice developed insulitis and diabetes. |
| 2627 | 11729828 | In vitro secretion of interleukin 2 and expression of IL-2 receptor in peripheral blood lymphocytes in high risk of insulin-dependent diabetes mellitus subjects. |
| 2628 | 11729828 | Interleukin 2 (IL-2)--a Th1 lymphocyte-derived cytokine is at present considered to play an important role in the etiopathogenesis of insulin-dependent diabetes mellitus. |
| 2629 | 11729828 | In the previous studies increased, decreased and unchanged IL-2 levels in patients with recent onset of insulin-dependent diabetes mellitus (IDDM) were found. |
| 2630 | 11729828 | The aim of our study was to estimate in vitro secretion of IL-2 and CD25 antigen expression by the peripheral blood T lymphocytes in subjects at the preclinical stage of IDDM (prediabetes), but still without metabolic disturbances. |
| 2631 | 11729828 | In 27 first degree relatives of IDDM patients with antibodies against different pancreatic islet cell antigens (ICA, GADA, IAA, IA-2) CD25 antigen expression on peripheral blood lymphocytes T was measured by flow cytometry and IL-2 concentration in supernatants of 48 and 72 h cultures of peripheral whole blood with 10 microg/ml PHA was estimated by ELISA. |
| 2632 | 11729828 | In the studied high risk IDDM subjects the decreased CD25 expression in peripheral CD4+ lymphocytes T and a negative correlation between the percentage of CD25+ cells and islet cell antibodies (ICA) titres was observed. |
| 2633 | 11729828 | A significant increase of IL-2 secretion at 72 h of PHA stimulation was shown in first degree relatives of IDDM patients with a combination of 3 or more antipancreatic-B cell antibodies. |
| 2634 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 2635 | 11739486 | A ligand for the chemokine receptor CCR7 can influence the homeostatic proliferation of CD4 T cells and progression of autoimmunity. |
| 2636 | 11739486 | Although the mechanisms are unknown, we find that the chemokine CCL21 (also known as TCA4, SLC, 6Ckine), a ligand for the chemokine receptor CCR7, can regulate homeostasis of CD4 (but not CD8) T cells. |
| 2637 | 11739486 | In the absence of CCR7 ligands, transferred CD4 T cells failed to expand in lymphopenic hosts, whereas in the presence of CCL21 overexpression, homeostatic CD4 T cell proliferation occurred even in nonlymphopenic recipients. |
| 2638 | 11739486 | These results suggest that CD4 T cells use local concentrations of CCR7 ligands as an index of T cell steady state numbers and that homeostatic expansion of the T cell population may be a contributing factor in the development of autoimmune disease. |
| 2639 | 11739486 | A ligand for the chemokine receptor CCR7 can influence the homeostatic proliferation of CD4 T cells and progression of autoimmunity. |
| 2640 | 11739486 | Although the mechanisms are unknown, we find that the chemokine CCL21 (also known as TCA4, SLC, 6Ckine), a ligand for the chemokine receptor CCR7, can regulate homeostasis of CD4 (but not CD8) T cells. |
| 2641 | 11739486 | In the absence of CCR7 ligands, transferred CD4 T cells failed to expand in lymphopenic hosts, whereas in the presence of CCL21 overexpression, homeostatic CD4 T cell proliferation occurred even in nonlymphopenic recipients. |
| 2642 | 11739486 | These results suggest that CD4 T cells use local concentrations of CCR7 ligands as an index of T cell steady state numbers and that homeostatic expansion of the T cell population may be a contributing factor in the development of autoimmune disease. |
| 2643 | 11739486 | A ligand for the chemokine receptor CCR7 can influence the homeostatic proliferation of CD4 T cells and progression of autoimmunity. |
| 2644 | 11739486 | Although the mechanisms are unknown, we find that the chemokine CCL21 (also known as TCA4, SLC, 6Ckine), a ligand for the chemokine receptor CCR7, can regulate homeostasis of CD4 (but not CD8) T cells. |
| 2645 | 11739486 | In the absence of CCR7 ligands, transferred CD4 T cells failed to expand in lymphopenic hosts, whereas in the presence of CCL21 overexpression, homeostatic CD4 T cell proliferation occurred even in nonlymphopenic recipients. |
| 2646 | 11739486 | These results suggest that CD4 T cells use local concentrations of CCR7 ligands as an index of T cell steady state numbers and that homeostatic expansion of the T cell population may be a contributing factor in the development of autoimmune disease. |
| 2647 | 11739486 | A ligand for the chemokine receptor CCR7 can influence the homeostatic proliferation of CD4 T cells and progression of autoimmunity. |
| 2648 | 11739486 | Although the mechanisms are unknown, we find that the chemokine CCL21 (also known as TCA4, SLC, 6Ckine), a ligand for the chemokine receptor CCR7, can regulate homeostasis of CD4 (but not CD8) T cells. |
| 2649 | 11739486 | In the absence of CCR7 ligands, transferred CD4 T cells failed to expand in lymphopenic hosts, whereas in the presence of CCL21 overexpression, homeostatic CD4 T cell proliferation occurred even in nonlymphopenic recipients. |
| 2650 | 11739486 | These results suggest that CD4 T cells use local concentrations of CCR7 ligands as an index of T cell steady state numbers and that homeostatic expansion of the T cell population may be a contributing factor in the development of autoimmune disease. |
| 2651 | 11781061 | T cells clones recognizing insulin, both CD4 and CD8, can transfer disease to young mice or immunodeficient animals. |
| 2652 | 11781358 | We also report low numbers of resting CD4(+) CD25(+) T cells in IMD patients, a subset of T cells shown to have important immunoregulatory functions in abrogating autoimmunities in 3-day thymectomized experimental mice. |
| 2653 | 11781358 | Whereas a biased Th1 to Th2 cytokine profile has been suggested to underlie the pathogenesis of IMD in both species, we found defective production of IFN-gamma in our patients after in vitro stimulation of their PBMCs by phorbol-myristate acetate and ionomycin and both IFN-gamma and IL-4 deficiencies in V(alpha)24(+) NK T-enriched cells. |
| 2654 | 11785671 | Although there was no evidence of typical insulitis in early disease development (day 10), in both rats and mice, macrophages, CD4+ and CD8+ cells were present in the islets of Langerhans as diffuse mononuclear infiltrates with the expression of IFN-gamma, and inducible NO synthase (iNOS). |
| 2655 | 11793013 | Data obtained on non-obese diabetic (NOD) mice suggest that macrophages and CD4+ T-cells are the main cellular effectors, whereas CD8+ T-cells are more important initiators of the immune process leading to beta-cell death. |
| 2656 | 11793013 | Perforin could be the effector molecule utilized by CD8+ T-cell initiation, whereas CD4+ mediated beta-cell destruction is mostly dependent on Fas/FasL and the cytokines IFNgamma and TNF-alpha. |
| 2657 | 11793013 | The macrophage cytokine IL-1beta in combination with IFN-gamma and TNF-alpha, plays an important role for beta-cell dysfunction and death. |
| 2658 | 11793013 | Signal transduction by these cytokines involves: (i) binding to specific receptors, (ii) signal transduction by cytosolic kinases (especially the so-called mitogen- and stress-activated protein kinases) and/or phosphatases, (iii) mobilization of diverse transcription factors - with nuclear factor kappaB (NF-kappaB), AP-1 and STAT-1 probably playing key roles for beta-cell apoptosis; (iv) up-regulation or down-regulation of gene transcription. |
| 2659 | 11793013 | Data obtained on non-obese diabetic (NOD) mice suggest that macrophages and CD4+ T-cells are the main cellular effectors, whereas CD8+ T-cells are more important initiators of the immune process leading to beta-cell death. |
| 2660 | 11793013 | Perforin could be the effector molecule utilized by CD8+ T-cell initiation, whereas CD4+ mediated beta-cell destruction is mostly dependent on Fas/FasL and the cytokines IFNgamma and TNF-alpha. |
| 2661 | 11793013 | The macrophage cytokine IL-1beta in combination with IFN-gamma and TNF-alpha, plays an important role for beta-cell dysfunction and death. |
| 2662 | 11793013 | Signal transduction by these cytokines involves: (i) binding to specific receptors, (ii) signal transduction by cytosolic kinases (especially the so-called mitogen- and stress-activated protein kinases) and/or phosphatases, (iii) mobilization of diverse transcription factors - with nuclear factor kappaB (NF-kappaB), AP-1 and STAT-1 probably playing key roles for beta-cell apoptosis; (iv) up-regulation or down-regulation of gene transcription. |
| 2663 | 11797119 | Here we report a case of large granular lymphocyte disease unusually expressing CD4+CD8+ clonal T cells and atypical cell morphology in bone marrow. |
| 2664 | 11812739 | Antidiabetogenic MHC class II molecules may thus afford diabetes resistance by presenting, on dendritic cells and macrophages, tolerogenic peptides to a subset of highly diabetogenic and MHC-promiscuous CD4(+) T-cells that play a critical role in the initiation of diabetes. |
| 2665 | 11826762 | It shares many of these functions with other cytokines such as IL-15, which complicates the interpretation of the IL-2-deficient phenotype. |
| 2666 | 11826762 | The autoimmune phenotype associated with IL-2 deficiency results from the dysregulated activity of thymus-derived TCR alpha beta CD4+ and/or CD8+ T cells. |
| 2667 | 11826762 | The IL-2R signal responsible for maintaining homeostasis is not dependent on either the Shc or Stat5 pathways, therefore AICD, which is Stat5-dependent in vitro, cannot be the critical mechanism. |
| 2668 | 11826762 | Finally, expression of the IL-2R in the thymus and not the periphery appears sufficient to suppress the autoimmune phenotype, suggesting that IL-2 signaling may be required for some aspect of thymocyte selection and/or differentiation that has so far gone undetected. |
| 2669 | 11862219 | The antidiabetogenic effects of DEF rely on the induction of anergy in splenic autoreactive CD4+ T cells via alteration of early T cell receptor signaling and stimulation of interleukin 10-secreting T regulatory type 1 cells in the pancreas. |
| 2670 | 11869680 | Pancreatic lymph node-derived CD4(+)CD25(+) Treg cells: highly potent regulators of diabetes that require TRANCE-RANK signals. |
| 2671 | 11869680 | Here we show in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans. |
| 2672 | 11869680 | PLN-derived Treg cells are extremely potent; only 2 x 10(3) cells are needed to prevent diabetes development, and their capacity to regulate is dependent on TNF-related activation induced cytokine-receptor activator of NFkappaB signals. |
| 2673 | 11869680 | Indeed, blockade of this pathway results in decreased frequency of CD4(+)CD25(+) Treg cells in the PLN, resulting in intra-islet differentiation of CD8(+) T cells into CTLs and rapid progression to diabetes. |
| 2674 | 11869680 | Pancreatic lymph node-derived CD4(+)CD25(+) Treg cells: highly potent regulators of diabetes that require TRANCE-RANK signals. |
| 2675 | 11869680 | Here we show in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans. |
| 2676 | 11869680 | PLN-derived Treg cells are extremely potent; only 2 x 10(3) cells are needed to prevent diabetes development, and their capacity to regulate is dependent on TNF-related activation induced cytokine-receptor activator of NFkappaB signals. |
| 2677 | 11869680 | Indeed, blockade of this pathway results in decreased frequency of CD4(+)CD25(+) Treg cells in the PLN, resulting in intra-islet differentiation of CD8(+) T cells into CTLs and rapid progression to diabetes. |
| 2678 | 11869680 | Pancreatic lymph node-derived CD4(+)CD25(+) Treg cells: highly potent regulators of diabetes that require TRANCE-RANK signals. |
| 2679 | 11869680 | Here we show in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans. |
| 2680 | 11869680 | PLN-derived Treg cells are extremely potent; only 2 x 10(3) cells are needed to prevent diabetes development, and their capacity to regulate is dependent on TNF-related activation induced cytokine-receptor activator of NFkappaB signals. |
| 2681 | 11869680 | Indeed, blockade of this pathway results in decreased frequency of CD4(+)CD25(+) Treg cells in the PLN, resulting in intra-islet differentiation of CD8(+) T cells into CTLs and rapid progression to diabetes. |
| 2682 | 11877486 | We report here that CD4(+) and CD4(-)CD8(-) (double negative [DN]) NKT cell subsets represent functionally distinct lineages with marked differences in their profile of cytokine secretion and pattern of expression of chemokine receptors, integrins, and NK receptors. |
| 2683 | 11877486 | CD4(+) NKT cells were the exclusive producers of interleukin (IL)-4 and IL-13 upon primary stimulation, whereas DN NKT cells had a strict Th1 profile and prominently expressed several NK lineage receptors. |
| 2684 | 11877486 | We report here that CD4(+) and CD4(-)CD8(-) (double negative [DN]) NKT cell subsets represent functionally distinct lineages with marked differences in their profile of cytokine secretion and pattern of expression of chemokine receptors, integrins, and NK receptors. |
| 2685 | 11877486 | CD4(+) NKT cells were the exclusive producers of interleukin (IL)-4 and IL-13 upon primary stimulation, whereas DN NKT cells had a strict Th1 profile and prominently expressed several NK lineage receptors. |
| 2686 | 11878772 | A new type of antigen presenting molecule (dimeric MHC class-II/peptide, DEF) endowed with antigen-specific immunomodulatory effects such as induction of Th2 polarization and T-cell anergy is also described as a potential antidiabetogenic agent. |
| 2687 | 11878772 | According to our preliminary results, the MHC II/peptide-based approach may provide rational grounds for further development of antigen-specific immunotherapeutic agents such as human-like MHC lI/peptide chimeras endowed with efficient down-regulatory effects in CD4 T-cell-mediated autoimmune diseases such as Type 1 diabetes, multiple sclerosis, primary biliary cirrhosis, and rheumatoid arthritis. |
| 2688 | 11884430 | Adoptive transfer experiments with CD62L(-/-) CD4(+) T cells prepared from BDC2.5 TCR transgenic mice revealed no apparent defects in migration to pancreatic lymph nodes, proliferation in response to beta cell Ag, or induction of diabetes in NOD.scid recipients. |
| 2689 | 11888156 | The protocol requires the presence of CD4+ T cells, interferon-gamma, and CTLA4, and involves the deletion of CD8+ alloreactive T cells. |
| 2690 | 11890612 | Modulation of CD4 T cell function by soluble MHC II-peptide chimeras. |
| 2691 | 11890612 | Co-ligation of TCR and CD4 co-receptor on T cells by MHC II-peptide complexes (signal 1) leads to various T cell functions depending on the nature of TCR and CD4 co-ligation, and whether costimulatory receptors (signal 2) such as CD28, CTLA-4, CD40L are involved in this interaction. |
| 2692 | 11890612 | Modulation of CD4 T cell function by soluble MHC II-peptide chimeras. |
| 2693 | 11890612 | Co-ligation of TCR and CD4 co-receptor on T cells by MHC II-peptide complexes (signal 1) leads to various T cell functions depending on the nature of TCR and CD4 co-ligation, and whether costimulatory receptors (signal 2) such as CD28, CTLA-4, CD40L are involved in this interaction. |
| 2694 | 11891296 | To date, no marker for autoimmune T cells has been described, although it was previously demonstrated that autoimmune mice have a large population of CD4(+) cells that express CD40. |
| 2695 | 11891296 | We show that autoimmune diabetes-prone nonobese diabetic mice have high levels of CD40(+)CD4(+) T cells in the thymus, spleen, and importantly, in the pancreas. |
| 2696 | 11891296 | Finally, as demonstrated by adoptive transfers, CD4(+)CD40(+) cells infiltrate the pancreatic islets causing beta-cell degranulation and ultimately diabetes. |
| 2697 | 11891296 | To date, no marker for autoimmune T cells has been described, although it was previously demonstrated that autoimmune mice have a large population of CD4(+) cells that express CD40. |
| 2698 | 11891296 | We show that autoimmune diabetes-prone nonobese diabetic mice have high levels of CD40(+)CD4(+) T cells in the thymus, spleen, and importantly, in the pancreas. |
| 2699 | 11891296 | Finally, as demonstrated by adoptive transfers, CD4(+)CD40(+) cells infiltrate the pancreatic islets causing beta-cell degranulation and ultimately diabetes. |
| 2700 | 11891296 | To date, no marker for autoimmune T cells has been described, although it was previously demonstrated that autoimmune mice have a large population of CD4(+) cells that express CD40. |
| 2701 | 11891296 | We show that autoimmune diabetes-prone nonobese diabetic mice have high levels of CD40(+)CD4(+) T cells in the thymus, spleen, and importantly, in the pancreas. |
| 2702 | 11891296 | Finally, as demonstrated by adoptive transfers, CD4(+)CD40(+) cells infiltrate the pancreatic islets causing beta-cell degranulation and ultimately diabetes. |
| 2703 | 11899083 | Despite of some controversy, most of the studies in humans and animal models suggest that CD4 (Th1) T cells are directly involved in the autoimmune attack by secretion of pro-inflammatory cytokines and recruitment of cytotoxic CD8 T cells. |
| 2704 | 11905849 | Complexity of human immune response profiles for CD4+ T cell epitopes from the diabetes autoantigen GAD65. |
| 2705 | 11905849 | We have investigated recognition of the GAD65 protein, one of the well-characterized autoantigens in type I diabetes, among individuals carrying the HLA-DR4 haplotypes characteristic of susceptibility to IDDM. |
| 2706 | 11905849 | The majority of T cell responses were restricted by DRB1 molecules; however, DRB4 restricted responses were also observed. |
| 2707 | 11978632 | Type 1 diabetes is a chronic progressive autoimmune disease characterized by mononuclear cell infiltration, dominated by interleukin-12 (IL-12)-dependent Th1 cells, of the pancreatic islets, with subsequent destruction of insulin-producing beta-cells. |
| 2708 | 11978632 | Thus, a short treatment of adult NOD mice with an analog of 1,25-dihydroxyvitamin D(3) inhibits IL-12 production, blocks pancreatic infiltration of Th1 cells, enhances CD4(+)CD25(+) regulatory cells, and arrests the progression of type 1 diabetes, suggesting its possible application in the treatment of human autoimmune diabetes. |
| 2709 | 11978633 | T-cell activation defined in flow cytometry by CD4(high) and/or CD25 markers were observed in all type 1 diabetic patients and some at-risk subjects, but not in normal control subjects. |
| 2710 | 11978635 | Fas/Fas ligand interactions play an essential role in the initiation of murine autoimmune diabetes. |
| 2711 | 11978635 | Apoptosis via Fas/Fas ligand (FasL) interactions has been proposed to be a major T-cell-mediated effector mechanism in autoimmune diabetes. |
| 2712 | 11978635 | To elucidate the role of Fas/FasL interactions in NOD diabetes, the effects of neutralizing anti-FasL antibody on autoimmune responses were evaluated. |
| 2713 | 11978635 | Islet-specific CD8(+) and CD4(+) T-cells expressed FasL upon activation and mediated FasL-dependent cytotoxicity against Fas-expressing target cells in vitro, although their cytotoxicity against islet cells was not blocked by anti-FasL antibody. |
| 2714 | 11978635 | On the other hand, blockade of Fas/FasL interactions significantly inhibited CD4(+) T-cell-dependent diabetes in adoptive transfer models. |
| 2715 | 11978635 | These results suggest a substantial contribution of Fas/FasL interactions to CD4(+), but not CD8(+), T-cell-mediated destruction of pancreatic beta-cells. |
| 2716 | 11978635 | These results suggest that Fas/FasL interactions contribute to CD4(+) T-cell-mediated beta-cell destruction and play an essential role in the initiation of autoimmune NOD diabetes. |
| 2717 | 11978635 | Fas/Fas ligand interactions play an essential role in the initiation of murine autoimmune diabetes. |
| 2718 | 11978635 | Apoptosis via Fas/Fas ligand (FasL) interactions has been proposed to be a major T-cell-mediated effector mechanism in autoimmune diabetes. |
| 2719 | 11978635 | To elucidate the role of Fas/FasL interactions in NOD diabetes, the effects of neutralizing anti-FasL antibody on autoimmune responses were evaluated. |
| 2720 | 11978635 | Islet-specific CD8(+) and CD4(+) T-cells expressed FasL upon activation and mediated FasL-dependent cytotoxicity against Fas-expressing target cells in vitro, although their cytotoxicity against islet cells was not blocked by anti-FasL antibody. |
| 2721 | 11978635 | On the other hand, blockade of Fas/FasL interactions significantly inhibited CD4(+) T-cell-dependent diabetes in adoptive transfer models. |
| 2722 | 11978635 | These results suggest a substantial contribution of Fas/FasL interactions to CD4(+), but not CD8(+), T-cell-mediated destruction of pancreatic beta-cells. |
| 2723 | 11978635 | These results suggest that Fas/FasL interactions contribute to CD4(+) T-cell-mediated beta-cell destruction and play an essential role in the initiation of autoimmune NOD diabetes. |
| 2724 | 11978635 | Fas/Fas ligand interactions play an essential role in the initiation of murine autoimmune diabetes. |
| 2725 | 11978635 | Apoptosis via Fas/Fas ligand (FasL) interactions has been proposed to be a major T-cell-mediated effector mechanism in autoimmune diabetes. |
| 2726 | 11978635 | To elucidate the role of Fas/FasL interactions in NOD diabetes, the effects of neutralizing anti-FasL antibody on autoimmune responses were evaluated. |
| 2727 | 11978635 | Islet-specific CD8(+) and CD4(+) T-cells expressed FasL upon activation and mediated FasL-dependent cytotoxicity against Fas-expressing target cells in vitro, although their cytotoxicity against islet cells was not blocked by anti-FasL antibody. |
| 2728 | 11978635 | On the other hand, blockade of Fas/FasL interactions significantly inhibited CD4(+) T-cell-dependent diabetes in adoptive transfer models. |
| 2729 | 11978635 | These results suggest a substantial contribution of Fas/FasL interactions to CD4(+), but not CD8(+), T-cell-mediated destruction of pancreatic beta-cells. |
| 2730 | 11978635 | These results suggest that Fas/FasL interactions contribute to CD4(+) T-cell-mediated beta-cell destruction and play an essential role in the initiation of autoimmune NOD diabetes. |
| 2731 | 11978635 | Fas/Fas ligand interactions play an essential role in the initiation of murine autoimmune diabetes. |
| 2732 | 11978635 | Apoptosis via Fas/Fas ligand (FasL) interactions has been proposed to be a major T-cell-mediated effector mechanism in autoimmune diabetes. |
| 2733 | 11978635 | To elucidate the role of Fas/FasL interactions in NOD diabetes, the effects of neutralizing anti-FasL antibody on autoimmune responses were evaluated. |
| 2734 | 11978635 | Islet-specific CD8(+) and CD4(+) T-cells expressed FasL upon activation and mediated FasL-dependent cytotoxicity against Fas-expressing target cells in vitro, although their cytotoxicity against islet cells was not blocked by anti-FasL antibody. |
| 2735 | 11978635 | On the other hand, blockade of Fas/FasL interactions significantly inhibited CD4(+) T-cell-dependent diabetes in adoptive transfer models. |
| 2736 | 11978635 | These results suggest a substantial contribution of Fas/FasL interactions to CD4(+), but not CD8(+), T-cell-mediated destruction of pancreatic beta-cells. |
| 2737 | 11978635 | These results suggest that Fas/FasL interactions contribute to CD4(+) T-cell-mediated beta-cell destruction and play an essential role in the initiation of autoimmune NOD diabetes. |
| 2738 | 11992736 | In the direct PLNA, diclofenac also increased the percent of T cells in the PLN with activated phenotypes (CD44(high)CD62L(low) and CD44(high)CD62L(high)). |
| 2739 | 11992736 | Finally, an increase in the intracellular level of IL-4, but not INFgamma, was detected in CD4(+) PLN cells following the injection of diclofenac mixed with TNP-OVA. |
| 2740 | 11994496 | We examined the expression of IFN-gamma, a characteristic Th1 cytokine, and IL-4, a characteristic Th2 cytokine, in islet infiltrates of female and male NOD mice at various ages. |
| 2741 | 11994496 | IFN-gamma was significantly higher in young females, whereas IL-4 was higher in young males. |
| 2742 | 11994496 | CD4(+) T cells isolated from lymph nodes of female mice and activated with anti-CD3 and anti-CD28 Abs produced more IFN-gamma, but less IL-4, as compared with males. |
| 2743 | 11994496 | Treatment of CD4(+) T cells with estrogen significantly increased, whereas testosterone treatment decreased the IL-12-induced production of IFN-gamma. |
| 2744 | 11994496 | We then examined whether the change in IL-12-induced IFN-gamma production by treatment with sex hormones was due to the regulation of STAT4 activation. |
| 2745 | 11994496 | We found that estrogen treatment increased the phosphorylation of STAT4 in IL-12-stimulated T cells. |
| 2746 | 11994496 | We conclude that the increased susceptibility of female NOD mice to the development of autoimmune diabetes could be due to the enhancement of the Th1 immune response through the increase of IL-12-induced STAT4 activation by estrogen. |
| 2747 | 11994496 | We examined the expression of IFN-gamma, a characteristic Th1 cytokine, and IL-4, a characteristic Th2 cytokine, in islet infiltrates of female and male NOD mice at various ages. |
| 2748 | 11994496 | IFN-gamma was significantly higher in young females, whereas IL-4 was higher in young males. |
| 2749 | 11994496 | CD4(+) T cells isolated from lymph nodes of female mice and activated with anti-CD3 and anti-CD28 Abs produced more IFN-gamma, but less IL-4, as compared with males. |
| 2750 | 11994496 | Treatment of CD4(+) T cells with estrogen significantly increased, whereas testosterone treatment decreased the IL-12-induced production of IFN-gamma. |
| 2751 | 11994496 | We then examined whether the change in IL-12-induced IFN-gamma production by treatment with sex hormones was due to the regulation of STAT4 activation. |
| 2752 | 11994496 | We found that estrogen treatment increased the phosphorylation of STAT4 in IL-12-stimulated T cells. |
| 2753 | 11994496 | We conclude that the increased susceptibility of female NOD mice to the development of autoimmune diabetes could be due to the enhancement of the Th1 immune response through the increase of IL-12-induced STAT4 activation by estrogen. |
| 2754 | 12028557 | Inefficient deletion of CD4 and CD8 single-positive, heat stable antigen (HSA)hi medullary thymocytes was also observed in hyporesponsive donors. |
| 2755 | 12034374 | Similarly, the dramatic decreases in the size of the CD4(+)CD8(+) population of cells in the thymus and in the number of thymocytes in the S and G2/M phases of the cell cycle observed in wild-type mice administered PPs were much less extensive in PPARalpha-null mice. |
| 2756 | 12039407 | Flow cytometric analyses found that autoreactive T-cell lines from patients induced by beta-cell antigens consisted of four major subsets (CD4(+)CD56(-), CD4(+)CD56(+), CD8(+)CD56(-), and CD8(+)CD56(+)) and that CD56(+) NKT cells might be derived from CD56(-) T cells. |
| 2757 | 12039407 | Moreover, the proportion of CD56(+) NKT cells in the T-cell lines was influenced by time course of repeated antigen stimulation. beta-cell antigen-specific CD56(+) NKT (CD4(+) or CD8(+)) cells were more aggressive (HLA-restricted and -unrestricted) effector cells lysing target cells such as K562, Jurkat, P815 plus anti-CD3 antibody, and autologous B cells sensitized by beta-cell peptides, when compared with their CD56(-) counterparts. beta-cell antigen- specific CD4(+)CD56(+) NKT cells showed non-HLA-restricted cytotoxicity to human beta cells, insulinoma cell line CM, and to islet cell lines TRM-6 and HP62 expressing CD56 but not to four CD56(-) pancreatic cell lines of non- islet origin. |
| 2758 | 12039407 | The CD4(+)CD56(+) NKT cells showed stronger cytotoxicity to CM, TRM-6 and HP62 cells than did CD4(+)CD56(-) T cells. |
| 2759 | 12039407 | Moreover, isotope-unlabelled CD56(+) cells and anti-CD56 antibodies were able to inhibit cytotoxicity of CD4(+)CD56(+) NKT to CD56(+) target cells. |
| 2760 | 12039407 | Flow cytometric analyses found that autoreactive T-cell lines from patients induced by beta-cell antigens consisted of four major subsets (CD4(+)CD56(-), CD4(+)CD56(+), CD8(+)CD56(-), and CD8(+)CD56(+)) and that CD56(+) NKT cells might be derived from CD56(-) T cells. |
| 2761 | 12039407 | Moreover, the proportion of CD56(+) NKT cells in the T-cell lines was influenced by time course of repeated antigen stimulation. beta-cell antigen-specific CD56(+) NKT (CD4(+) or CD8(+)) cells were more aggressive (HLA-restricted and -unrestricted) effector cells lysing target cells such as K562, Jurkat, P815 plus anti-CD3 antibody, and autologous B cells sensitized by beta-cell peptides, when compared with their CD56(-) counterparts. beta-cell antigen- specific CD4(+)CD56(+) NKT cells showed non-HLA-restricted cytotoxicity to human beta cells, insulinoma cell line CM, and to islet cell lines TRM-6 and HP62 expressing CD56 but not to four CD56(-) pancreatic cell lines of non- islet origin. |
| 2762 | 12039407 | The CD4(+)CD56(+) NKT cells showed stronger cytotoxicity to CM, TRM-6 and HP62 cells than did CD4(+)CD56(-) T cells. |
| 2763 | 12039407 | Moreover, isotope-unlabelled CD56(+) cells and anti-CD56 antibodies were able to inhibit cytotoxicity of CD4(+)CD56(+) NKT to CD56(+) target cells. |
| 2764 | 12039407 | Flow cytometric analyses found that autoreactive T-cell lines from patients induced by beta-cell antigens consisted of four major subsets (CD4(+)CD56(-), CD4(+)CD56(+), CD8(+)CD56(-), and CD8(+)CD56(+)) and that CD56(+) NKT cells might be derived from CD56(-) T cells. |
| 2765 | 12039407 | Moreover, the proportion of CD56(+) NKT cells in the T-cell lines was influenced by time course of repeated antigen stimulation. beta-cell antigen-specific CD56(+) NKT (CD4(+) or CD8(+)) cells were more aggressive (HLA-restricted and -unrestricted) effector cells lysing target cells such as K562, Jurkat, P815 plus anti-CD3 antibody, and autologous B cells sensitized by beta-cell peptides, when compared with their CD56(-) counterparts. beta-cell antigen- specific CD4(+)CD56(+) NKT cells showed non-HLA-restricted cytotoxicity to human beta cells, insulinoma cell line CM, and to islet cell lines TRM-6 and HP62 expressing CD56 but not to four CD56(-) pancreatic cell lines of non- islet origin. |
| 2766 | 12039407 | The CD4(+)CD56(+) NKT cells showed stronger cytotoxicity to CM, TRM-6 and HP62 cells than did CD4(+)CD56(-) T cells. |
| 2767 | 12039407 | Moreover, isotope-unlabelled CD56(+) cells and anti-CD56 antibodies were able to inhibit cytotoxicity of CD4(+)CD56(+) NKT to CD56(+) target cells. |
| 2768 | 12039407 | Flow cytometric analyses found that autoreactive T-cell lines from patients induced by beta-cell antigens consisted of four major subsets (CD4(+)CD56(-), CD4(+)CD56(+), CD8(+)CD56(-), and CD8(+)CD56(+)) and that CD56(+) NKT cells might be derived from CD56(-) T cells. |
| 2769 | 12039407 | Moreover, the proportion of CD56(+) NKT cells in the T-cell lines was influenced by time course of repeated antigen stimulation. beta-cell antigen-specific CD56(+) NKT (CD4(+) or CD8(+)) cells were more aggressive (HLA-restricted and -unrestricted) effector cells lysing target cells such as K562, Jurkat, P815 plus anti-CD3 antibody, and autologous B cells sensitized by beta-cell peptides, when compared with their CD56(-) counterparts. beta-cell antigen- specific CD4(+)CD56(+) NKT cells showed non-HLA-restricted cytotoxicity to human beta cells, insulinoma cell line CM, and to islet cell lines TRM-6 and HP62 expressing CD56 but not to four CD56(-) pancreatic cell lines of non- islet origin. |
| 2770 | 12039407 | The CD4(+)CD56(+) NKT cells showed stronger cytotoxicity to CM, TRM-6 and HP62 cells than did CD4(+)CD56(-) T cells. |
| 2771 | 12039407 | Moreover, isotope-unlabelled CD56(+) cells and anti-CD56 antibodies were able to inhibit cytotoxicity of CD4(+)CD56(+) NKT to CD56(+) target cells. |
| 2772 | 12049723 | CD154-dependent priming of diabetogenic CD4(+) T cells dissociated from activation of antigen-presenting cells. |
| 2773 | 12049723 | We followed the fate of K(d)- or I-A(g7)-restricted beta cell-autoreactive T cells in monoclonal TCR-transgenic NOD mice expressing or lacking CD154. 8.3-NOD.RAG-2(-/-)/CD154(-/-) mice, which bear autoreactive CD8(+) T cells, developed diabetes with the same incidence and tempo as 8.3-NOD.RAG-2(-/-)/CD154(+) mice. |
| 2774 | 12049723 | Recruitment of CD154(-/-) 8.3-CD8(+) CTL was accelerated by CD154(+)CD4(+) T cells, by expression of a B7.1 transgene in beta cells or by treatment of the mice with CpG-DNA or an agonistic anti-CD40 antibody. |
| 2775 | 12049723 | In contrast, the autoreactive CD4(+) T cells maturing in 4.1-NOD.RAG-2(-/-) mice lost their diabetogenic potential if they lacked CD154, even in the presence of CD154(+)CD4(+) T cells, B7.1 molecules on beta cells, CpG-DNA treatment, or systemic CD40 ligation. |
| 2776 | 12049723 | These results demonstrate the existence of a novel, CD154-dependent pathway of CD4(+) T cell activation that is independent of CD40-mediated activation of APCs. |
| 2777 | 12049723 | CD154-dependent priming of diabetogenic CD4(+) T cells dissociated from activation of antigen-presenting cells. |
| 2778 | 12049723 | We followed the fate of K(d)- or I-A(g7)-restricted beta cell-autoreactive T cells in monoclonal TCR-transgenic NOD mice expressing or lacking CD154. 8.3-NOD.RAG-2(-/-)/CD154(-/-) mice, which bear autoreactive CD8(+) T cells, developed diabetes with the same incidence and tempo as 8.3-NOD.RAG-2(-/-)/CD154(+) mice. |
| 2779 | 12049723 | Recruitment of CD154(-/-) 8.3-CD8(+) CTL was accelerated by CD154(+)CD4(+) T cells, by expression of a B7.1 transgene in beta cells or by treatment of the mice with CpG-DNA or an agonistic anti-CD40 antibody. |
| 2780 | 12049723 | In contrast, the autoreactive CD4(+) T cells maturing in 4.1-NOD.RAG-2(-/-) mice lost their diabetogenic potential if they lacked CD154, even in the presence of CD154(+)CD4(+) T cells, B7.1 molecules on beta cells, CpG-DNA treatment, or systemic CD40 ligation. |
| 2781 | 12049723 | These results demonstrate the existence of a novel, CD154-dependent pathway of CD4(+) T cell activation that is independent of CD40-mediated activation of APCs. |
| 2782 | 12049723 | CD154-dependent priming of diabetogenic CD4(+) T cells dissociated from activation of antigen-presenting cells. |
| 2783 | 12049723 | We followed the fate of K(d)- or I-A(g7)-restricted beta cell-autoreactive T cells in monoclonal TCR-transgenic NOD mice expressing or lacking CD154. 8.3-NOD.RAG-2(-/-)/CD154(-/-) mice, which bear autoreactive CD8(+) T cells, developed diabetes with the same incidence and tempo as 8.3-NOD.RAG-2(-/-)/CD154(+) mice. |
| 2784 | 12049723 | Recruitment of CD154(-/-) 8.3-CD8(+) CTL was accelerated by CD154(+)CD4(+) T cells, by expression of a B7.1 transgene in beta cells or by treatment of the mice with CpG-DNA or an agonistic anti-CD40 antibody. |
| 2785 | 12049723 | In contrast, the autoreactive CD4(+) T cells maturing in 4.1-NOD.RAG-2(-/-) mice lost their diabetogenic potential if they lacked CD154, even in the presence of CD154(+)CD4(+) T cells, B7.1 molecules on beta cells, CpG-DNA treatment, or systemic CD40 ligation. |
| 2786 | 12049723 | These results demonstrate the existence of a novel, CD154-dependent pathway of CD4(+) T cell activation that is independent of CD40-mediated activation of APCs. |
| 2787 | 12049723 | CD154-dependent priming of diabetogenic CD4(+) T cells dissociated from activation of antigen-presenting cells. |
| 2788 | 12049723 | We followed the fate of K(d)- or I-A(g7)-restricted beta cell-autoreactive T cells in monoclonal TCR-transgenic NOD mice expressing or lacking CD154. 8.3-NOD.RAG-2(-/-)/CD154(-/-) mice, which bear autoreactive CD8(+) T cells, developed diabetes with the same incidence and tempo as 8.3-NOD.RAG-2(-/-)/CD154(+) mice. |
| 2789 | 12049723 | Recruitment of CD154(-/-) 8.3-CD8(+) CTL was accelerated by CD154(+)CD4(+) T cells, by expression of a B7.1 transgene in beta cells or by treatment of the mice with CpG-DNA or an agonistic anti-CD40 antibody. |
| 2790 | 12049723 | In contrast, the autoreactive CD4(+) T cells maturing in 4.1-NOD.RAG-2(-/-) mice lost their diabetogenic potential if they lacked CD154, even in the presence of CD154(+)CD4(+) T cells, B7.1 molecules on beta cells, CpG-DNA treatment, or systemic CD40 ligation. |
| 2791 | 12049723 | These results demonstrate the existence of a novel, CD154-dependent pathway of CD4(+) T cell activation that is independent of CD40-mediated activation of APCs. |
| 2792 | 12073618 | To define the immunopathologic mechanisms underlying pulmonary tuberculosis in patients with DM, the production of IFN-gamma by CD4+ T cells or PBMC were followed up longitudinally during antituberculous chemotherapy. |
| 2793 | 12073618 | At the time of diagnosis, IFN-gamma production by CD4+ T cells in either tuberculosis patients without DM (TB) or with DM was significantly lower than that in the healthy control. |
| 2794 | 12073618 | CD4+ T cells in tuberculosis patients with DM under poor control (DM(p)TB) produced significantly less IFN-gamma than did patients with DM under good control (DM(g)TB). |
| 2795 | 12073618 | To define the immunopathologic mechanisms underlying pulmonary tuberculosis in patients with DM, the production of IFN-gamma by CD4+ T cells or PBMC were followed up longitudinally during antituberculous chemotherapy. |
| 2796 | 12073618 | At the time of diagnosis, IFN-gamma production by CD4+ T cells in either tuberculosis patients without DM (TB) or with DM was significantly lower than that in the healthy control. |
| 2797 | 12073618 | CD4+ T cells in tuberculosis patients with DM under poor control (DM(p)TB) produced significantly less IFN-gamma than did patients with DM under good control (DM(g)TB). |
| 2798 | 12073618 | To define the immunopathologic mechanisms underlying pulmonary tuberculosis in patients with DM, the production of IFN-gamma by CD4+ T cells or PBMC were followed up longitudinally during antituberculous chemotherapy. |
| 2799 | 12073618 | At the time of diagnosis, IFN-gamma production by CD4+ T cells in either tuberculosis patients without DM (TB) or with DM was significantly lower than that in the healthy control. |
| 2800 | 12073618 | CD4+ T cells in tuberculosis patients with DM under poor control (DM(p)TB) produced significantly less IFN-gamma than did patients with DM under good control (DM(g)TB). |
| 2801 | 12079263 | Hypergammaglobulinaemia, increased serum levels of total IgG or IgG4, positive autoantibodies such as antinuclear antibody, anti-lactoferrin antibody, anti-CA-II antibody, rheumatoid factor and anti-smooth muscle antibody, were often observed in patients with AIP. |
| 2802 | 12079263 | Major subgroups of lymphocytes infiltrating areas around pancreatic ducts were CD4(+) T-cells producing IFN-gamma. |
| 2803 | 12110118 | The disease is T-cell mediated, involving both CD4 and CD8 cells. |
| 2804 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 2805 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 2806 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 2807 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 2808 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 2809 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 2810 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 2811 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 2812 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 2813 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 2814 | 12115623 | We previously demonstrated that immunotherapy with dendritic cells (DC) prevented diabetes development in prediabetic NOD mice and that this effect was optimal when using a stimulatory DC population generated from bone marrow cells cultured with granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4. |
| 2815 | 12115623 | In this study, we have investigated the mechanism by which GM-CSF- and IL-4-cultured DC prevent diabetes in prediabetic NOD mice. |
| 2816 | 12115623 | Furthermore, sorted CD45RB(lo) CD25+ CD4+ T cells from the spleen of DC-treated mice produced high amounts of Th2 cytokines following anti-TCR stimulation, suggesting that these cells are responsible for the apparent Th2 shift. |
| 2817 | 12118894 | Furthermore, combined blockade of the CD28/B7 and CD154/CD40 costimulatory pathways induces tolerance in multiple CD4+ T-cell dependent allograft models. |
| 2818 | 12118894 | Analysis of the costimulatory capacity of different antigen presenting cell (APC) populations demonstrated that APCs resident within the donor skin, Langerhans cells, are potent stimulators not requiring CD28- or CD154-dependent costimulation for direct major histocompatibility complex (MHC) antigen presentation. |
| 2819 | 12118894 | These results complement previous work examining the role of costimulation on CD8+ T cells, supporting a model in which the effectiveness of costimulatory blockade in the setting of transplantation may be selective for the indirect pathway of MHC alloantigen presentation. |
| 2820 | 12145162 | CC chemokine receptor 5 (CCR5) is expressed preferentially by CD4(+) T helper 1 (Th1) cells. |
| 2821 | 12145162 | In CCR5(-/-) mice, intragraft mRNA expression of interleukin-4 and -5 was increased, whereas that of interferon-gamma was decreased, corresponding to a Th2 pattern of T-cell activation in the target tissues compared with a Th1 pattern observed in controls. |
| 2822 | 12147632 | In addition, anti-CD45RB treatment led to reduced expression of LFA-1 and CD62 ligand (CD62L) on CD4 T cells, independent of antigenic challenge. |
| 2823 | 12147632 | LFA-1 may enhance co-stimulation, and both LFA-1 and CD62L are involved in T cell trafficking. |
| 2824 | 12163561 | The presence of activated, antigen-specific CD4(+) T cells converts this tolerogenic encounter into an immunogenic one by promoting extensive proliferation of CD8(+) T cells and their development into effectors. |
| 2825 | 12163561 | Surprisingly, activation of APCs with an agonistic antibody specific for CD40 could not substitute for CD4(+) help in this task. |
| 2826 | 12163561 | The presence of activated, antigen-specific CD4(+) T cells converts this tolerogenic encounter into an immunogenic one by promoting extensive proliferation of CD8(+) T cells and their development into effectors. |
| 2827 | 12163561 | Surprisingly, activation of APCs with an agonistic antibody specific for CD40 could not substitute for CD4(+) help in this task. |
| 2828 | 12173299 | In parallel, the proliferative response of CD4+ T-cells to the primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. |
| 2829 | 12173299 | Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. |
| 2830 | 12173299 | FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. |
| 2831 | 12182467 | Benign insulitis with macrophages, B cells, CD4 > CD8 T cells and low levels of IL-2R, IL-2, IFN-gamma and IL-4 was seen in islets from the native pancreas and in long surviving pancreas isografts in mice that remained in remission. |
| 2832 | 12186840 | CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. |
| 2833 | 12186840 | These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. |
| 2834 | 12186840 | Lymphocytes from these TCR transgenic mice proliferate and make interferon gamma, interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and IL-10 when stimulated in vitro with GAD65 peptide 286-300, yet these TCR transgenic animals do not spontaneously develop diabetes, and insulitis is virtually undetectable. |
| 2835 | 12186840 | Furthermore, in vitro activated CD4 T cells from GAD 286 TCR transgenic mice express higher levels of CTL-associated antigen (CTLA)-4 than nontransgenic littermates. |
| 2836 | 12186840 | CD4(+) T cells, or p286-tetramer(+)CD4(+) Tcells, from GAD65 286-300-specific TCR transgenic mice delay diabetes induced in NOD.scid mice by diabetic NOD spleen cells. |
| 2837 | 12186840 | CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. |
| 2838 | 12186840 | These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. |
| 2839 | 12186840 | Lymphocytes from these TCR transgenic mice proliferate and make interferon gamma, interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and IL-10 when stimulated in vitro with GAD65 peptide 286-300, yet these TCR transgenic animals do not spontaneously develop diabetes, and insulitis is virtually undetectable. |
| 2840 | 12186840 | Furthermore, in vitro activated CD4 T cells from GAD 286 TCR transgenic mice express higher levels of CTL-associated antigen (CTLA)-4 than nontransgenic littermates. |
| 2841 | 12186840 | CD4(+) T cells, or p286-tetramer(+)CD4(+) Tcells, from GAD65 286-300-specific TCR transgenic mice delay diabetes induced in NOD.scid mice by diabetic NOD spleen cells. |
| 2842 | 12186840 | CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. |
| 2843 | 12186840 | These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. |
| 2844 | 12186840 | Lymphocytes from these TCR transgenic mice proliferate and make interferon gamma, interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and IL-10 when stimulated in vitro with GAD65 peptide 286-300, yet these TCR transgenic animals do not spontaneously develop diabetes, and insulitis is virtually undetectable. |
| 2845 | 12186840 | Furthermore, in vitro activated CD4 T cells from GAD 286 TCR transgenic mice express higher levels of CTL-associated antigen (CTLA)-4 than nontransgenic littermates. |
| 2846 | 12186840 | CD4(+) T cells, or p286-tetramer(+)CD4(+) Tcells, from GAD65 286-300-specific TCR transgenic mice delay diabetes induced in NOD.scid mice by diabetic NOD spleen cells. |
| 2847 | 12186840 | CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. |
| 2848 | 12186840 | These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. |
| 2849 | 12186840 | Lymphocytes from these TCR transgenic mice proliferate and make interferon gamma, interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and IL-10 when stimulated in vitro with GAD65 peptide 286-300, yet these TCR transgenic animals do not spontaneously develop diabetes, and insulitis is virtually undetectable. |
| 2850 | 12186840 | Furthermore, in vitro activated CD4 T cells from GAD 286 TCR transgenic mice express higher levels of CTL-associated antigen (CTLA)-4 than nontransgenic littermates. |
| 2851 | 12186840 | CD4(+) T cells, or p286-tetramer(+)CD4(+) Tcells, from GAD65 286-300-specific TCR transgenic mice delay diabetes induced in NOD.scid mice by diabetic NOD spleen cells. |
| 2852 | 12193712 | Whether or not peptide II(33-47) is the only proinsulin determinant recognized by CD4 T cells remains unclear. |
| 2853 | 12193715 | The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7. |
| 2854 | 12193715 | Recently, CD4(+)CD25(+) T cells have been implicated in the control of diabetes, suggesting that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveillance. |
| 2855 | 12193715 | Here we show that CD4(+)CD25(+) splenocytes inhibit diabetes in cotransfer with islet-infiltrating cells. |
| 2856 | 12193715 | Furthermore, CD62L expression is necessary for this disease-delaying effect of CD4(+)CD25(+) cells in vivo, but not for their suppressor function in vitro. |
| 2857 | 12193715 | We demonstrate that the CD4(+)CD25(+)CD62L(+) splenocytes express CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-inflammatory protein-3beta), lymphoid chemokines, whereas CD4(+)CD25(+)CD62L(-) splenocytes preferentially express CCR2, CCR4, and CXCR3 and migrate toward the corresponding inflammatory chemokines. |
| 2858 | 12193715 | These data demonstrate that CD4(+)CD25(+)CD62L(+), but not CD4(+)CD25(+)CD62L(-), splenocytes delay diabetes transfer, and that CD4(+)CD25(+) suppressor T cells are comprised of at least two subpopulations that behave differently in cotransfer in vivo and express distinct chemokine receptor and chemotactic response profiles despite demonstrating equivalent suppressor functions in vitro. |
| 2859 | 12193715 | The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7. |
| 2860 | 12193715 | Recently, CD4(+)CD25(+) T cells have been implicated in the control of diabetes, suggesting that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveillance. |
| 2861 | 12193715 | Here we show that CD4(+)CD25(+) splenocytes inhibit diabetes in cotransfer with islet-infiltrating cells. |
| 2862 | 12193715 | Furthermore, CD62L expression is necessary for this disease-delaying effect of CD4(+)CD25(+) cells in vivo, but not for their suppressor function in vitro. |
| 2863 | 12193715 | We demonstrate that the CD4(+)CD25(+)CD62L(+) splenocytes express CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-inflammatory protein-3beta), lymphoid chemokines, whereas CD4(+)CD25(+)CD62L(-) splenocytes preferentially express CCR2, CCR4, and CXCR3 and migrate toward the corresponding inflammatory chemokines. |
| 2864 | 12193715 | These data demonstrate that CD4(+)CD25(+)CD62L(+), but not CD4(+)CD25(+)CD62L(-), splenocytes delay diabetes transfer, and that CD4(+)CD25(+) suppressor T cells are comprised of at least two subpopulations that behave differently in cotransfer in vivo and express distinct chemokine receptor and chemotactic response profiles despite demonstrating equivalent suppressor functions in vitro. |
| 2865 | 12193715 | The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7. |
| 2866 | 12193715 | Recently, CD4(+)CD25(+) T cells have been implicated in the control of diabetes, suggesting that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveillance. |
| 2867 | 12193715 | Here we show that CD4(+)CD25(+) splenocytes inhibit diabetes in cotransfer with islet-infiltrating cells. |
| 2868 | 12193715 | Furthermore, CD62L expression is necessary for this disease-delaying effect of CD4(+)CD25(+) cells in vivo, but not for their suppressor function in vitro. |
| 2869 | 12193715 | We demonstrate that the CD4(+)CD25(+)CD62L(+) splenocytes express CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-inflammatory protein-3beta), lymphoid chemokines, whereas CD4(+)CD25(+)CD62L(-) splenocytes preferentially express CCR2, CCR4, and CXCR3 and migrate toward the corresponding inflammatory chemokines. |
| 2870 | 12193715 | These data demonstrate that CD4(+)CD25(+)CD62L(+), but not CD4(+)CD25(+)CD62L(-), splenocytes delay diabetes transfer, and that CD4(+)CD25(+) suppressor T cells are comprised of at least two subpopulations that behave differently in cotransfer in vivo and express distinct chemokine receptor and chemotactic response profiles despite demonstrating equivalent suppressor functions in vitro. |
| 2871 | 12193715 | The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7. |
| 2872 | 12193715 | Recently, CD4(+)CD25(+) T cells have been implicated in the control of diabetes, suggesting that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveillance. |
| 2873 | 12193715 | Here we show that CD4(+)CD25(+) splenocytes inhibit diabetes in cotransfer with islet-infiltrating cells. |
| 2874 | 12193715 | Furthermore, CD62L expression is necessary for this disease-delaying effect of CD4(+)CD25(+) cells in vivo, but not for their suppressor function in vitro. |
| 2875 | 12193715 | We demonstrate that the CD4(+)CD25(+)CD62L(+) splenocytes express CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-inflammatory protein-3beta), lymphoid chemokines, whereas CD4(+)CD25(+)CD62L(-) splenocytes preferentially express CCR2, CCR4, and CXCR3 and migrate toward the corresponding inflammatory chemokines. |
| 2876 | 12193715 | These data demonstrate that CD4(+)CD25(+)CD62L(+), but not CD4(+)CD25(+)CD62L(-), splenocytes delay diabetes transfer, and that CD4(+)CD25(+) suppressor T cells are comprised of at least two subpopulations that behave differently in cotransfer in vivo and express distinct chemokine receptor and chemotactic response profiles despite demonstrating equivalent suppressor functions in vitro. |
| 2877 | 12193715 | The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7. |
| 2878 | 12193715 | Recently, CD4(+)CD25(+) T cells have been implicated in the control of diabetes, suggesting that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveillance. |
| 2879 | 12193715 | Here we show that CD4(+)CD25(+) splenocytes inhibit diabetes in cotransfer with islet-infiltrating cells. |
| 2880 | 12193715 | Furthermore, CD62L expression is necessary for this disease-delaying effect of CD4(+)CD25(+) cells in vivo, but not for their suppressor function in vitro. |
| 2881 | 12193715 | We demonstrate that the CD4(+)CD25(+)CD62L(+) splenocytes express CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-inflammatory protein-3beta), lymphoid chemokines, whereas CD4(+)CD25(+)CD62L(-) splenocytes preferentially express CCR2, CCR4, and CXCR3 and migrate toward the corresponding inflammatory chemokines. |
| 2882 | 12193715 | These data demonstrate that CD4(+)CD25(+)CD62L(+), but not CD4(+)CD25(+)CD62L(-), splenocytes delay diabetes transfer, and that CD4(+)CD25(+) suppressor T cells are comprised of at least two subpopulations that behave differently in cotransfer in vivo and express distinct chemokine receptor and chemotactic response profiles despite demonstrating equivalent suppressor functions in vitro. |
| 2883 | 12193715 | The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7. |
| 2884 | 12193715 | Recently, CD4(+)CD25(+) T cells have been implicated in the control of diabetes, suggesting that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveillance. |
| 2885 | 12193715 | Here we show that CD4(+)CD25(+) splenocytes inhibit diabetes in cotransfer with islet-infiltrating cells. |
| 2886 | 12193715 | Furthermore, CD62L expression is necessary for this disease-delaying effect of CD4(+)CD25(+) cells in vivo, but not for their suppressor function in vitro. |
| 2887 | 12193715 | We demonstrate that the CD4(+)CD25(+)CD62L(+) splenocytes express CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-inflammatory protein-3beta), lymphoid chemokines, whereas CD4(+)CD25(+)CD62L(-) splenocytes preferentially express CCR2, CCR4, and CXCR3 and migrate toward the corresponding inflammatory chemokines. |
| 2888 | 12193715 | These data demonstrate that CD4(+)CD25(+)CD62L(+), but not CD4(+)CD25(+)CD62L(-), splenocytes delay diabetes transfer, and that CD4(+)CD25(+) suppressor T cells are comprised of at least two subpopulations that behave differently in cotransfer in vivo and express distinct chemokine receptor and chemotactic response profiles despite demonstrating equivalent suppressor functions in vitro. |
| 2889 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 2890 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 2891 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 2892 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 2893 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 2894 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 2895 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 2896 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 2897 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 2898 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 2899 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 2900 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 2901 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 2902 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 2903 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 2904 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 2905 | 12229124 | Cytologic examination of the ascitic fluid revealed numerous abnormal lymphocytes which by flow cytometry demonstrated expression of CD5, CD19, CD20, and CD4. |
| 2906 | 12296863 | No preferential inactivation was shown in freshly sorted CD4+, CD8+, CD19+ cells or in IL-2 cultured CD4 and CD8 T cells, indicating that peripheral blood lymphocytes in these women are randomly selected. |
| 2907 | 12296863 | Moreover, only one single FOXP3 transcript was expressed by CD4 T cell clones analysed by RT-PCR, confirming that this gene is subject to X- inactivation. |
| 2908 | 12296863 | No preferential inactivation was shown in freshly sorted CD4+, CD8+, CD19+ cells or in IL-2 cultured CD4 and CD8 T cells, indicating that peripheral blood lymphocytes in these women are randomly selected. |
| 2909 | 12296863 | Moreover, only one single FOXP3 transcript was expressed by CD4 T cell clones analysed by RT-PCR, confirming that this gene is subject to X- inactivation. |
| 2910 | 12365794 | Fas and Fas ligand immunolocalization in pancreatic islets of NOD mice during spontaneous and cyclophosphamide-accelerated diabetes. |
| 2911 | 12365794 | Here, dual-label immunohistochemistry was employed to examine the intra-islet expression, distribution and cellular sources of Fas and FasL in the NOD mouse, during spontaneous diabetes (days 21, 40 and 90) and following acceleration of diabetes with cyclophosphamide (days 0, 4, 7, 11 and 14 after cyclophosphamide administration). |
| 2912 | 12365794 | FasL was expressed constitutively in most beta cells but not in glucagon or somatostatin cells or islet inflammatory cells and paralleled the loss of insulin immunolabelling with advancing disease. |
| 2913 | 12365794 | During spontaneous and cyclophosphamide diabetes, it was observed in a higher proportion of islet infiltrating macrophages than CD4 and CD8 T cells, concomitant with advancing insulitis. |
| 2914 | 12365794 | In cyclophosphamide-treated mice, the proportion of Fas-positive intra-islet CD4 and CD8 T cells at day 14 (with and without diabetes) was considerably higher than at days 0, 4, 7 and 11. |
| 2915 | 12365794 | Our results show constitutive expression of FasL in beta cells in the NOD mouse and predominant expression of Fas in intra-islet macrophages and to a lesser extent in T cells prior to diabetes onset. |
| 2916 | 12365794 | Interleukin-1beta in intra-islet macrophages may induce Fas and inducible nitric oxide synthase expression in an autocrine and paracrine manner and mediate beta cell destruction or even death of some macrophages and T cells. |
| 2917 | 12365794 | Fas and Fas ligand immunolocalization in pancreatic islets of NOD mice during spontaneous and cyclophosphamide-accelerated diabetes. |
| 2918 | 12365794 | Here, dual-label immunohistochemistry was employed to examine the intra-islet expression, distribution and cellular sources of Fas and FasL in the NOD mouse, during spontaneous diabetes (days 21, 40 and 90) and following acceleration of diabetes with cyclophosphamide (days 0, 4, 7, 11 and 14 after cyclophosphamide administration). |
| 2919 | 12365794 | FasL was expressed constitutively in most beta cells but not in glucagon or somatostatin cells or islet inflammatory cells and paralleled the loss of insulin immunolabelling with advancing disease. |
| 2920 | 12365794 | During spontaneous and cyclophosphamide diabetes, it was observed in a higher proportion of islet infiltrating macrophages than CD4 and CD8 T cells, concomitant with advancing insulitis. |
| 2921 | 12365794 | In cyclophosphamide-treated mice, the proportion of Fas-positive intra-islet CD4 and CD8 T cells at day 14 (with and without diabetes) was considerably higher than at days 0, 4, 7 and 11. |
| 2922 | 12365794 | Our results show constitutive expression of FasL in beta cells in the NOD mouse and predominant expression of Fas in intra-islet macrophages and to a lesser extent in T cells prior to diabetes onset. |
| 2923 | 12365794 | Interleukin-1beta in intra-islet macrophages may induce Fas and inducible nitric oxide synthase expression in an autocrine and paracrine manner and mediate beta cell destruction or even death of some macrophages and T cells. |
| 2924 | 12390307 | Protection induced by CTB-insulin was transferred to naive recipients by splenic CD4+ T cells. |
| 2925 | 12390307 | Reverse transcription-polymerase chain reaction analysis of recipients' pancreatic glands revealed an increase of TGF-beta and IL-10 transcripts after donor mice tolerization, while levels of IFN-gamma and IL-4 RNAs were unchanged. |
| 2926 | 12390307 | Higher amounts of IL-4 and IFN-gamma were noticed in pancreatic lymph nodes of tolerized mice upon in vitro stimulation. |
| 2927 | 12391193 | CD4-dependent generation of dominant transplantation tolerance induced by simultaneous perturbation of CD154 and LFA-1 pathways. |
| 2928 | 12391193 | CD154 and LFA-1 (CD11a) represent conceptually distinct pathways of receptor/ligand interactions (costimulation and adhesion/homing, respectively) that have been effectively targeted to induce long-term allograft acceptance and tolerance. |
| 2929 | 12391193 | In vitro analysis indicated that simultaneous targeting of CD154 and LFA-1 resulted in profound inhibition of alloreactivity, suggesting that combined anti-CD154/anti-LFA-1 therapy could be highly effective in vivo. |
| 2930 | 12391193 | Thus, we evaluated combining mAb therapies targeting CD154 and LFA-1 for inducing transplantation tolerance to pancreatic islet allografts. |
| 2931 | 12391193 | Therefore, simultaneous perturbation of CD154 and LFA-1 molecules can result in profound tolerance induction not accomplished through individual monotherapy approaches. |
| 2932 | 12401711 | We also found that the tendency of NOD mice to resist tolerance induction by costimulation blockade is mediated by both CD4+ and CD8+ T-cells, not directly linked to the presence of autoimmunity, and conferred by non-MHC background genes. |
| 2933 | 12401715 | Diabetes was characterized by diffuse CD4(+)CD8(+) T-cell infiltration of pancreatic islets and severe insulin deficiency, and ppIns, proinsulin, and insulin DNA were equally effective for disease induction. |
| 2934 | 12419281 | Insulin, phogrin and phogrin-peptide 7 (aa 755-777) but not phogrin-peptide 2 (aa 640-659) or tetanus toxin peptide were recognized as antigens. |
| 2935 | 12419281 | Islet cell-reactive and phogrin peptide 7-specific CD4(+) T-cell lines were generated from splenocytes of unprimed 4-week-old NOD females and shown to secrete Th1-type cytokines. |
| 2936 | 12420105 | Psoriasis is characterized by a dermal and epidermal infiltrate comprised predominantly of CD4(+) and CD8(+) T cells, respectively. |
| 2937 | 12420105 | Using an immunoperoxidase technique, cryostat sections were stained using antibodies to T-cell markers CD2, CD3, CD4 and CD8; cutaneous leucocyte associated antigen; NK cell markers CD16, CD56, CD57, CD94 and CD158a; and the NK-T cell marker CD161. |
| 2938 | 12420105 | There were significantly more cells expressing T cell markers, NK cell markers CD16, CD57, CD94 and CD158a and NK-T cell marker CD161 in involved skin than in uninvolved or normal skin ( P<0.01). |
| 2939 | 12420105 | Psoriasis is characterized by a dermal and epidermal infiltrate comprised predominantly of CD4(+) and CD8(+) T cells, respectively. |
| 2940 | 12420105 | Using an immunoperoxidase technique, cryostat sections were stained using antibodies to T-cell markers CD2, CD3, CD4 and CD8; cutaneous leucocyte associated antigen; NK cell markers CD16, CD56, CD57, CD94 and CD158a; and the NK-T cell marker CD161. |
| 2941 | 12420105 | There were significantly more cells expressing T cell markers, NK cell markers CD16, CD57, CD94 and CD158a and NK-T cell marker CD161 in involved skin than in uninvolved or normal skin ( P<0.01). |
| 2942 | 12426635 | Kinetics of TNF-alpha and IFN-gamma mRNA expression in islets and spleen of NOD mice. |
| 2943 | 12426635 | Cytokines produced by islet-infiltrating mononuclear cells may be directly cytotoxic and can be involved in islet destruction coordinated by CD4+ and CD8+ cells. |
| 2944 | 12426635 | We utilized a semiquantitative RT-PCR assay to analyze in vitro the mRNA expression of TNF-alpha and IFN-gamma cytokine genes in isolated islets (N = 100) and spleen cells (5 x 10(5) cells) from female NOD mice during the development of diabetes and from female CBA-j mice as a related control strain that does not develop diabetes. |
| 2945 | 12426635 | An increase in IFN-gamma expression in islets was observed for females aged 28 weeks (149 +/- 29 arbitrary units (AU), P<0.05, Student t-test) with advanced destructive insulitis when compared with CBA-j mice, while TNF-alpha was expressed in both NOD and CBA-j female islets at the same level at all ages studied. |
| 2946 | 12426635 | The data suggest that IFN-gamma and TNF-alpha expression in pancreatic islets of female NOD mice is associated with beta cell destruction and overt diabetes. |
| 2947 | 12437993 | Expression of ABCB1 (MDR1, P-glycoprotein) increases with age in CD4(+) and CD8(+) T-lymphocytes indicating that P-glycoprotein may be involved in the secretion of cytokines, growth factors, and cytotoxic molecules. |
| 2948 | 12437993 | Polymorphisms in the sulfonylurea receptor gene (ABCC8, SUR1) are associated with non-insulin-dependent diabetes mellitus (NIDDM). |
| 2949 | 12444125 | CTLA-4 is critical to the regulation of CD4 T cell homeostasis in vivo. |
| 2950 | 12444170 | Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. |
| 2951 | 12444170 | In this study, we demonstrate that increased IFN-gamma, decreased IL-4, and decreased IL-10 production in NOD T cells is CD4 T cell intrinsic. |
| 2952 | 12444170 | NOD CD4(+) T cells purified and stimulated with anti-CD3/anti-CD28 Abs generated greater IFN-gamma, less IL-4, and less IL-10 than B6.G7 CD4(+) T cells. |
| 2953 | 12444170 | Moreover, the increased IFN-gamma:IL-4 cytokine ratio was independent of the genetic background of APCs, since NOD CD4(+) T cells generated increased IFN-gamma and decreased IL-4 compared with B6.G7 CD4(+) T cells, regardless of whether they were stimulated with NOD or B6.G7 APCs. |
| 2954 | 12444170 | Cell cycle analysis showed that the cytokine differences were not due to cycle/proliferative differences between NOD and B6.G7, since stimulated CD4(+) T cells from both strains showed quantitatively identical entry into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater numbers of IFN-gamma-positive cells with each subsequent cell division. |
| 2955 | 12444170 | Moreover, 7-aminoactinomycin D and 5-bromo-2'-deoxyuridine analysis showed indistinguishable entry into G(0)/G(1), S, and G(2)/M phases of the cell cycle for both NOD and B6.G7 CD4(+) cells, with both strains generating IFN-gamma predominantly in the S phase. |
| 2956 | 12444170 | Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. |
| 2957 | 12444170 | In this study, we demonstrate that increased IFN-gamma, decreased IL-4, and decreased IL-10 production in NOD T cells is CD4 T cell intrinsic. |
| 2958 | 12444170 | NOD CD4(+) T cells purified and stimulated with anti-CD3/anti-CD28 Abs generated greater IFN-gamma, less IL-4, and less IL-10 than B6.G7 CD4(+) T cells. |
| 2959 | 12444170 | Moreover, the increased IFN-gamma:IL-4 cytokine ratio was independent of the genetic background of APCs, since NOD CD4(+) T cells generated increased IFN-gamma and decreased IL-4 compared with B6.G7 CD4(+) T cells, regardless of whether they were stimulated with NOD or B6.G7 APCs. |
| 2960 | 12444170 | Cell cycle analysis showed that the cytokine differences were not due to cycle/proliferative differences between NOD and B6.G7, since stimulated CD4(+) T cells from both strains showed quantitatively identical entry into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater numbers of IFN-gamma-positive cells with each subsequent cell division. |
| 2961 | 12444170 | Moreover, 7-aminoactinomycin D and 5-bromo-2'-deoxyuridine analysis showed indistinguishable entry into G(0)/G(1), S, and G(2)/M phases of the cell cycle for both NOD and B6.G7 CD4(+) cells, with both strains generating IFN-gamma predominantly in the S phase. |
| 2962 | 12444170 | Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. |
| 2963 | 12444170 | In this study, we demonstrate that increased IFN-gamma, decreased IL-4, and decreased IL-10 production in NOD T cells is CD4 T cell intrinsic. |
| 2964 | 12444170 | NOD CD4(+) T cells purified and stimulated with anti-CD3/anti-CD28 Abs generated greater IFN-gamma, less IL-4, and less IL-10 than B6.G7 CD4(+) T cells. |
| 2965 | 12444170 | Moreover, the increased IFN-gamma:IL-4 cytokine ratio was independent of the genetic background of APCs, since NOD CD4(+) T cells generated increased IFN-gamma and decreased IL-4 compared with B6.G7 CD4(+) T cells, regardless of whether they were stimulated with NOD or B6.G7 APCs. |
| 2966 | 12444170 | Cell cycle analysis showed that the cytokine differences were not due to cycle/proliferative differences between NOD and B6.G7, since stimulated CD4(+) T cells from both strains showed quantitatively identical entry into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater numbers of IFN-gamma-positive cells with each subsequent cell division. |
| 2967 | 12444170 | Moreover, 7-aminoactinomycin D and 5-bromo-2'-deoxyuridine analysis showed indistinguishable entry into G(0)/G(1), S, and G(2)/M phases of the cell cycle for both NOD and B6.G7 CD4(+) cells, with both strains generating IFN-gamma predominantly in the S phase. |
| 2968 | 12444170 | Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. |
| 2969 | 12444170 | In this study, we demonstrate that increased IFN-gamma, decreased IL-4, and decreased IL-10 production in NOD T cells is CD4 T cell intrinsic. |
| 2970 | 12444170 | NOD CD4(+) T cells purified and stimulated with anti-CD3/anti-CD28 Abs generated greater IFN-gamma, less IL-4, and less IL-10 than B6.G7 CD4(+) T cells. |
| 2971 | 12444170 | Moreover, the increased IFN-gamma:IL-4 cytokine ratio was independent of the genetic background of APCs, since NOD CD4(+) T cells generated increased IFN-gamma and decreased IL-4 compared with B6.G7 CD4(+) T cells, regardless of whether they were stimulated with NOD or B6.G7 APCs. |
| 2972 | 12444170 | Cell cycle analysis showed that the cytokine differences were not due to cycle/proliferative differences between NOD and B6.G7, since stimulated CD4(+) T cells from both strains showed quantitatively identical entry into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater numbers of IFN-gamma-positive cells with each subsequent cell division. |
| 2973 | 12444170 | Moreover, 7-aminoactinomycin D and 5-bromo-2'-deoxyuridine analysis showed indistinguishable entry into G(0)/G(1), S, and G(2)/M phases of the cell cycle for both NOD and B6.G7 CD4(+) cells, with both strains generating IFN-gamma predominantly in the S phase. |
| 2974 | 12444170 | Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. |
| 2975 | 12444170 | In this study, we demonstrate that increased IFN-gamma, decreased IL-4, and decreased IL-10 production in NOD T cells is CD4 T cell intrinsic. |
| 2976 | 12444170 | NOD CD4(+) T cells purified and stimulated with anti-CD3/anti-CD28 Abs generated greater IFN-gamma, less IL-4, and less IL-10 than B6.G7 CD4(+) T cells. |
| 2977 | 12444170 | Moreover, the increased IFN-gamma:IL-4 cytokine ratio was independent of the genetic background of APCs, since NOD CD4(+) T cells generated increased IFN-gamma and decreased IL-4 compared with B6.G7 CD4(+) T cells, regardless of whether they were stimulated with NOD or B6.G7 APCs. |
| 2978 | 12444170 | Cell cycle analysis showed that the cytokine differences were not due to cycle/proliferative differences between NOD and B6.G7, since stimulated CD4(+) T cells from both strains showed quantitatively identical entry into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater numbers of IFN-gamma-positive cells with each subsequent cell division. |
| 2979 | 12444170 | Moreover, 7-aminoactinomycin D and 5-bromo-2'-deoxyuridine analysis showed indistinguishable entry into G(0)/G(1), S, and G(2)/M phases of the cell cycle for both NOD and B6.G7 CD4(+) cells, with both strains generating IFN-gamma predominantly in the S phase. |
| 2980 | 12444170 | Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. |
| 2981 | 12444170 | In this study, we demonstrate that increased IFN-gamma, decreased IL-4, and decreased IL-10 production in NOD T cells is CD4 T cell intrinsic. |
| 2982 | 12444170 | NOD CD4(+) T cells purified and stimulated with anti-CD3/anti-CD28 Abs generated greater IFN-gamma, less IL-4, and less IL-10 than B6.G7 CD4(+) T cells. |
| 2983 | 12444170 | Moreover, the increased IFN-gamma:IL-4 cytokine ratio was independent of the genetic background of APCs, since NOD CD4(+) T cells generated increased IFN-gamma and decreased IL-4 compared with B6.G7 CD4(+) T cells, regardless of whether they were stimulated with NOD or B6.G7 APCs. |
| 2984 | 12444170 | Cell cycle analysis showed that the cytokine differences were not due to cycle/proliferative differences between NOD and B6.G7, since stimulated CD4(+) T cells from both strains showed quantitatively identical entry into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater numbers of IFN-gamma-positive cells with each subsequent cell division. |
| 2985 | 12444170 | Moreover, 7-aminoactinomycin D and 5-bromo-2'-deoxyuridine analysis showed indistinguishable entry into G(0)/G(1), S, and G(2)/M phases of the cell cycle for both NOD and B6.G7 CD4(+) cells, with both strains generating IFN-gamma predominantly in the S phase. |
| 2986 | 12451259 | Role of CD4+ and CD8+ T cells in the rejection of concordant pancreas xenografts. |
| 2987 | 12464673 | CCR4 was found exclusively on memory CD4(+) T cells during the progression of disease in NOD mice. |
| 2988 | 12464673 | Cells expressing the CCR4 ligand TARC (thymus- and activation-regulated chemokine) were detected within infiltrated islets from prediabetic mice. |
| 2989 | 12464673 | Interestingly, neutralization of macrophage-derived chemokine (MDC) with Ab caused a significant reduction of CCR4-positive T cells within the pancreatic infiltrates and inhibited the development of insulitis and diabetes. |
| 2990 | 12464673 | Furthermore, enhanced recruitment of CCR4-bearing cells in NOD mice resulting from transgenic expression of MDC resulted in acceleration of clinical disease. |
| 2991 | 12473243 | Purified CD62L+CD4+ cells from CTB-insulin fed mice significantly reduced the capacity of diabetogenic T cells to transfer diabetes in syngeneic recipients. |
| 2992 | 12473243 | In vitro stimulated CD62L+CD4+ cells from the spleen of fed animals secreted lower amounts of IL-4 and IL-10 but comparable levels of TGFbeta than CD62L-cells. |
| 2993 | 12473243 | A reduced IFN-gamma production between the two cell subsets was specifically observed in CTB-insulin fed mice. |
| 2994 | 12473243 | Taken together, our results suggest that L-selectin and alpha4-integrin have distinct but complementary roles in the generation and function of regulatory CD4+ T cells following CTB-insulin administration. |
| 2995 | 12473243 | Purified CD62L+CD4+ cells from CTB-insulin fed mice significantly reduced the capacity of diabetogenic T cells to transfer diabetes in syngeneic recipients. |
| 2996 | 12473243 | In vitro stimulated CD62L+CD4+ cells from the spleen of fed animals secreted lower amounts of IL-4 and IL-10 but comparable levels of TGFbeta than CD62L-cells. |
| 2997 | 12473243 | A reduced IFN-gamma production between the two cell subsets was specifically observed in CTB-insulin fed mice. |
| 2998 | 12473243 | Taken together, our results suggest that L-selectin and alpha4-integrin have distinct but complementary roles in the generation and function of regulatory CD4+ T cells following CTB-insulin administration. |
| 2999 | 12473243 | Purified CD62L+CD4+ cells from CTB-insulin fed mice significantly reduced the capacity of diabetogenic T cells to transfer diabetes in syngeneic recipients. |
| 3000 | 12473243 | In vitro stimulated CD62L+CD4+ cells from the spleen of fed animals secreted lower amounts of IL-4 and IL-10 but comparable levels of TGFbeta than CD62L-cells. |
| 3001 | 12473243 | A reduced IFN-gamma production between the two cell subsets was specifically observed in CTB-insulin fed mice. |
| 3002 | 12473243 | Taken together, our results suggest that L-selectin and alpha4-integrin have distinct but complementary roles in the generation and function of regulatory CD4+ T cells following CTB-insulin administration. |
| 3003 | 12479819 | The presence of NKT cells did not block the initial activation and expansion of the CD4(+) T cells but did inhibit their IL-2 and IFN-gamma production and later proliferation, resulting in an anergic phenotype. |
| 3004 | 12500188 | These observations were further confirmed by the results of CD4(+) enzyme-linked immunospot assay for interferon (IFN)-gamma and interleukin (IL)-4 and intracellular cytokine staining of IFN-gamma producing CD8(+) cells. |
| 3005 | 12502802 | A comparison of the frequency of gamma interferon (IFN-gamma)-producing CD4(+) and CD8(+) T cells in peripheral blood by ELISpot assay did not reveal any correlation between viral clearance and T-cell responses. |
| 3006 | 12502802 | In addition, analyses of IFN-gamma, IFN-alpha, and interleukin-4 mRNA levels in liver biopsies, presumably indicative of intrahepatic T-cell responses, revealed no distinct pattern in these chimpanzees with respect to infection outcome. |
| 3007 | 12517935 | Either IL-2 or IL-12 is sufficient to direct Th1 differentiation by nonobese diabetic T cells. |
| 3008 | 12517935 | We found that CD4(+) T cells from nonobese diabetic mice spontaneously differentiate into IFN-gamma-producing Th1 cells in response to polyclonal TCR stimulation in the absence of IL-12 and IFN-gamma. |
| 3009 | 12517935 | Instead, IL-2 was necessary and sufficient to direct T cell differentiation to the Th1 lineage by nonobese diabetic CD4(+) T cells. |
| 3010 | 12517935 | Either IL-2 or IL-12 is sufficient to direct Th1 differentiation by nonobese diabetic T cells. |
| 3011 | 12517935 | We found that CD4(+) T cells from nonobese diabetic mice spontaneously differentiate into IFN-gamma-producing Th1 cells in response to polyclonal TCR stimulation in the absence of IL-12 and IFN-gamma. |
| 3012 | 12517935 | Instead, IL-2 was necessary and sufficient to direct T cell differentiation to the Th1 lineage by nonobese diabetic CD4(+) T cells. |
| 3013 | 12520519 | Dendritic cells (DCs) not only induce but also modulate T cell activation. 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] induces DCs with a tolerogenic phenotype, characterized by decreased expression of CD40, CD80, and CD86 costimulatory molecules, low IL-12 and enhanced IL-10 secretion. |
| 3014 | 12520519 | The enhancement of CD4(+)CD25(+) regulatory T cells, able to mediate transplantation tolerance and to arrest type 1 diabetes development by a short oral treatment with VDR ligands, suggests possible clinical applications of this approach. |
| 3015 | 12538715 | FcR-binding "classical" anti-CD3 mAb is a potent immunosuppressive drug that alters CD4(+) and CD8(+) T cell function in vivo via anergy induction and programmed cell death (PCD). |
| 3016 | 12538715 | Anti-CD3-mediated PCD was Fas independent but was mediated by the mitochondria-initiated apoptosis that was abrogated in Bcl-x(L)-transgenic T cells. |
| 3017 | 12538715 | The PCD was more pronounced in CD28-deficient mice consistent with defective Bcl-x(L) up-regulation. |
| 3018 | 12538715 | Residual T cells isolated from anti-CD3-treated wild-type, CD28(-/-), and Bcl-x(L)-transgenic mice were hyporesponsive. |
| 3019 | 12538715 | The hyporesponsiveness was more pronounced in CD28(-/-) and wild-type mice treated with anti-B7-2, suggesting that CD28 interaction with B7-2 regulates T cell responsiveness in anti-CD3-treated animals. |
| 3020 | 12540604 | Specifically, and contrary to published reports, the thymocyte subset distribution, the rate and composition of thymic export, and the composition of the peripheral T-cell pool, including the proportion of CD25(+)CD4(+) T-cells, are essentially normal in prediabetic NOD mice. |
| 3021 | 12540606 | Accelerated diabetes in rat insulin promoter-tumor necrosis factor-alpha transgenic nonobese diabetic mice lacking major histocompatibility class II molecules. |
| 3022 | 12540606 | Surprisingly, although diabetes was evident in the F1 intercross expressing rat insulin promoter (RIP)-TNF, offspring lacking either endogenous or transgenic class II molecules developed accelerated diabetes with high frequency in both sexes. |
| 3023 | 12540606 | Thus, neonatal expression of TNF-alpha in an islet-specific manner bypassed the requirement of CD4(+) T-cells and resulted in diabetes that could be mediated by CD8(+) T-cells. |
| 3024 | 12559622 | We found that the myocardium of these patients was infiltrated by CD4(+) and CD8(+) T lymphocytes as well as macrophages. |
| 3025 | 12559622 | Finally, mRNA for interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha was detected in the cardiac specimens, although at a lower level compared with specimens from hearts without signs of viral infections. |
| 3026 | 12563296 | Recent data indicate that transforming growth factor-beta-dependent CD4+CD25+ regulatory T cells might have a central role in this effect. |
| 3027 | 12569167 | In a trial of an FcR nonbinding humanized anti-CD3 mAb hOKT3gamma1(Ala-Ala) for treatment of patients with type 1 diabetes, we found significant increases in IL-10 and IL-5 in the serum of 63% and 72% of patients, respectively, and TNF-alpha and IL-6 levels that were lower than those previously reported following OKT3 therapy. |
| 3028 | 12569167 | However, the production of IL-10, compared to IFN-gamma on a molar basis, was greater after culture with hOKT3gamma1(Ala-Ala) than with OKT3. |
| 3029 | 12569167 | Flow cytometric studies confirmed that OKT3 induced IFN-gamma and IL-10 production, but hOKT3gamma1(Ala-Ala) induced only detectable IL-10 production in CD45RO(+) cells. |
| 3030 | 12569167 | Moreover, in vivo, we found IL-10(+)CD4(+) T cells after drug treatment. |
| 3031 | 12569167 | These cells were heterogeneous but generally CD45RO(+), CTLA-4(-), and expressed CCR4. |
| 3032 | 12574341 | This hyperactivation was detected for different NF-kappaB complexes and correlated with increased IkappaBalpha degradation. |
| 3033 | 12574341 | Furthermore, increased NF-kappaB activation resulted in an enhanced capacity of NOD vs NOR or BALB/c Mphi to secrete IL-12(p70), TNF-alpha, and IL-1alpha, which was inhibited upon infection with an adenoviral recombinant encoding a modified form of IkappaBalpha. |
| 3034 | 12574341 | In contrast, elevated NF-kappaB activation had no significant effect on the capacity of NOD Mphi to stimulate CD4(+) or CD8(+) T cells in an Ag-specific manner. |
| 3035 | 12594305 | Skewing their cytokine production from a Th1 (primarily IFN-gamma) to a Th2 (primarily IL-4 and IL-10) pattern is a widely proposed approach to dampen the pathogenicity of autoreactive diabetogenic T cells. |
| 3036 | 12594305 | Murine CD4 T cells are characterized by a reciprocal relationship between the production of IFN-gamma and expression of the beta-chain component of its receptor (IFN-gamma RB). |
| 3037 | 12594305 | Thus, NOD mice constitutively expressing a CD2 promoter-driven IFN-gamma RB transgene in all T cells are Th1-deficient. |
| 3038 | 12604308 | We report that insulin promoter murine CD80 (RIP-CD80) transgenic mice are extraordinarily susceptible to autoantigen-induced diabetes, while spontaneous disease is rare. |
| 3039 | 12604308 | While both RIP-GP(+)and RIP-CD80(+)GP(+)mice mounted moderate CD4-independent CTL responses, only CD80(+)GP(+)mice developed severe insulitis and diabetes due to islet-infiltration of activated, gp33-specific, CD8(+)T cells. |
| 3040 | 12604308 | We conclude that aberrant CD80-expression in a peripheral tissue disrupts that tissue's natural resistance to CD8 T cell-mediated autoimmune destruction. |
| 3041 | 12604315 | We have recently reported that in patients with anti-glutamic acid decarboxylase (GAD) 65(+)diabetes with residual beta-cell function, most with a 'high-titer' (>10U/ml) required insulin within 5 years, whereas most with a 'low-titer' (1.3-9.9U/ml) did not need insulin for over 15-20 years after the onset. |
| 3042 | 12604315 | Although GAD65-reactive CD4(+)cells in the periphery were detected in both groups, a significant positive correlation between serum IP-10 level and the number of GAD65-reactive CD4(+)cells was observed only in the high-titer group. |
| 3043 | 12604315 | Therefore, it has been speculated that the co-existence of GAD65-reactive IFN-gamma-producing CD4(+)cells and a high serum IP-10 level may be important for rapid disease progression as seen in the high-titer group. |
| 3044 | 12604315 | We have recently reported that in patients with anti-glutamic acid decarboxylase (GAD) 65(+)diabetes with residual beta-cell function, most with a 'high-titer' (>10U/ml) required insulin within 5 years, whereas most with a 'low-titer' (1.3-9.9U/ml) did not need insulin for over 15-20 years after the onset. |
| 3045 | 12604315 | Although GAD65-reactive CD4(+)cells in the periphery were detected in both groups, a significant positive correlation between serum IP-10 level and the number of GAD65-reactive CD4(+)cells was observed only in the high-titer group. |
| 3046 | 12604315 | Therefore, it has been speculated that the co-existence of GAD65-reactive IFN-gamma-producing CD4(+)cells and a high serum IP-10 level may be important for rapid disease progression as seen in the high-titer group. |
| 3047 | 12618479 | A crucial role of CD4 T cells as a functional source of CD154 in the initiation of insulin-dependent diabetes mellitus in the non-obese diabetic mouse. |
| 3048 | 12618479 | Although the critical requirement of CD4 T cells in type I (insulin-dependent) diabetes mellitus (T1DM) has been well documented, information on the exact role(s) of CD4 T cells in T1DM development is still limited. |
| 3049 | 12618479 | Without CD154, CD4 T cells were not capable of mediating help in disease development in NOD mice. |
| 3050 | 12618479 | Taken collectively, these results indicated that CD4 T cells play a crucial role in T1DM as a source of CD154, and that the role of CD154 on CD4 T cells in insulitis may not be just to facilitate priming and expanding of auto-reactive CD8 T cells by activating antigen-presenting cells bearing islet antigens. |
| 3051 | 12618479 | A crucial role of CD4 T cells as a functional source of CD154 in the initiation of insulin-dependent diabetes mellitus in the non-obese diabetic mouse. |
| 3052 | 12618479 | Although the critical requirement of CD4 T cells in type I (insulin-dependent) diabetes mellitus (T1DM) has been well documented, information on the exact role(s) of CD4 T cells in T1DM development is still limited. |
| 3053 | 12618479 | Without CD154, CD4 T cells were not capable of mediating help in disease development in NOD mice. |
| 3054 | 12618479 | Taken collectively, these results indicated that CD4 T cells play a crucial role in T1DM as a source of CD154, and that the role of CD154 on CD4 T cells in insulitis may not be just to facilitate priming and expanding of auto-reactive CD8 T cells by activating antigen-presenting cells bearing islet antigens. |
| 3055 | 12618479 | A crucial role of CD4 T cells as a functional source of CD154 in the initiation of insulin-dependent diabetes mellitus in the non-obese diabetic mouse. |
| 3056 | 12618479 | Although the critical requirement of CD4 T cells in type I (insulin-dependent) diabetes mellitus (T1DM) has been well documented, information on the exact role(s) of CD4 T cells in T1DM development is still limited. |
| 3057 | 12618479 | Without CD154, CD4 T cells were not capable of mediating help in disease development in NOD mice. |
| 3058 | 12618479 | Taken collectively, these results indicated that CD4 T cells play a crucial role in T1DM as a source of CD154, and that the role of CD154 on CD4 T cells in insulitis may not be just to facilitate priming and expanding of auto-reactive CD8 T cells by activating antigen-presenting cells bearing islet antigens. |
| 3059 | 12618479 | A crucial role of CD4 T cells as a functional source of CD154 in the initiation of insulin-dependent diabetes mellitus in the non-obese diabetic mouse. |
| 3060 | 12618479 | Although the critical requirement of CD4 T cells in type I (insulin-dependent) diabetes mellitus (T1DM) has been well documented, information on the exact role(s) of CD4 T cells in T1DM development is still limited. |
| 3061 | 12618479 | Without CD154, CD4 T cells were not capable of mediating help in disease development in NOD mice. |
| 3062 | 12618479 | Taken collectively, these results indicated that CD4 T cells play a crucial role in T1DM as a source of CD154, and that the role of CD154 on CD4 T cells in insulitis may not be just to facilitate priming and expanding of auto-reactive CD8 T cells by activating antigen-presenting cells bearing islet antigens. |
| 3063 | 12641818 | Also CD4+ and CD8+ lymphocytes infiltrated in and/or around pancreatic islets in the CpG ODN-treated mice. |
| 3064 | 12646622 | Infections that induce autoimmune diabetes in BBDR rats modulate CD4+CD25+ T cell populations. |
| 3065 | 12646622 | Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4(+)CD25(+) T cells in both BBDR rats and normal WF rats. |
| 3066 | 12646622 | Surprisingly, RV infection increased CD4(+)CD25(+) T cells in pancreatic lymph nodes of BBDR but not WF rats. |
| 3067 | 12646622 | This increase appeared to be due to the accumulation of nonproliferating CD4(+)CD25(+) T cells. |
| 3068 | 12646622 | The results imply that the reduction in splenic CD4(+)CD25(+) cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4(+)CD25(+) cells is both virus and rat strain specific. |
| 3069 | 12646622 | More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulatory CD4(+)CD25(+) T cell function. |
| 3070 | 12646622 | Infections that induce autoimmune diabetes in BBDR rats modulate CD4+CD25+ T cell populations. |
| 3071 | 12646622 | Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4(+)CD25(+) T cells in both BBDR rats and normal WF rats. |
| 3072 | 12646622 | Surprisingly, RV infection increased CD4(+)CD25(+) T cells in pancreatic lymph nodes of BBDR but not WF rats. |
| 3073 | 12646622 | This increase appeared to be due to the accumulation of nonproliferating CD4(+)CD25(+) T cells. |
| 3074 | 12646622 | The results imply that the reduction in splenic CD4(+)CD25(+) cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4(+)CD25(+) cells is both virus and rat strain specific. |
| 3075 | 12646622 | More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulatory CD4(+)CD25(+) T cell function. |
| 3076 | 12646622 | Infections that induce autoimmune diabetes in BBDR rats modulate CD4+CD25+ T cell populations. |
| 3077 | 12646622 | Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4(+)CD25(+) T cells in both BBDR rats and normal WF rats. |
| 3078 | 12646622 | Surprisingly, RV infection increased CD4(+)CD25(+) T cells in pancreatic lymph nodes of BBDR but not WF rats. |
| 3079 | 12646622 | This increase appeared to be due to the accumulation of nonproliferating CD4(+)CD25(+) T cells. |
| 3080 | 12646622 | The results imply that the reduction in splenic CD4(+)CD25(+) cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4(+)CD25(+) cells is both virus and rat strain specific. |
| 3081 | 12646622 | More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulatory CD4(+)CD25(+) T cell function. |
| 3082 | 12646622 | Infections that induce autoimmune diabetes in BBDR rats modulate CD4+CD25+ T cell populations. |
| 3083 | 12646622 | Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4(+)CD25(+) T cells in both BBDR rats and normal WF rats. |
| 3084 | 12646622 | Surprisingly, RV infection increased CD4(+)CD25(+) T cells in pancreatic lymph nodes of BBDR but not WF rats. |
| 3085 | 12646622 | This increase appeared to be due to the accumulation of nonproliferating CD4(+)CD25(+) T cells. |
| 3086 | 12646622 | The results imply that the reduction in splenic CD4(+)CD25(+) cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4(+)CD25(+) cells is both virus and rat strain specific. |
| 3087 | 12646622 | More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulatory CD4(+)CD25(+) T cell function. |
| 3088 | 12646622 | Infections that induce autoimmune diabetes in BBDR rats modulate CD4+CD25+ T cell populations. |
| 3089 | 12646622 | Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4(+)CD25(+) T cells in both BBDR rats and normal WF rats. |
| 3090 | 12646622 | Surprisingly, RV infection increased CD4(+)CD25(+) T cells in pancreatic lymph nodes of BBDR but not WF rats. |
| 3091 | 12646622 | This increase appeared to be due to the accumulation of nonproliferating CD4(+)CD25(+) T cells. |
| 3092 | 12646622 | The results imply that the reduction in splenic CD4(+)CD25(+) cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4(+)CD25(+) cells is both virus and rat strain specific. |
| 3093 | 12646622 | More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulatory CD4(+)CD25(+) T cell function. |
| 3094 | 12646622 | Infections that induce autoimmune diabetes in BBDR rats modulate CD4+CD25+ T cell populations. |
| 3095 | 12646622 | Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4(+)CD25(+) T cells in both BBDR rats and normal WF rats. |
| 3096 | 12646622 | Surprisingly, RV infection increased CD4(+)CD25(+) T cells in pancreatic lymph nodes of BBDR but not WF rats. |
| 3097 | 12646622 | This increase appeared to be due to the accumulation of nonproliferating CD4(+)CD25(+) T cells. |
| 3098 | 12646622 | The results imply that the reduction in splenic CD4(+)CD25(+) cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4(+)CD25(+) cells is both virus and rat strain specific. |
| 3099 | 12646622 | More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulatory CD4(+)CD25(+) T cell function. |
| 3100 | 12657523 | Both the CD4(+) and CD8(+) subsets of T cells are required for the normal development of IDDM in NOD mice. |
| 3101 | 12657523 | We have isolated a GAD(65) reactive, cytotoxic CD8(+) T cell clone R1 that produces large quantities of IFNgamma and accelerates the onset of insulitis. |
| 3102 | 12657523 | This clone proliferates and produces IFNgamma in response to GAD(65) presenting APCs and kills GAD(65) presenting targets. |
| 3103 | 12657523 | Furthermore, it expresses TNFalpha, CD25, CD28, CD44, CD45 and LFA1, but not CD95L This is the first example of a GAD(65)specific CD8(+) T cell clone that accelerates the onset of the insulitis, although it does not appear to accelerate the onset of diabetes. |
| 3104 | 12663785 | Kinetics of CD4+ and CD8+ memory T-cell responses during hepatitis C virus rechallenge of previously recovered chimpanzees. |
| 3105 | 12663785 | The animal that most rapidly cleared circulating HCV as determined by nested reverse transcription-PCR (RT-PCR) displayed the most vigorous and sustained response of gamma interferon (IFN-gamma)-producing and proliferating CD4(+) T cells in the blood. |
| 3106 | 12663785 | Vigorous CD4(+) T-cell proliferation during viremia was followed by an increased frequency and a phenotypic and functional change of the tetramer(+) CD8(+) T-cell population. |
| 3107 | 12663785 | Kinetics of CD4+ and CD8+ memory T-cell responses during hepatitis C virus rechallenge of previously recovered chimpanzees. |
| 3108 | 12663785 | The animal that most rapidly cleared circulating HCV as determined by nested reverse transcription-PCR (RT-PCR) displayed the most vigorous and sustained response of gamma interferon (IFN-gamma)-producing and proliferating CD4(+) T cells in the blood. |
| 3109 | 12663785 | Vigorous CD4(+) T-cell proliferation during viremia was followed by an increased frequency and a phenotypic and functional change of the tetramer(+) CD8(+) T-cell population. |
| 3110 | 12663785 | Kinetics of CD4+ and CD8+ memory T-cell responses during hepatitis C virus rechallenge of previously recovered chimpanzees. |
| 3111 | 12663785 | The animal that most rapidly cleared circulating HCV as determined by nested reverse transcription-PCR (RT-PCR) displayed the most vigorous and sustained response of gamma interferon (IFN-gamma)-producing and proliferating CD4(+) T cells in the blood. |
| 3112 | 12663785 | Vigorous CD4(+) T-cell proliferation during viremia was followed by an increased frequency and a phenotypic and functional change of the tetramer(+) CD8(+) T-cell population. |
| 3113 | 12694582 | Preceding the clinical diagnosis of type I DM is a preclinical stage characterized by autoantibodies to insulin, glutamic acid decarboxylase (GAD) and a tyrosine phosphatase-like molecule (IA-2). |
| 3114 | 12694582 | In contrast, the progression to clinical disease appears associated with class I alleles A24, A30 and B18 while A1, A28, B14 and B56 appear negatively associated. |
| 3115 | 12694582 | These results are consistent with the view that CD4+ T cells responding to peptides in the context of class 2 molecules are responsible for initiating autoantibody production, while the destruction of islet cells leading to clinical expression of the disease is the function of CD8+ T cells recognizing relevant peptides in the context of class I molecules. |
| 3116 | 12697265 | In humans, genetic defects decreasing Fas function cause the Autoimmune Lymphoproliferative Syndrome (ALPS) where autoimmunities are associated with accumulation of polyclonal lymphocytes in the secondary lymphoid tissues and expansion of T cells lacking both CD4 and CD8 (DN cells). |
| 3117 | 12711326 | Prevention of autoimmune diabetes in NOD mice by troglitazone is associated with modulation of ICAM-1 expression on pancreatic islet cells and IFN-gamma expression in splenic T cells. |
| 3118 | 12711326 | Thiazolidinediones acting as PPAR-gamma agonists are a new generation of oral antidiabetics addressing insulin resistance as a main feature of type-2 diabetes. |
| 3119 | 12711326 | To investigate whether TGZ acts by affecting the ICAM-1/LFA-1 pathway and/or the Th1/Th2 cytokine balance in NOD mice, we analysed the IL-1beta-induced ICAM-1 expression on islet-cells and the LFA-1, CD25, IL-2, IFN-gamma, IL-4, and IL-10 expression on splenocytes. |
| 3120 | 12711326 | After 200 days of oral TGZ administration, islet cells from TGZ-treated NOD mice showed a reduced ICAM-1 expression in response to the pro-inflammatory cytokine IL-1beta. |
| 3121 | 12711326 | The expression of the ligand LFA-1 on CD4(+) and CD8(+) T-cells was comparable to that of placebo- and untreated controls. |
| 3122 | 12727648 | Dendritic cells (DCs) not only induce but also modulate T cell activation. 1,25-Dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)] induces DCs with a tolerogenic phenotype, characterized by decreased expression of CD40, CD80, and CD86 co-stimulatory molecules, low IL-12, and enhanced IL-10 secretion. |
| 3123 | 12727648 | Graft acceptance is associated with impaired development of type 1 CD4(+) and CD8(+) cells and an increased percentage of CD4(+)CD25(+) regulatory cells expressing CD152 in the spleen and in the draining lymph node. |
| 3124 | 12727648 | CD4(+)CD25(+) cells that are able to inhibit the T cell response to a pancreatic autoantigen and to significantly delay disease transfer by pathogenic CD4(+)CD25(-) cells are also induced by treatment of adult nonobese diabetic (NOD) mice with a selected vitamin D receptor (VDR) ligand. |
| 3125 | 12727648 | The enhancement of CD4(+)CD25(+) regulatory T cells able to mediate transplantation tolerance and to arrest type 1 diabetes development by a short oral treatment with small organic compounds that induce tolerogenic DCs, like VDR ligands, suggests possible clinical applications of this approach. |
| 3126 | 12727648 | Dendritic cells (DCs) not only induce but also modulate T cell activation. 1,25-Dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)] induces DCs with a tolerogenic phenotype, characterized by decreased expression of CD40, CD80, and CD86 co-stimulatory molecules, low IL-12, and enhanced IL-10 secretion. |
| 3127 | 12727648 | Graft acceptance is associated with impaired development of type 1 CD4(+) and CD8(+) cells and an increased percentage of CD4(+)CD25(+) regulatory cells expressing CD152 in the spleen and in the draining lymph node. |
| 3128 | 12727648 | CD4(+)CD25(+) cells that are able to inhibit the T cell response to a pancreatic autoantigen and to significantly delay disease transfer by pathogenic CD4(+)CD25(-) cells are also induced by treatment of adult nonobese diabetic (NOD) mice with a selected vitamin D receptor (VDR) ligand. |
| 3129 | 12727648 | The enhancement of CD4(+)CD25(+) regulatory T cells able to mediate transplantation tolerance and to arrest type 1 diabetes development by a short oral treatment with small organic compounds that induce tolerogenic DCs, like VDR ligands, suggests possible clinical applications of this approach. |
| 3130 | 12727648 | Dendritic cells (DCs) not only induce but also modulate T cell activation. 1,25-Dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)] induces DCs with a tolerogenic phenotype, characterized by decreased expression of CD40, CD80, and CD86 co-stimulatory molecules, low IL-12, and enhanced IL-10 secretion. |
| 3131 | 12727648 | Graft acceptance is associated with impaired development of type 1 CD4(+) and CD8(+) cells and an increased percentage of CD4(+)CD25(+) regulatory cells expressing CD152 in the spleen and in the draining lymph node. |
| 3132 | 12727648 | CD4(+)CD25(+) cells that are able to inhibit the T cell response to a pancreatic autoantigen and to significantly delay disease transfer by pathogenic CD4(+)CD25(-) cells are also induced by treatment of adult nonobese diabetic (NOD) mice with a selected vitamin D receptor (VDR) ligand. |
| 3133 | 12727648 | The enhancement of CD4(+)CD25(+) regulatory T cells able to mediate transplantation tolerance and to arrest type 1 diabetes development by a short oral treatment with small organic compounds that induce tolerogenic DCs, like VDR ligands, suggests possible clinical applications of this approach. |
| 3134 | 12727928 | Here we show that proinsulin B24-C36 peptide binds to I-A(g7), the MHC class II molecule of the NOD mouse, and, after intranasal administration, induces regulatory CD4(+) T cells that, in the absence of CD8(+) T cells, block the adoptive transfer of diabetes. |
| 3135 | 12727928 | We then determined that B24-C36, and its core sequence B25-C34, bind to K(d), the NOD mouse MHC class I molecule, and elicit CD8(+) CTLs. |
| 3136 | 12727928 | When the CD8(+) T lymphocyte epitope was truncated at the C34 valine anchor residue for binding to K(d), the residual CD4(+) T cell epitope, B24-C32/33, significantly inhibited diabetes development after a single intranasal dose. |
| 3137 | 12727928 | Here we show that proinsulin B24-C36 peptide binds to I-A(g7), the MHC class II molecule of the NOD mouse, and, after intranasal administration, induces regulatory CD4(+) T cells that, in the absence of CD8(+) T cells, block the adoptive transfer of diabetes. |
| 3138 | 12727928 | We then determined that B24-C36, and its core sequence B25-C34, bind to K(d), the NOD mouse MHC class I molecule, and elicit CD8(+) CTLs. |
| 3139 | 12727928 | When the CD8(+) T lymphocyte epitope was truncated at the C34 valine anchor residue for binding to K(d), the residual CD4(+) T cell epitope, B24-C32/33, significantly inhibited diabetes development after a single intranasal dose. |
| 3140 | 12742378 | We have recently described an impaired proliferative response of CD4(+) T-cells to primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. |
| 3141 | 12742378 | In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the immune response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). |
| 3142 | 12742378 | Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the immune response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). |
| 3143 | 12742378 | Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). |
| 3144 | 12742378 | When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. |
| 3145 | 12742378 | We have recently described an impaired proliferative response of CD4(+) T-cells to primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. |
| 3146 | 12742378 | In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the immune response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). |
| 3147 | 12742378 | Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the immune response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). |
| 3148 | 12742378 | Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). |
| 3149 | 12742378 | When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. |
| 3150 | 12742378 | We have recently described an impaired proliferative response of CD4(+) T-cells to primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. |
| 3151 | 12742378 | In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the immune response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). |
| 3152 | 12742378 | Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the immune response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). |
| 3153 | 12742378 | Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). |
| 3154 | 12742378 | When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. |
| 3155 | 12742378 | We have recently described an impaired proliferative response of CD4(+) T-cells to primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. |
| 3156 | 12742378 | In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the immune response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). |
| 3157 | 12742378 | Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the immune response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). |
| 3158 | 12742378 | Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). |
| 3159 | 12742378 | When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. |
| 3160 | 12748380 | Adoptive transfer of lymphocytes from HCV-LP-immunized mice to naive mice provided protection against vvHCV.S challenge, and this transferred immunity can be abrogated by either CD4 or CD8 depletion. |
| 3161 | 12748380 | Our results suggest that HCV-LPs can induce humoral and cellular immune responses that are protective in a surrogate HCV challenge model and that a strong cellular immunity provided by both CD4 and CD8 effector lymphocytes may be important for protection from HCV infection. |
| 3162 | 12748380 | Adoptive transfer of lymphocytes from HCV-LP-immunized mice to naive mice provided protection against vvHCV.S challenge, and this transferred immunity can be abrogated by either CD4 or CD8 depletion. |
| 3163 | 12748380 | Our results suggest that HCV-LPs can induce humoral and cellular immune responses that are protective in a surrogate HCV challenge model and that a strong cellular immunity provided by both CD4 and CD8 effector lymphocytes may be important for protection from HCV infection. |
| 3164 | 12753807 | Moreover, both CD4(+)and CD8(+)subsets were affected. |
| 3165 | 12753807 | Gene expression analysis using real-time RT-PCR additionally revealed low expression of Fas and FasL, the death receptor system activating caspase 8 and contributing to AICD. |
| 3166 | 12759426 | IL-12 administration accelerates autoimmune diabetes in both wild-type and IFN-gamma-deficient nonobese diabetic mice, revealing pathogenic and protective effects of IL-12-induced IFN-gamma. |
| 3167 | 12759426 | IL-12 administration to nonobese diabetic (NOD) mice induces IFN-gamma-secreting type 1 T cells and high circulating IFN-gamma levels and accelerates insulin-dependent diabetes mellitus (IDDM). |
| 3168 | 12759426 | Here we show that IL-12-induced IFN-gamma production is dispensable for diabetes acceleration, because exogenous IL-12 could enhance IDDM development in IFN-gamma-deficient as well as in IFN-gamma-sufficient NOD mice. |
| 3169 | 12759426 | Both in IFN-gamma(+/-) and IFN-gamma(-/-) NOD mice, IL-12 administration generates a massive and destructive insulitis characterized by T cells, macrophages, and CD11c(+) dendritic cells, and increases the number of pancreatic CD4(+) cells secreting IL-2 and TNF-alpha. |
| 3170 | 12759426 | Surprisingly, IL-12-induced IFN-gamma hinders pancreatic B cell infiltration and inhibits the capacity of APCs to activate T cells. |
| 3171 | 12759426 | Although pancreatic CD4(+) T cells from IL-12-treated IFN-gamma(-/-) mice fail to up-regulate the P-selectin ligand, suggesting that their entry into the pancreas may be impaired, T cell expansion is favored in these mice compared with IL-12-treated IFN-gamma(+/-) mice because IL-12 administration in the absence of IFN-gamma leads to enhanced cell proliferation and reduced T cell apoptosis. |
| 3172 | 12759426 | NO, an effector molecule in beta cell destruction, is produced ex vivo in high quantity by pancreas-infiltrating cells through a mechanism involving IL-12-induced IFN-gamma. |
| 3173 | 12759426 | Conversely, in IL-12-treated IFN-gamma-deficient mice, other pathways of beta cell death appear to be increased, as indicated by the up-regulated expression of Fas ligand on Th1 cells in the absence of IFN-gamma. |
| 3174 | 12759426 | These data demonstrate that IFN-gamma has a dual role, pathogenic and protective, in IDDM development, and its deletion allows IL-12 to establish alternative pathways leading to diabetes acceleration. |
| 3175 | 12759426 | IL-12 administration accelerates autoimmune diabetes in both wild-type and IFN-gamma-deficient nonobese diabetic mice, revealing pathogenic and protective effects of IL-12-induced IFN-gamma. |
| 3176 | 12759426 | IL-12 administration to nonobese diabetic (NOD) mice induces IFN-gamma-secreting type 1 T cells and high circulating IFN-gamma levels and accelerates insulin-dependent diabetes mellitus (IDDM). |
| 3177 | 12759426 | Here we show that IL-12-induced IFN-gamma production is dispensable for diabetes acceleration, because exogenous IL-12 could enhance IDDM development in IFN-gamma-deficient as well as in IFN-gamma-sufficient NOD mice. |
| 3178 | 12759426 | Both in IFN-gamma(+/-) and IFN-gamma(-/-) NOD mice, IL-12 administration generates a massive and destructive insulitis characterized by T cells, macrophages, and CD11c(+) dendritic cells, and increases the number of pancreatic CD4(+) cells secreting IL-2 and TNF-alpha. |
| 3179 | 12759426 | Surprisingly, IL-12-induced IFN-gamma hinders pancreatic B cell infiltration and inhibits the capacity of APCs to activate T cells. |
| 3180 | 12759426 | Although pancreatic CD4(+) T cells from IL-12-treated IFN-gamma(-/-) mice fail to up-regulate the P-selectin ligand, suggesting that their entry into the pancreas may be impaired, T cell expansion is favored in these mice compared with IL-12-treated IFN-gamma(+/-) mice because IL-12 administration in the absence of IFN-gamma leads to enhanced cell proliferation and reduced T cell apoptosis. |
| 3181 | 12759426 | NO, an effector molecule in beta cell destruction, is produced ex vivo in high quantity by pancreas-infiltrating cells through a mechanism involving IL-12-induced IFN-gamma. |
| 3182 | 12759426 | Conversely, in IL-12-treated IFN-gamma-deficient mice, other pathways of beta cell death appear to be increased, as indicated by the up-regulated expression of Fas ligand on Th1 cells in the absence of IFN-gamma. |
| 3183 | 12759426 | These data demonstrate that IFN-gamma has a dual role, pathogenic and protective, in IDDM development, and its deletion allows IL-12 to establish alternative pathways leading to diabetes acceleration. |
| 3184 | 12763479 | TCR-activated NOD splenic CD4+ and CD8+ T cells are more resistant to AICD than control strain C57BL/6, BALB/c, and NOR T cells. |
| 3185 | 12763479 | NOR CD4+ but not CD8+ T cells are resistant to TCR-induced AICD. |
| 3186 | 12763479 | Whereas c-FLIP expression is reduced in activated T cells from control strains, it persists in activated NOD CD8+ T cells and is accompanied by diminished activity of caspase-3 and -8. |
| 3187 | 12763479 | IL-4 reduces this c-FLIP expression and increases caspase-3 and -8 activity in activated NOD CD8+ T cells. |
| 3188 | 12763479 | Moreover, IL-4 and CD28 costimulation restores the susceptibility of NOD CD8+ T cells to AICD, and this is associated with increased expression of CD25, CD95, CD95L, and TNFR2. |
| 3189 | 12763479 | TCR-activated NOD splenic CD4+ and CD8+ T cells are more resistant to AICD than control strain C57BL/6, BALB/c, and NOR T cells. |
| 3190 | 12763479 | NOR CD4+ but not CD8+ T cells are resistant to TCR-induced AICD. |
| 3191 | 12763479 | Whereas c-FLIP expression is reduced in activated T cells from control strains, it persists in activated NOD CD8+ T cells and is accompanied by diminished activity of caspase-3 and -8. |
| 3192 | 12763479 | IL-4 reduces this c-FLIP expression and increases caspase-3 and -8 activity in activated NOD CD8+ T cells. |
| 3193 | 12763479 | Moreover, IL-4 and CD28 costimulation restores the susceptibility of NOD CD8+ T cells to AICD, and this is associated with increased expression of CD25, CD95, CD95L, and TNFR2. |
| 3194 | 12765954 | Cellular xenograft rejection involves a pronounced contribution of CD4 T-cells recognizing antigens in association with recipient MHC class II molecules. |
| 3195 | 12765954 | Although all types of grafts rejected acutely in wild-type mice, this response demonstrated markedly differing dependence on host MHC class II antigen presentation, depending on the donor species. |
| 3196 | 12765955 | Reduced insulitis in L-AGE versus H-AGE mice (P < 0.01) was marked by GAD- and insulin-unresponsive pancreatic interleukin (IL)-4-positive CD4+ cells compared with the GAD- and insulin-responsive interferon (IFN)-gamma-positive T-cells from H-AGE mice (P < 0.005). |
| 3197 | 12765955 | Splenocytes from L-AGE mice consisted of GAD- and insulin-responsive IL-10-positive CD4+ cells compared with the IFN-gamma-positive T-cells from H-AGE mice (P < 0.005). |
| 3198 | 12765955 | Reduced insulitis in L-AGE versus H-AGE mice (P < 0.01) was marked by GAD- and insulin-unresponsive pancreatic interleukin (IL)-4-positive CD4+ cells compared with the GAD- and insulin-responsive interferon (IFN)-gamma-positive T-cells from H-AGE mice (P < 0.005). |
| 3199 | 12765955 | Splenocytes from L-AGE mice consisted of GAD- and insulin-responsive IL-10-positive CD4+ cells compared with the IFN-gamma-positive T-cells from H-AGE mice (P < 0.005). |
| 3200 | 12818140 | The %age number of CD19+, CD5+/CD20+ B lymphocytes and CD3+, CD4+, CD8+, CD4+/DR+, CD8+/DR+ T lymphocytes subpopulations were investigated in the peripheral blood. |
| 3201 | 12818140 | The elevated number of CD5+ B lymphocytes correlated with presence of activated lymphocytes T (CD4+/DR+ and CD8+/DR+). |
| 3202 | 12818140 | The total number of CD19+, CCD3+, CD4+, CD8+ lymphocytes was on comparable level in both groups. |
| 3203 | 12818140 | The %age number of CD19+, CD5+/CD20+ B lymphocytes and CD3+, CD4+, CD8+, CD4+/DR+, CD8+/DR+ T lymphocytes subpopulations were investigated in the peripheral blood. |
| 3204 | 12818140 | The elevated number of CD5+ B lymphocytes correlated with presence of activated lymphocytes T (CD4+/DR+ and CD8+/DR+). |
| 3205 | 12818140 | The total number of CD19+, CCD3+, CD4+, CD8+ lymphocytes was on comparable level in both groups. |
| 3206 | 12818140 | The %age number of CD19+, CD5+/CD20+ B lymphocytes and CD3+, CD4+, CD8+, CD4+/DR+, CD8+/DR+ T lymphocytes subpopulations were investigated in the peripheral blood. |
| 3207 | 12818140 | The elevated number of CD5+ B lymphocytes correlated with presence of activated lymphocytes T (CD4+/DR+ and CD8+/DR+). |
| 3208 | 12818140 | The total number of CD19+, CCD3+, CD4+, CD8+ lymphocytes was on comparable level in both groups. |
| 3209 | 12819471 | Clinically, IPEX manifests most commonly with diarrhea, insulin-dependent diabetes mellitus, thyroid disorders, and eczema. |
| 3210 | 12819471 | FOXP3, the gene responsible for IPEX, maps to chromosome Xp11.23-Xq13.3 and encodes a putative DNA-binding protein of the forkhead family. |
| 3211 | 12819471 | Recent data indicate that FOXP3 is expressed primarily in the CD4+CD25+ regulatory T-cell subset, where it may function as a transcriptional repressor and key modulator of regulatory T-cell fate and function. |
| 3212 | 12866664 | Concomitant with the insulin receptors, two other growth factor receptors (IGF-1 and IL-2) also emerge on the T lymphocyte cell surface along with intracellular signal transduction mechanisms and insulin degrading enzyme (IDE). |
| 3213 | 12866664 | In activated T-lymphocytes, insulin stimulates glucose uptake, glucose oxidation, pyruvate flux and pyruvate dehydrogenase activity, amino acid transport, lipid metabolism and protein synthesis. |
| 3214 | 12866664 | Our studies show that patients with diabetic ketoacidosis and hyperglycemia have increased proinflammatory cytokines and activated CD4+ and CD8+ T lymphocytes. |
| 3215 | 12866664 | The mechanisms underlying insulin action, in general, or in the CD4+ and CD8+ T-lymphocytes, in particular, have not been clearly elucidated. |
| 3216 | 12866664 | Concomitant with the insulin receptors, two other growth factor receptors (IGF-1 and IL-2) also emerge on the T lymphocyte cell surface along with intracellular signal transduction mechanisms and insulin degrading enzyme (IDE). |
| 3217 | 12866664 | In activated T-lymphocytes, insulin stimulates glucose uptake, glucose oxidation, pyruvate flux and pyruvate dehydrogenase activity, amino acid transport, lipid metabolism and protein synthesis. |
| 3218 | 12866664 | Our studies show that patients with diabetic ketoacidosis and hyperglycemia have increased proinflammatory cytokines and activated CD4+ and CD8+ T lymphocytes. |
| 3219 | 12866664 | The mechanisms underlying insulin action, in general, or in the CD4+ and CD8+ T-lymphocytes, in particular, have not been clearly elucidated. |
| 3220 | 12874472 | In vivo CD4(+) and CD8(+) T cell-depleting strategies and genetically altered mice that did not express MHC class I or class II antigens were used to study the allorecognition and effector pathways of islet allograft rejection in different strains of mice, including autoimmunity-prone nonobese diabetic (NOD) mice. |
| 3221 | 12874472 | In BALB/c mice, islet rejection depended on both CD4(+) and CD8(+) T cells. |
| 3222 | 12874472 | In C57BL/6 mice, CD8(+) T cells could eventually mediate islet rejection by themselves, but they produced rejection more efficiently with help from CD4(+) T cells stimulated through either the direct or indirect pathway. |
| 3223 | 12874472 | In vivo CD4(+) and CD8(+) T cell-depleting strategies and genetically altered mice that did not express MHC class I or class II antigens were used to study the allorecognition and effector pathways of islet allograft rejection in different strains of mice, including autoimmunity-prone nonobese diabetic (NOD) mice. |
| 3224 | 12874472 | In BALB/c mice, islet rejection depended on both CD4(+) and CD8(+) T cells. |
| 3225 | 12874472 | In C57BL/6 mice, CD8(+) T cells could eventually mediate islet rejection by themselves, but they produced rejection more efficiently with help from CD4(+) T cells stimulated through either the direct or indirect pathway. |
| 3226 | 12874472 | In vivo CD4(+) and CD8(+) T cell-depleting strategies and genetically altered mice that did not express MHC class I or class II antigens were used to study the allorecognition and effector pathways of islet allograft rejection in different strains of mice, including autoimmunity-prone nonobese diabetic (NOD) mice. |
| 3227 | 12874472 | In BALB/c mice, islet rejection depended on both CD4(+) and CD8(+) T cells. |
| 3228 | 12874472 | In C57BL/6 mice, CD8(+) T cells could eventually mediate islet rejection by themselves, but they produced rejection more efficiently with help from CD4(+) T cells stimulated through either the direct or indirect pathway. |
| 3229 | 12885158 | To study how these T cells interact following encounter with the self-protein they recognize in the periphery, we have developed an adoptive transfer system in which HEL-specific TCR transgenic CD4 T cells are transferred to mice expressing HEL protein in the pancreas under the control of the rat insulin promoter. |
| 3230 | 12887108 | The strong associations between poor vitamin D nutrition, particular VDR alleles, and susceptibility to chronic mycobacterial infections, together with evidence that 1alpha,25-(OH)2D3 served as a vaccine adjuvant enhancing antibody-mediated immunity, suggest a model wherein high levels of 1alpha,25-(OH)2D3-liganded VDR transcriptional activity may promote the CD4+ T helper 2 (Th2) cell-mediated and mucosal antibody responses to cutaneous antigens in vivo. |
| 3231 | 12887108 | Studies done in animal models of multiple sclerosis (MS), insulin-dependent diabetes mellitus (IDDM), inflammatory bowel disease (IBD), and transplantation support a model wherein the 1alpha,25-(OH)2D3 may augment the function of suppressor T cells that maintain self tolerance to organ-specific self antigens. |
| 3232 | 12917258 | Inflammatory sites associated with tissue destruction often contain a complex mixture of cells including macrophages as well as CD8+ and CD4+ T cells. |
| 3233 | 12917258 | CD8+ T cells triggered NO production by macrophages, while macrophages triggered IFN-gamma production by CD8+ T cells. |
| 3234 | 12917258 | Antibodies specific for ICAM-1 and LFA-1 inhibited both cooperative islet destruction and cross-stimulation of CD8+ T cells and macrophages. |
| 3235 | 12928371 | Systemic overexpression of IL-10 induces CD4+CD25+ cell populations in vivo and ameliorates type 1 diabetes in nonobese diabetic mice in a dose-dependent fashion. |
| 3236 | 12928371 | The rAAV-IL-10 therapy attenuated pancreatic insulitis, decreased MHC II expression on CD11b+ cells, increased the population of CD11b+ cells, and modulated insulin autoantibody production. |
| 3237 | 12928371 | Interestingly, rAAV-IL-10 therapy dramatically increased the percentage of CD4+CD25+ regulatory T cells. |
| 3238 | 12928371 | Systemic overexpression of IL-10 induces CD4+CD25+ cell populations in vivo and ameliorates type 1 diabetes in nonobese diabetic mice in a dose-dependent fashion. |
| 3239 | 12928371 | The rAAV-IL-10 therapy attenuated pancreatic insulitis, decreased MHC II expression on CD11b+ cells, increased the population of CD11b+ cells, and modulated insulin autoantibody production. |
| 3240 | 12928371 | Interestingly, rAAV-IL-10 therapy dramatically increased the percentage of CD4+CD25+ regulatory T cells. |
| 3241 | 12930356 | Critical roles of CD30/CD30L interactions in murine autoimmune diabetes. |
| 3242 | 12930356 | CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. |
| 3243 | 12930356 | In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. |
| 3244 | 12930356 | Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4+ or CD8+ T cells in the spleen and pancreatic lymph node of younger NOD mice. |
| 3245 | 12930356 | In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. |
| 3246 | 12930356 | In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4+ or CD8+ T cell lines into NOD-SCID mice. |
| 3247 | 12930356 | These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice. |
| 3248 | 12930356 | Critical roles of CD30/CD30L interactions in murine autoimmune diabetes. |
| 3249 | 12930356 | CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. |
| 3250 | 12930356 | In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. |
| 3251 | 12930356 | Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4+ or CD8+ T cells in the spleen and pancreatic lymph node of younger NOD mice. |
| 3252 | 12930356 | In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. |
| 3253 | 12930356 | In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4+ or CD8+ T cell lines into NOD-SCID mice. |
| 3254 | 12930356 | These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice. |
| 3255 | 12930356 | Critical roles of CD30/CD30L interactions in murine autoimmune diabetes. |
| 3256 | 12930356 | CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. |
| 3257 | 12930356 | In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. |
| 3258 | 12930356 | Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4+ or CD8+ T cells in the spleen and pancreatic lymph node of younger NOD mice. |
| 3259 | 12930356 | In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. |
| 3260 | 12930356 | In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4+ or CD8+ T cell lines into NOD-SCID mice. |
| 3261 | 12930356 | These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice. |
| 3262 | 12937416 | Here we report that treatment with CD3epsilon-specific antibodies induces transferable T-cell-mediated tolerance involving CD4+CD25+ cells. |
| 3263 | 12937416 | However, these CD4+CD25+ T cells are distinct from naturally occurring regulatory T cells that control physiological autoreactivity. |
| 3264 | 12937416 | The central role of TGF-beta was further suggested by its increased, long-lasting production by CD4+ T cells from tolerant mice. |
| 3265 | 12937416 | Here we report that treatment with CD3epsilon-specific antibodies induces transferable T-cell-mediated tolerance involving CD4+CD25+ cells. |
| 3266 | 12937416 | However, these CD4+CD25+ T cells are distinct from naturally occurring regulatory T cells that control physiological autoreactivity. |
| 3267 | 12937416 | The central role of TGF-beta was further suggested by its increased, long-lasting production by CD4+ T cells from tolerant mice. |
| 3268 | 12937416 | Here we report that treatment with CD3epsilon-specific antibodies induces transferable T-cell-mediated tolerance involving CD4+CD25+ cells. |
| 3269 | 12937416 | However, these CD4+CD25+ T cells are distinct from naturally occurring regulatory T cells that control physiological autoreactivity. |
| 3270 | 12937416 | The central role of TGF-beta was further suggested by its increased, long-lasting production by CD4+ T cells from tolerant mice. |
| 3271 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3272 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3273 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3274 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3275 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3276 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3277 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3278 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3279 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3280 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3281 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3282 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3283 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3284 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3285 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3286 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3287 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3288 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3289 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3290 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3291 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3292 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3293 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3294 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3295 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3296 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3297 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3298 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3299 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3300 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3301 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3302 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3303 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3304 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3305 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3306 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3307 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3308 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3309 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3310 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3311 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3312 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3313 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3314 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3315 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3316 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3317 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3318 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3319 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3320 | 12974752 | As expected, an added benefit was the much smaller oral antigen dose required to induce CD4+ insulin-B specific regulatory cells that bystander-suppress autoaggressive responses. |
| 3321 | 14500627 | Cutting edge: CD28 controls peripheral homeostasis of CD4+CD25+ regulatory T cells. |
| 3322 | 14500627 | CD28/B7 blockade leads to exacerbated autoimmune disease in the nonobese diabetic mouse strain as a result of a marked reduction in the number of CD4(+)CD25(+) regulatory T cells (Tregs). |
| 3323 | 14500627 | CD28 engagement promotes survival by regulating IL-2 production by conventional T cells and CD25 expression on Tregs. |
| 3324 | 14500627 | Cutting edge: CD28 controls peripheral homeostasis of CD4+CD25+ regulatory T cells. |
| 3325 | 14500627 | CD28/B7 blockade leads to exacerbated autoimmune disease in the nonobese diabetic mouse strain as a result of a marked reduction in the number of CD4(+)CD25(+) regulatory T cells (Tregs). |
| 3326 | 14500627 | CD28 engagement promotes survival by regulating IL-2 production by conventional T cells and CD25 expression on Tregs. |
| 3327 | 14530324 | CD4(+)CD25(-) T cells showed a higher proliferation and produced more IFN-gamma, but less IL-4 and IL-10, whereas CD4(+)CD25(+) T suppressor cells produced significantly lower levels of IL-10 in 16- compared with 8-wk-old NOD mice. |
| 3328 | 14530324 | An increased percentage of CD4(+)CD25(-) T cells expressing CD54 was present in 16-wk-old and in diabetic NOD, but not in BALB/c mice. |
| 3329 | 14530324 | Costimulation via CD54 increased the proliferation of CD4(+)CD25(-) T cells from 16-, but not 8-wk-old NOD mice, and blocking CD54 prevented their proliferation, consistent with the role of CD54 in diabetes development. |
| 3330 | 14530324 | CD4(+)CD25(-) T cells showed a higher proliferation and produced more IFN-gamma, but less IL-4 and IL-10, whereas CD4(+)CD25(+) T suppressor cells produced significantly lower levels of IL-10 in 16- compared with 8-wk-old NOD mice. |
| 3331 | 14530324 | An increased percentage of CD4(+)CD25(-) T cells expressing CD54 was present in 16-wk-old and in diabetic NOD, but not in BALB/c mice. |
| 3332 | 14530324 | Costimulation via CD54 increased the proliferation of CD4(+)CD25(-) T cells from 16-, but not 8-wk-old NOD mice, and blocking CD54 prevented their proliferation, consistent with the role of CD54 in diabetes development. |
| 3333 | 14530324 | CD4(+)CD25(-) T cells showed a higher proliferation and produced more IFN-gamma, but less IL-4 and IL-10, whereas CD4(+)CD25(+) T suppressor cells produced significantly lower levels of IL-10 in 16- compared with 8-wk-old NOD mice. |
| 3334 | 14530324 | An increased percentage of CD4(+)CD25(-) T cells expressing CD54 was present in 16-wk-old and in diabetic NOD, but not in BALB/c mice. |
| 3335 | 14530324 | Costimulation via CD54 increased the proliferation of CD4(+)CD25(-) T cells from 16-, but not 8-wk-old NOD mice, and blocking CD54 prevented their proliferation, consistent with the role of CD54 in diabetes development. |
| 3336 | 14530340 | Tetramer-positive cells were identified in the immature CD4(+)CD8(low) population that arises during positive selection, and in larger numbers in the more mature CD4(+)CD8(-) population. |
| 3337 | 14530378 | To directly test this hypothesis, we have generated a beta cell-specific knockout of the Fas gene in a transgenic model of type 1 autoimmune diabetes in which CD4+ T cells with a transgenic TCR specific for influenza hemagglutinin (HA) are causing diabetes in mice that express HA under control of the rat insulin promoter. |
| 3338 | 14554080 | However, while infiltrating T cells were found within the pancreas, depletion of the CD4 T cell population prior to secondary infection or use of CD8 knock-out mice had no effect on the development of virus-mediated hyperglycemia. |
| 3339 | 14556005 | We report here that the T(H) type 1 (T(H)1)-specific Tim-3 (T cell immunoglobulin domain, mucin domain) protein functions to inhibit aggressive T(H)1-mediated auto- and alloimmune responses. |
| 3340 | 14556005 | These effects were mediated, at least in part, by dampening of the antigen-specific immunosuppressive function of CD4(+)CD25(+) regulatory T cell populations. |
| 3341 | 14561706 | The CD1d-reactive tetramer-positive CD4+ T cells augmented anti-dsDNA Ab secretion about tenfold. |
| 3342 | 14568923 | Thymic-derived dysregulated tolerance has been suggested to occur in type 1 diabetes via impaired generation of CD4(+)CD25(+) T regulatory cells, leading to autoimmune beta cell destruction. |
| 3343 | 14568923 | In this study, we demonstrate that Notch3 expression is a characteristic feature of CD4(+)CD25(+) cells. |
| 3344 | 14568923 | The failure to develop the disease is associated with an increase of CD4(+)CD25(+) T regulatory cells, accumulating in lymphoid organs, in pancreas infiltrates and paralleled by increased expression of IL-4 and IL-10. |
| 3345 | 14568923 | Accordingly, CD4(+) T cells from Notch3-transgenic mice inhibit the development of hyperglycemia and insulitis when injected into streptozotocin-treated wild-type mice and display in vitro suppressive activity. |
| 3346 | 14568923 | Thymic-derived dysregulated tolerance has been suggested to occur in type 1 diabetes via impaired generation of CD4(+)CD25(+) T regulatory cells, leading to autoimmune beta cell destruction. |
| 3347 | 14568923 | In this study, we demonstrate that Notch3 expression is a characteristic feature of CD4(+)CD25(+) cells. |
| 3348 | 14568923 | The failure to develop the disease is associated with an increase of CD4(+)CD25(+) T regulatory cells, accumulating in lymphoid organs, in pancreas infiltrates and paralleled by increased expression of IL-4 and IL-10. |
| 3349 | 14568923 | Accordingly, CD4(+) T cells from Notch3-transgenic mice inhibit the development of hyperglycemia and insulitis when injected into streptozotocin-treated wild-type mice and display in vitro suppressive activity. |
| 3350 | 14568923 | Thymic-derived dysregulated tolerance has been suggested to occur in type 1 diabetes via impaired generation of CD4(+)CD25(+) T regulatory cells, leading to autoimmune beta cell destruction. |
| 3351 | 14568923 | In this study, we demonstrate that Notch3 expression is a characteristic feature of CD4(+)CD25(+) cells. |
| 3352 | 14568923 | The failure to develop the disease is associated with an increase of CD4(+)CD25(+) T regulatory cells, accumulating in lymphoid organs, in pancreas infiltrates and paralleled by increased expression of IL-4 and IL-10. |
| 3353 | 14568923 | Accordingly, CD4(+) T cells from Notch3-transgenic mice inhibit the development of hyperglycemia and insulitis when injected into streptozotocin-treated wild-type mice and display in vitro suppressive activity. |
| 3354 | 14568923 | Thymic-derived dysregulated tolerance has been suggested to occur in type 1 diabetes via impaired generation of CD4(+)CD25(+) T regulatory cells, leading to autoimmune beta cell destruction. |
| 3355 | 14568923 | In this study, we demonstrate that Notch3 expression is a characteristic feature of CD4(+)CD25(+) cells. |
| 3356 | 14568923 | The failure to develop the disease is associated with an increase of CD4(+)CD25(+) T regulatory cells, accumulating in lymphoid organs, in pancreas infiltrates and paralleled by increased expression of IL-4 and IL-10. |
| 3357 | 14568923 | Accordingly, CD4(+) T cells from Notch3-transgenic mice inhibit the development of hyperglycemia and insulitis when injected into streptozotocin-treated wild-type mice and display in vitro suppressive activity. |
| 3358 | 14597769 | Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+CD25- T cells. |
| 3359 | 14597769 | CD4+CD25+ regulatory T (TR) cells have been described in both humans and mice. |
| 3360 | 14597769 | Recently, the forkhead/winged helix transcription factor, FoxP3, has been shown to be important for the function of TR cells in mice. |
| 3361 | 14597769 | In this study, human TR cells were examined and, in results similar to those of studies done in mice, expression of FoxP3 was found exclusively in CD4+CD25+ T cells and correlated with the suppressive activity of these cells. |
| 3362 | 14597769 | In contrast to the mouse studies, activation of human CD4+CD25- T cells led to expression of FoxP3. |
| 3363 | 14597769 | Expression of FoxP3 in activated human CD4+CD25+ cells also correlated with suppression of proliferation by these cells in freshly isolated CD4+CD25- T cells from the same donor. |
| 3364 | 14597769 | Thus, in humans, during activation of CD4+CD25- T cells in an immune response, two populations of cells may arise, effector CD4+CD25+ and regulatory CD4+CD25+ T cells, with expression of FoxP3 correlated with regulatory activity. |
| 3365 | 14597769 | Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+CD25- T cells. |
| 3366 | 14597769 | CD4+CD25+ regulatory T (TR) cells have been described in both humans and mice. |
| 3367 | 14597769 | Recently, the forkhead/winged helix transcription factor, FoxP3, has been shown to be important for the function of TR cells in mice. |
| 3368 | 14597769 | In this study, human TR cells were examined and, in results similar to those of studies done in mice, expression of FoxP3 was found exclusively in CD4+CD25+ T cells and correlated with the suppressive activity of these cells. |
| 3369 | 14597769 | In contrast to the mouse studies, activation of human CD4+CD25- T cells led to expression of FoxP3. |
| 3370 | 14597769 | Expression of FoxP3 in activated human CD4+CD25+ cells also correlated with suppression of proliferation by these cells in freshly isolated CD4+CD25- T cells from the same donor. |
| 3371 | 14597769 | Thus, in humans, during activation of CD4+CD25- T cells in an immune response, two populations of cells may arise, effector CD4+CD25+ and regulatory CD4+CD25+ T cells, with expression of FoxP3 correlated with regulatory activity. |
| 3372 | 14597769 | Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+CD25- T cells. |
| 3373 | 14597769 | CD4+CD25+ regulatory T (TR) cells have been described in both humans and mice. |
| 3374 | 14597769 | Recently, the forkhead/winged helix transcription factor, FoxP3, has been shown to be important for the function of TR cells in mice. |
| 3375 | 14597769 | In this study, human TR cells were examined and, in results similar to those of studies done in mice, expression of FoxP3 was found exclusively in CD4+CD25+ T cells and correlated with the suppressive activity of these cells. |
| 3376 | 14597769 | In contrast to the mouse studies, activation of human CD4+CD25- T cells led to expression of FoxP3. |
| 3377 | 14597769 | Expression of FoxP3 in activated human CD4+CD25+ cells also correlated with suppression of proliferation by these cells in freshly isolated CD4+CD25- T cells from the same donor. |
| 3378 | 14597769 | Thus, in humans, during activation of CD4+CD25- T cells in an immune response, two populations of cells may arise, effector CD4+CD25+ and regulatory CD4+CD25+ T cells, with expression of FoxP3 correlated with regulatory activity. |
| 3379 | 14597769 | Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+CD25- T cells. |
| 3380 | 14597769 | CD4+CD25+ regulatory T (TR) cells have been described in both humans and mice. |
| 3381 | 14597769 | Recently, the forkhead/winged helix transcription factor, FoxP3, has been shown to be important for the function of TR cells in mice. |
| 3382 | 14597769 | In this study, human TR cells were examined and, in results similar to those of studies done in mice, expression of FoxP3 was found exclusively in CD4+CD25+ T cells and correlated with the suppressive activity of these cells. |
| 3383 | 14597769 | In contrast to the mouse studies, activation of human CD4+CD25- T cells led to expression of FoxP3. |
| 3384 | 14597769 | Expression of FoxP3 in activated human CD4+CD25+ cells also correlated with suppression of proliferation by these cells in freshly isolated CD4+CD25- T cells from the same donor. |
| 3385 | 14597769 | Thus, in humans, during activation of CD4+CD25- T cells in an immune response, two populations of cells may arise, effector CD4+CD25+ and regulatory CD4+CD25+ T cells, with expression of FoxP3 correlated with regulatory activity. |
| 3386 | 14597769 | Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+CD25- T cells. |
| 3387 | 14597769 | CD4+CD25+ regulatory T (TR) cells have been described in both humans and mice. |
| 3388 | 14597769 | Recently, the forkhead/winged helix transcription factor, FoxP3, has been shown to be important for the function of TR cells in mice. |
| 3389 | 14597769 | In this study, human TR cells were examined and, in results similar to those of studies done in mice, expression of FoxP3 was found exclusively in CD4+CD25+ T cells and correlated with the suppressive activity of these cells. |
| 3390 | 14597769 | In contrast to the mouse studies, activation of human CD4+CD25- T cells led to expression of FoxP3. |
| 3391 | 14597769 | Expression of FoxP3 in activated human CD4+CD25+ cells also correlated with suppression of proliferation by these cells in freshly isolated CD4+CD25- T cells from the same donor. |
| 3392 | 14597769 | Thus, in humans, during activation of CD4+CD25- T cells in an immune response, two populations of cells may arise, effector CD4+CD25+ and regulatory CD4+CD25+ T cells, with expression of FoxP3 correlated with regulatory activity. |
| 3393 | 14597769 | Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+CD25- T cells. |
| 3394 | 14597769 | CD4+CD25+ regulatory T (TR) cells have been described in both humans and mice. |
| 3395 | 14597769 | Recently, the forkhead/winged helix transcription factor, FoxP3, has been shown to be important for the function of TR cells in mice. |
| 3396 | 14597769 | In this study, human TR cells were examined and, in results similar to those of studies done in mice, expression of FoxP3 was found exclusively in CD4+CD25+ T cells and correlated with the suppressive activity of these cells. |
| 3397 | 14597769 | In contrast to the mouse studies, activation of human CD4+CD25- T cells led to expression of FoxP3. |
| 3398 | 14597769 | Expression of FoxP3 in activated human CD4+CD25+ cells also correlated with suppression of proliferation by these cells in freshly isolated CD4+CD25- T cells from the same donor. |
| 3399 | 14597769 | Thus, in humans, during activation of CD4+CD25- T cells in an immune response, two populations of cells may arise, effector CD4+CD25+ and regulatory CD4+CD25+ T cells, with expression of FoxP3 correlated with regulatory activity. |
| 3400 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3401 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3402 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3403 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3404 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3405 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3406 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3407 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3408 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3409 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3410 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3411 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3412 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3413 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3414 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3415 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3416 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3417 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3418 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3419 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3420 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3421 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3422 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3423 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3424 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3425 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3426 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3427 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3428 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3429 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3430 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3431 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3432 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3433 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3434 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3435 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3436 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3437 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3438 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3439 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3440 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3441 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3442 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3443 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3444 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3445 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3446 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3447 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3448 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3449 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3450 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3451 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3452 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3453 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3454 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3455 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3456 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3457 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3458 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3459 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3460 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3461 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3462 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3463 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3464 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3465 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3466 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3467 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3468 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3469 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3470 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3471 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3472 | 14609212 | The role of CD28 and CTLA4 in the function and homeostasis of CD4+CD25+ regulatory T cells. |
| 3473 | 14609212 | CD4+CD25+ T cells regulate a variety of autoimmune and alloimmune responses including the development of autoimmune diabetes in non-obese diabetic (NOD) mice. |
| 3474 | 14609212 | We have examined the role of CD28/CTLA4/B7 interactions in the expansion and survival of CD4+CD25+ regulatory T cells (T(reg)) in this setting. |
| 3475 | 14609212 | In addition, analysis of T(reg) from CTLA4-deficient mice suggests that CTLA4 expression is not required for their development or function. |
| 3476 | 14609212 | The role of CD28 and CTLA4 in the function and homeostasis of CD4+CD25+ regulatory T cells. |
| 3477 | 14609212 | CD4+CD25+ T cells regulate a variety of autoimmune and alloimmune responses including the development of autoimmune diabetes in non-obese diabetic (NOD) mice. |
| 3478 | 14609212 | We have examined the role of CD28/CTLA4/B7 interactions in the expansion and survival of CD4+CD25+ regulatory T cells (T(reg)) in this setting. |
| 3479 | 14609212 | In addition, analysis of T(reg) from CTLA4-deficient mice suggests that CTLA4 expression is not required for their development or function. |
| 3480 | 14609212 | The role of CD28 and CTLA4 in the function and homeostasis of CD4+CD25+ regulatory T cells. |
| 3481 | 14609212 | CD4+CD25+ T cells regulate a variety of autoimmune and alloimmune responses including the development of autoimmune diabetes in non-obese diabetic (NOD) mice. |
| 3482 | 14609212 | We have examined the role of CD28/CTLA4/B7 interactions in the expansion and survival of CD4+CD25+ regulatory T cells (T(reg)) in this setting. |
| 3483 | 14609212 | In addition, analysis of T(reg) from CTLA4-deficient mice suggests that CTLA4 expression is not required for their development or function. |
| 3484 | 14609216 | Naso-respirtory insulin (which avoids insulin degradation) induces CD8+ alpha(alpha) TCR gamma(delta) T(reg) whereas peptides that bind to the NOD MHC class II molecule, I-Ag7, insulin B9-23 and proinsulin B24-C36, induce CD4+ T(regs) Following naso-respiratory delivery of insulin to NOD mice increased numbers of CD8+ gamma(delta) T cells expressing interleukin (IL)10 are detected in the pancreatic lymph nodes. |
| 3485 | 14609216 | CD8+ gamma(delta) T(reg) are conceivably physiological and insulin-specific, induced by exposure to insulin in maternal milk. |
| 3486 | 14609218 | In several autoimmune models, feedback regulation employing both CD4+ and CD8+ T cells of TCR specificity can be shown to occur and to account for remission from the transient disease state, or for its prevention. |
| 3487 | 14609218 | In this model, the acetylated 1-9 N-terminal antigenic determinant from myelin basic protein (MBP) induces a transient paralytic disease owing to the activation of self-directed, high-affinity, CD4+ T cells. |
| 3488 | 14609218 | A CD4+ T cell directed against a TCR determinant in the framework region of the Vbeta chain, and a CD8+ T cell directed against an upstream, distinct framework determinant, both of which are necessary for regulation, bring about a reversal of the disease process. |
| 3489 | 14609218 | In several autoimmune models, feedback regulation employing both CD4+ and CD8+ T cells of TCR specificity can be shown to occur and to account for remission from the transient disease state, or for its prevention. |
| 3490 | 14609218 | In this model, the acetylated 1-9 N-terminal antigenic determinant from myelin basic protein (MBP) induces a transient paralytic disease owing to the activation of self-directed, high-affinity, CD4+ T cells. |
| 3491 | 14609218 | A CD4+ T cell directed against a TCR determinant in the framework region of the Vbeta chain, and a CD8+ T cell directed against an upstream, distinct framework determinant, both of which are necessary for regulation, bring about a reversal of the disease process. |
| 3492 | 14609218 | In several autoimmune models, feedback regulation employing both CD4+ and CD8+ T cells of TCR specificity can be shown to occur and to account for remission from the transient disease state, or for its prevention. |
| 3493 | 14609218 | In this model, the acetylated 1-9 N-terminal antigenic determinant from myelin basic protein (MBP) induces a transient paralytic disease owing to the activation of self-directed, high-affinity, CD4+ T cells. |
| 3494 | 14609218 | A CD4+ T cell directed against a TCR determinant in the framework region of the Vbeta chain, and a CD8+ T cell directed against an upstream, distinct framework determinant, both of which are necessary for regulation, bring about a reversal of the disease process. |
| 3495 | 14609223 | CD4+ lymphocytes with specificity for insulin can be induced by immunization with the insulin B chain via the oral route or by DNA vaccination. |
| 3496 | 14609223 | In comparison to non-regulatory insulin B-specific cell lines, they produce high amounts of interleukin (IL)4 and IL10, whereas interferon (IFN)gamma and tumour necrosis factor (TNF)alpha levels are comparable. |
| 3497 | 14609223 | We propose that this is achieved by modulation of antigen presenting cells that lose the ability to propagate aggressive responses after exposure to IL4 or IL10 in vitro. |
| 3498 | 14609223 | In order to avoid induction of insulin B-specific autoaggressive T cells we have demonstrated that administration of IL4 or IL10 at the time of immunization is beneficial and therefore should be part of a potential future clinical application. |
| 3499 | 14609225 | In the thymus these regulatory cells are CD25+-like CD4+ cells shown to control physiologic organ-specific autoimmunity. |
| 3500 | 14609225 | In contrast, in the periphery, both CD4+CD25+ and CD4+CD25- cells exhibit regulatory capacities. |
| 3501 | 14609225 | Additionally, onset of autoimmune diabetes was preceded by a functional abnormality of CD4+CD25+ regulatory T cells as assessed by their inability to suppress in vitro the proliferation of polyclonally activated CD25- T cells. |
| 3502 | 14609225 | Furthermore, we also obtained evidence in CD3-treated NOD for a significant increase (in the pancreatic and mesenteric lymph nodes but not in the spleen) in the proportion of CD4+CD25+CTLA4+ T cells which produce TGFbeta. |
| 3503 | 14609225 | In the thymus these regulatory cells are CD25+-like CD4+ cells shown to control physiologic organ-specific autoimmunity. |
| 3504 | 14609225 | In contrast, in the periphery, both CD4+CD25+ and CD4+CD25- cells exhibit regulatory capacities. |
| 3505 | 14609225 | Additionally, onset of autoimmune diabetes was preceded by a functional abnormality of CD4+CD25+ regulatory T cells as assessed by their inability to suppress in vitro the proliferation of polyclonally activated CD25- T cells. |
| 3506 | 14609225 | Furthermore, we also obtained evidence in CD3-treated NOD for a significant increase (in the pancreatic and mesenteric lymph nodes but not in the spleen) in the proportion of CD4+CD25+CTLA4+ T cells which produce TGFbeta. |
| 3507 | 14609225 | In the thymus these regulatory cells are CD25+-like CD4+ cells shown to control physiologic organ-specific autoimmunity. |
| 3508 | 14609225 | In contrast, in the periphery, both CD4+CD25+ and CD4+CD25- cells exhibit regulatory capacities. |
| 3509 | 14609225 | Additionally, onset of autoimmune diabetes was preceded by a functional abnormality of CD4+CD25+ regulatory T cells as assessed by their inability to suppress in vitro the proliferation of polyclonally activated CD25- T cells. |
| 3510 | 14609225 | Furthermore, we also obtained evidence in CD3-treated NOD for a significant increase (in the pancreatic and mesenteric lymph nodes but not in the spleen) in the proportion of CD4+CD25+CTLA4+ T cells which produce TGFbeta. |
| 3511 | 14609225 | In the thymus these regulatory cells are CD25+-like CD4+ cells shown to control physiologic organ-specific autoimmunity. |
| 3512 | 14609225 | In contrast, in the periphery, both CD4+CD25+ and CD4+CD25- cells exhibit regulatory capacities. |
| 3513 | 14609225 | Additionally, onset of autoimmune diabetes was preceded by a functional abnormality of CD4+CD25+ regulatory T cells as assessed by their inability to suppress in vitro the proliferation of polyclonally activated CD25- T cells. |
| 3514 | 14609225 | Furthermore, we also obtained evidence in CD3-treated NOD for a significant increase (in the pancreatic and mesenteric lymph nodes but not in the spleen) in the proportion of CD4+CD25+CTLA4+ T cells which produce TGFbeta. |
| 3515 | 14610290 | Our studies of the mechanism of the non-FcR binding anti-CD3 MAb indicate that the MAb delivers an activation signal to T cells resulting in disproportionate production of interleukin-10 (IL-10) relative to interferon-gamma(IFN-gamma) in vitro compared with FcR binding anti-CD3 MAb, and detectable levels of IL-10, IL-5, but rarely IFN-gamma or IL-2 in the serum after treatment. |
| 3516 | 14610290 | In addition, the drug induces a population of CD4+IL-10+ CCR4+ cells in vivo. |
| 3517 | 14624755 | Peripheral T cell lymphopenia (lyp) in the BioBreeding (BB) rat is linked to a frameshift mutation in Ian5, a member of the Immune Associated Nucleotide (Ian) gene family on rat chromosome 4. |
| 3518 | 14624755 | Analysis of thymic CD4 and CD8 T lymphocytes revealed no difference in the percentage of CD4(-)CD8(+)and CD4(+)CD8(-)subsets in lyp/lyp compared to +/+ F344 rats. |
| 3519 | 14624755 | Compared to F344 +/+ rats double positive CD4(+)CD8(+)T cells were increased only in lyp/lyp spleen (P=0.034) while double negative CD4(-)CD8(-)were increased in thymus (P=0.033), spleen (P=0.012), MLN (P<0.0001), and peripheral blood (P<0.0001). |
| 3520 | 14624755 | Peripheral T cell lymphopenia (lyp) in the BioBreeding (BB) rat is linked to a frameshift mutation in Ian5, a member of the Immune Associated Nucleotide (Ian) gene family on rat chromosome 4. |
| 3521 | 14624755 | Analysis of thymic CD4 and CD8 T lymphocytes revealed no difference in the percentage of CD4(-)CD8(+)and CD4(+)CD8(-)subsets in lyp/lyp compared to +/+ F344 rats. |
| 3522 | 14624755 | Compared to F344 +/+ rats double positive CD4(+)CD8(+)T cells were increased only in lyp/lyp spleen (P=0.034) while double negative CD4(-)CD8(-)were increased in thymus (P=0.033), spleen (P=0.012), MLN (P<0.0001), and peripheral blood (P<0.0001). |
| 3523 | 14634082 | We have shown recently that PPARgamma agonists inhibit EAE by blocking IL-12 production, IL-12 signaling, and neural Ag-induced Th1 differentiation. |
| 3524 | 14634082 | The exacerbation of EAE in PPARgamma(+/-) mice associates with an increased expansion of CD4(+) and CD8(+) T cells and expression of CD40 and MHC class II molecules in response to MOGp35-55 Ag. |
| 3525 | 14634096 | Systemic and pancreatic cytokine profiles deviated to a Th1-dominant state, and the the frequency of glutamic acid decarboxylase-reactive IFN-gamma-producing CD4(+) cells was also high in the IL-18 group. |
| 3526 | 14634096 | Moreover, it was suggested that the promoting effect of IL-18 might be associated with increased peripheral IL-12, CD86, and pancreatic IFN-inducible protein-10 mRNA expression levels. |
| 3527 | 14645156 | Autoantibodies and CD4 T cells target a beta cell retroviral envelope protein in non-obese diabetic mice. |
| 3528 | 14659909 | Using the CFSE assay we were able to measure directly the proliferation of human CD4(+) T cells from healthy donors in response to the type 1 diabetes autoantigens glutamic acid decarboxylase (GAD) and proinsulin (PI). |
| 3529 | 14662897 | To ascertain the role of CD8(+) T cell-induced beta cell lysis in the initiation of diabetes, we expressed a rat insulin promoter (RIP)-driven adenovirus E19 transgene in NOD mice. |
| 3530 | 14662897 | RIP-E19 expression inhibited MHC class I transport exclusively in beta cells and rendered these cells resistant to lysis by CD8(+) (but not CD4(+)) T cells, both in vitro and in vivo. |
| 3531 | 14670304 | CD40 ligation releases immature dendritic cells from the control of regulatory CD4+CD25+ T cells. |
| 3532 | 14670304 | We report that disruption of CD154 in nonobese diabetic (NOD) mice abrogates the helper function of CD4+CD25- T cells without impairing the regulatory activity of CD4+CD25+ T cells. |
| 3533 | 14670304 | Whereas CD4+ T cells from NOD mice enhanced a diabetogenic CD8+ T cell response in monoclonal TCR-transgenic NOD mice, CD4+ T cells from NOD.CD154(-/-) mice actively suppressed it. |
| 3534 | 14670304 | Suppression was mediated by regulatory CD4+CD25+ T cells capable of inhibiting CD8+ T cell responses induced by peptide-pulsed dendritic cells (DCs), but not peptide/MHC monomers. |
| 3535 | 14670304 | It involved inhibition of DC maturation, did not occur in the presence of CD154+ T-helper cells, and could be inhibited by activation of DCs with LPS, CpG DNA, or an agonistic anti-CD40 mAb. |
| 3536 | 14670304 | Thus, in at least some genetic backgrounds, CD154-CD40 interactions and innate stimuli release immature DCs from suppression by CD4+CD25+ T cells. |
| 3537 | 14670304 | CD40 ligation releases immature dendritic cells from the control of regulatory CD4+CD25+ T cells. |
| 3538 | 14670304 | We report that disruption of CD154 in nonobese diabetic (NOD) mice abrogates the helper function of CD4+CD25- T cells without impairing the regulatory activity of CD4+CD25+ T cells. |
| 3539 | 14670304 | Whereas CD4+ T cells from NOD mice enhanced a diabetogenic CD8+ T cell response in monoclonal TCR-transgenic NOD mice, CD4+ T cells from NOD.CD154(-/-) mice actively suppressed it. |
| 3540 | 14670304 | Suppression was mediated by regulatory CD4+CD25+ T cells capable of inhibiting CD8+ T cell responses induced by peptide-pulsed dendritic cells (DCs), but not peptide/MHC monomers. |
| 3541 | 14670304 | It involved inhibition of DC maturation, did not occur in the presence of CD154+ T-helper cells, and could be inhibited by activation of DCs with LPS, CpG DNA, or an agonistic anti-CD40 mAb. |
| 3542 | 14670304 | Thus, in at least some genetic backgrounds, CD154-CD40 interactions and innate stimuli release immature DCs from suppression by CD4+CD25+ T cells. |
| 3543 | 14670304 | CD40 ligation releases immature dendritic cells from the control of regulatory CD4+CD25+ T cells. |
| 3544 | 14670304 | We report that disruption of CD154 in nonobese diabetic (NOD) mice abrogates the helper function of CD4+CD25- T cells without impairing the regulatory activity of CD4+CD25+ T cells. |
| 3545 | 14670304 | Whereas CD4+ T cells from NOD mice enhanced a diabetogenic CD8+ T cell response in monoclonal TCR-transgenic NOD mice, CD4+ T cells from NOD.CD154(-/-) mice actively suppressed it. |
| 3546 | 14670304 | Suppression was mediated by regulatory CD4+CD25+ T cells capable of inhibiting CD8+ T cell responses induced by peptide-pulsed dendritic cells (DCs), but not peptide/MHC monomers. |
| 3547 | 14670304 | It involved inhibition of DC maturation, did not occur in the presence of CD154+ T-helper cells, and could be inhibited by activation of DCs with LPS, CpG DNA, or an agonistic anti-CD40 mAb. |
| 3548 | 14670304 | Thus, in at least some genetic backgrounds, CD154-CD40 interactions and innate stimuli release immature DCs from suppression by CD4+CD25+ T cells. |
| 3549 | 14670304 | CD40 ligation releases immature dendritic cells from the control of regulatory CD4+CD25+ T cells. |
| 3550 | 14670304 | We report that disruption of CD154 in nonobese diabetic (NOD) mice abrogates the helper function of CD4+CD25- T cells without impairing the regulatory activity of CD4+CD25+ T cells. |
| 3551 | 14670304 | Whereas CD4+ T cells from NOD mice enhanced a diabetogenic CD8+ T cell response in monoclonal TCR-transgenic NOD mice, CD4+ T cells from NOD.CD154(-/-) mice actively suppressed it. |
| 3552 | 14670304 | Suppression was mediated by regulatory CD4+CD25+ T cells capable of inhibiting CD8+ T cell responses induced by peptide-pulsed dendritic cells (DCs), but not peptide/MHC monomers. |
| 3553 | 14670304 | It involved inhibition of DC maturation, did not occur in the presence of CD154+ T-helper cells, and could be inhibited by activation of DCs with LPS, CpG DNA, or an agonistic anti-CD40 mAb. |
| 3554 | 14670304 | Thus, in at least some genetic backgrounds, CD154-CD40 interactions and innate stimuli release immature DCs from suppression by CD4+CD25+ T cells. |
| 3555 | 14670304 | CD40 ligation releases immature dendritic cells from the control of regulatory CD4+CD25+ T cells. |
| 3556 | 14670304 | We report that disruption of CD154 in nonobese diabetic (NOD) mice abrogates the helper function of CD4+CD25- T cells without impairing the regulatory activity of CD4+CD25+ T cells. |
| 3557 | 14670304 | Whereas CD4+ T cells from NOD mice enhanced a diabetogenic CD8+ T cell response in monoclonal TCR-transgenic NOD mice, CD4+ T cells from NOD.CD154(-/-) mice actively suppressed it. |
| 3558 | 14670304 | Suppression was mediated by regulatory CD4+CD25+ T cells capable of inhibiting CD8+ T cell responses induced by peptide-pulsed dendritic cells (DCs), but not peptide/MHC monomers. |
| 3559 | 14670304 | It involved inhibition of DC maturation, did not occur in the presence of CD154+ T-helper cells, and could be inhibited by activation of DCs with LPS, CpG DNA, or an agonistic anti-CD40 mAb. |
| 3560 | 14670304 | Thus, in at least some genetic backgrounds, CD154-CD40 interactions and innate stimuli release immature DCs from suppression by CD4+CD25+ T cells. |
| 3561 | 14673094 | It is not clear, however, whether a given subset, notably CD4+CD25+ regulatory T cells, protects from a wide spectrum of immune disorders, or whether specialized subsets of regulatory T cells control each given disease or group of diseases. |
| 3562 | 14679038 | Clearly, both CD4+ and CD8+ T cells are required, but activated CD4+ T cells are both necessary and sufficient in causing disease. |
| 3563 | 14679038 | It is still unclear whether the CD8+ T cell exerts its function as a classical effector cell or mainly as an immunomodulatory cell acting in synergy with the CD4+ T cell. |
| 3564 | 14679038 | The relative role of T cell effector mechanisms such as Fas/FasL, perforin/granzyme, and the TRAIL systems is unclear. |
| 3565 | 14679038 | Clearly, both CD4+ and CD8+ T cells are required, but activated CD4+ T cells are both necessary and sufficient in causing disease. |
| 3566 | 14679038 | It is still unclear whether the CD8+ T cell exerts its function as a classical effector cell or mainly as an immunomodulatory cell acting in synergy with the CD4+ T cell. |
| 3567 | 14679038 | The relative role of T cell effector mechanisms such as Fas/FasL, perforin/granzyme, and the TRAIL systems is unclear. |
| 3568 | 14679042 | Our approach takes advantage of the appearance of highly activated T cells expressing a CD25(+)/CD4(high+) phenotype induced by immobilized class II MHC monomer containing the GAD65 peptide. |
| 3569 | 14679043 | Nonobese diabetic (NOD) mice develop overt diabetes following prolonged periods of pancreatic islet inflammation involving both CD4+ and CD8+ T cells. |
| 3570 | 14679043 | We and others have shown that a significant fraction of NOD islet-associated CD8+ T cells express highly homologous TCRalpha chains (Valpha17 and Jalpha42 joined by the same N-region sequence) and that they recognize the peptide NRP-A7 in the context of the MHC class I molecule H-2K(d). |
| 3571 | 14679052 | Fas and Fas ligand immunoexpression in pancreatic islets of NOD mice during spontaneous and cyclophosphamide-accelerated diabetes. |
| 3572 | 14679052 | During insulin-dependent diabetes mellitus, beta cell destruction may involve activation of the Fas-Fas ligand (Fas-FasL) system. |
| 3573 | 14679052 | During spontaneous and cyclophosphamide diabetes, it was observed in a higher proportion of islet infiltrating macrophages than in CD4 and CD8 cells. |
| 3574 | 14679052 | In the cyclophosphamide group, Fas expression in intra-islet CD4 and CD8 cells showed an increase close to the onset of diabetes. |
| 3575 | 14679052 | At days 11 and 14, several intra-islet macrophages with immunolabeling for Fas also coexpressed interleukin-1beta and inducible nitric oxide synthase. |
| 3576 | 14679052 | Fas and Fas ligand immunoexpression in pancreatic islets of NOD mice during spontaneous and cyclophosphamide-accelerated diabetes. |
| 3577 | 14679052 | During insulin-dependent diabetes mellitus, beta cell destruction may involve activation of the Fas-Fas ligand (Fas-FasL) system. |
| 3578 | 14679052 | During spontaneous and cyclophosphamide diabetes, it was observed in a higher proportion of islet infiltrating macrophages than in CD4 and CD8 cells. |
| 3579 | 14679052 | In the cyclophosphamide group, Fas expression in intra-islet CD4 and CD8 cells showed an increase close to the onset of diabetes. |
| 3580 | 14679052 | At days 11 and 14, several intra-islet macrophages with immunolabeling for Fas also coexpressed interleukin-1beta and inducible nitric oxide synthase. |
| 3581 | 14679058 | From day 7, caspase-3 expression began to increase in intra-islet macrophages and reached a peak at days 11 and 14, when a small number of CD4 and CD8 T cells also showed positive labeling. |
| 3582 | 14679076 | Difference in gene expression profiles between human CD4+CD25+ and CD4+CD25- T cells. |
| 3583 | 14679076 | We studied the gene expression profiles of human CD4+CD25+ and CD4+CD25- T cells by using cDNA microarrays. |
| 3584 | 14679076 | Difference in gene expression profiles between human CD4+CD25+ and CD4+CD25- T cells. |
| 3585 | 14679076 | We studied the gene expression profiles of human CD4+CD25+ and CD4+CD25- T cells by using cDNA microarrays. |
| 3586 | 14679092 | We have previously shown that serum interferon-inducible protein-10 and glutamic acid decarboxylase-reactive CD4(+) interferon-gamma-producing cells in the peripheral blood are good markers for T cell-mediated autoimmunity in type 1 diabetes. |
| 3587 | 14679096 | Detection of GAD-reactive CD4+ cells in so-called "type 1B" diabetes. |
| 3588 | 14681852 | De novo emergence of growth factor receptors in activated human CD4+ and CD8+ T lymphocytes. |
| 3589 | 14681852 | Using phytohemagglutinin (PHA)-activated human T lymphocytes, we have demonstrated de novo emergence of growth factor receptors (insulin, insulin-like growth factor-1 [IGF-1], and interleukin-2 [IL-2]) in the CD4(+) and CD8(+) subsets determined by flow cytometry. |
| 3590 | 14681852 | These events, which are actinomycin- and cycloheximide-sensitive, occur only in activated, but not nonactivated, CD4(+) and CD8(+) lymphocytes. |
| 3591 | 14681852 | De novo emergence of growth factor receptors in activated human CD4+ and CD8+ T lymphocytes. |
| 3592 | 14681852 | Using phytohemagglutinin (PHA)-activated human T lymphocytes, we have demonstrated de novo emergence of growth factor receptors (insulin, insulin-like growth factor-1 [IGF-1], and interleukin-2 [IL-2]) in the CD4(+) and CD8(+) subsets determined by flow cytometry. |
| 3593 | 14681852 | These events, which are actinomycin- and cycloheximide-sensitive, occur only in activated, but not nonactivated, CD4(+) and CD8(+) lymphocytes. |
| 3594 | 14681852 | De novo emergence of growth factor receptors in activated human CD4+ and CD8+ T lymphocytes. |
| 3595 | 14681852 | Using phytohemagglutinin (PHA)-activated human T lymphocytes, we have demonstrated de novo emergence of growth factor receptors (insulin, insulin-like growth factor-1 [IGF-1], and interleukin-2 [IL-2]) in the CD4(+) and CD8(+) subsets determined by flow cytometry. |
| 3596 | 14681852 | These events, which are actinomycin- and cycloheximide-sensitive, occur only in activated, but not nonactivated, CD4(+) and CD8(+) lymphocytes. |
| 3597 | 14692396 | The IDDM and NIDDM patients had above-normal absolute lymphocyte counts, whereas the percentages of CD3, CD4 adn CD8 T lymphocytes were significantly reduced. |
| 3598 | 14692396 | The low intracellular reduced glutathione(GSH) and the unbalanced profile of key enzymes involved in GSH metabolism, gamma-glutamyltransferase (gamma-GT) and glutathione-S-transferase (GST), account for the increased oxidative status of PBMC from diabetic patients. |
| 3599 | 14707058 | MHC class II molecules play a role in the selection of autoreactive class I-restricted CD8 T cells that are essential contributors to type 1 diabetes development in nonobese diabetic mice. |
| 3600 | 14707058 | Development of autoreactive CD4 T cells contributing to type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice is either promoted or dominantly inhibited by particular MHC class II variants. |
| 3601 | 14707058 | In addition, it is now clear that when co-expressed with other susceptibility genes, some common MHC class I variants aberrantly mediate autoreactive CD8 T cell responses also essential to T1D development. |
| 3602 | 14707058 | However, it was unknown whether the development of diabetogenic CD8 T cells could also be dominantly inhibited by particular MHC variants. |
| 3603 | 14707058 | We addressed this issue by crossing NOD mice transgenically expressing the TCR from the diabetogenic CD8 T cell clone AI4 with NOD stocks congenic for MHC haplotypes that dominantly inhibit T1D. |
| 3604 | 14707058 | In contrast, heterozygous expression of some MHC haplotypes conferring T1D resistance anergized AI4 T cells through decreased TCR (H2(b)) or CD8 expression (H2(q)). |
| 3605 | 14707073 | Further analyses revealed that thymic deletion required both a hybrid MHC class II molecule, Ebeta(b) Ealpha(d), and the K(d) molecule presenting the HA epitope, which together synergize to effect deletion of CD4+CD8+ thymocytes. |
| 3606 | 14724691 | hIan5: the human ortholog to the rat Ian4/Iddm1/lyp is a new member of the Ian family that is overexpressed in B-cell lymphoid malignancies. |
| 3607 | 14724691 | Recently, the rat Ian4 (rIan4) was cloned and it appears to be identical to the gene Iddm1/lyp responsible for severe lymphopenia and the development of insulin-dependent diabetes in the BB-DP rat. |
| 3608 | 14724691 | Different blood fractions show high hIan5 expression in CD4- and CD8-positive T cells and monocytes, but not in B lymphocytes. |
| 3609 | 14734611 | CD4, CD8 T cells and B cells were present in islet infiltrates from 9-week-old L-selectin-sufficient and -deficient littermates. |
| 3610 | 14734611 | On the other hand, homing of activated, cloned insulin-specific autoaggressive CD8 T cells (TGNFC8 clone) is not affected in NOD/L-selectin-deficient recipients. |
| 3611 | 14735361 | We studied the histo- and immunopathology of the endocrine and exocrine pancreas and a number of other organs in a new insulin-dependent diabetes mellitus (IDDM) rat model (LEW.1AR1/Ztm- iddm rat). |
| 3612 | 14735361 | The islet infiltrate was composed mainly of ED1-positive macrophages and T lymphocytes, comprising a large number of CD8(+) lymphocytes and a few CD4(+) lymphocytes. |
| 3613 | 14741738 | The p38 mitogen-activated protein kinase (MAPK) pathway is important in Th1 immunity, macrophage activation, and apoptosis. |
| 3614 | 14741738 | Since they may be associated with beta-cell destruction during the development of type 1 diabetes, we investigated the role of the p38 MAPK pathway in female nonobese diabetic (NOD) mice. |
| 3615 | 14741738 | Phosphorylated p38 MAPK was observed immunohistochemically in CD4+ cells that had infiltrated into the islets and part of beta-cells, increasing in proportion to the severity of insulitis. |
| 3616 | 14741738 | Continuous oral administration of 0.08% FR167653, a specific p38 MAPK pathway inhibitor, significantly reduced the ex vivo production of interferon-gamma by splenic Th1 cells without affecting interleukin-4 production by Th2 cells. |
| 3617 | 14741738 | Treatment with FR167653 after insulitis had developed (i.e. from 10-30 weeks of age) also prevented diabetes, further suggesting that treatment with the p38 MAPK pathway inhibitor keeps insulitis benign in NOD mice, partly by inhibiting Th1 immunity. |
| 3618 | 14741738 | These findings suggest that p38 MAPK is a key mediator that switches insulitis from benign to destructive in the development of type 1 diabetes. |
| 3619 | 14766222 | We studied in vivo activation of CD4 and CD8 lymphocytes by measuring de novo growth factor receptor for insulin, IGF-1, and IL-2 in eight patients on admission and at resolution of DKA, and compared them with matched controls. |
| 3620 | 14961992 | The four insulin-independent patients showed prolonged CD4+ T-cell lymphocytopenia; inverted CD4:CD8 ratios; and increases in the percentage of CD4+CD25+ T cells. |
| 3621 | 14980436 | CD28 costimulation enhances the sensitivity of the ELISPOT assay for detection of antigen-specific memory effector CD4 and CD8 cell populations in human diseases. |
| 3622 | 14980436 | CD4 and CD8 IFN-gamma responses to viral (hepatitis C) and autoimmune antigens (islet cell) were tested in 10 hepatitis C and 8 type 1 diabetic as well as healthy control subjects. |
| 3623 | 14980436 | CD28 costimulation enhances the sensitivity of the ELISPOT assay for detection of antigen-specific memory effector CD4 and CD8 cell populations in human diseases. |
| 3624 | 14980436 | CD4 and CD8 IFN-gamma responses to viral (hepatitis C) and autoimmune antigens (islet cell) were tested in 10 hepatitis C and 8 type 1 diabetic as well as healthy control subjects. |
| 3625 | 14980439 | MHC tetramers have become essential tools for the analysis of antigen specific responses of CD8+ and CD4+ T cells. |
| 3626 | 15024185 | The expression of cytokine genes in the peritoneal macrophages and splenic CD4- and CD8-positive lymphocytes of the nonobese diabetic mice. |
| 3627 | 15024185 | In this study, we showed that the mRNA expression of the pro-inflammatory cytokines, TNF-alpha, IL-1 beta, IL-6, and GM-CSF, were increased while the anti-inflammatory cytokine, TGF-beta, decreased in the peritoneal macrophages of nonobese diabetic (NOD) mice. |
| 3628 | 15024185 | Surprisingly the expression of IFN-gamma and IL-2 by splenic CD4+ cells were lower in 5-week-old NOD mice as compared to the nonobese diabetic resistant (NOR) control mice, but their expression was higher in older NOD mice. |
| 3629 | 15024185 | The expression of IL-4 and IL-10 decreased in splenic CD4-positive lymphocytes. |
| 3630 | 15024185 | Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred. |
| 3631 | 15024185 | The expression of cytokine genes in the peritoneal macrophages and splenic CD4- and CD8-positive lymphocytes of the nonobese diabetic mice. |
| 3632 | 15024185 | In this study, we showed that the mRNA expression of the pro-inflammatory cytokines, TNF-alpha, IL-1 beta, IL-6, and GM-CSF, were increased while the anti-inflammatory cytokine, TGF-beta, decreased in the peritoneal macrophages of nonobese diabetic (NOD) mice. |
| 3633 | 15024185 | Surprisingly the expression of IFN-gamma and IL-2 by splenic CD4+ cells were lower in 5-week-old NOD mice as compared to the nonobese diabetic resistant (NOR) control mice, but their expression was higher in older NOD mice. |
| 3634 | 15024185 | The expression of IL-4 and IL-10 decreased in splenic CD4-positive lymphocytes. |
| 3635 | 15024185 | Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred. |
| 3636 | 15024185 | The expression of cytokine genes in the peritoneal macrophages and splenic CD4- and CD8-positive lymphocytes of the nonobese diabetic mice. |
| 3637 | 15024185 | In this study, we showed that the mRNA expression of the pro-inflammatory cytokines, TNF-alpha, IL-1 beta, IL-6, and GM-CSF, were increased while the anti-inflammatory cytokine, TGF-beta, decreased in the peritoneal macrophages of nonobese diabetic (NOD) mice. |
| 3638 | 15024185 | Surprisingly the expression of IFN-gamma and IL-2 by splenic CD4+ cells were lower in 5-week-old NOD mice as compared to the nonobese diabetic resistant (NOR) control mice, but their expression was higher in older NOD mice. |
| 3639 | 15024185 | The expression of IL-4 and IL-10 decreased in splenic CD4-positive lymphocytes. |
| 3640 | 15024185 | Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred. |
| 3641 | 15030582 | The coexpression of HLA and CD3, CD4, CD8, CD19 and CD14 molecules was evaluated by flow cytometry. |
| 3642 | 15030582 | Patients presented decreased percentage of double-positive CD4(+)/DQ(+) cells and increased percentage of CD19(+)/DR(+) cells, irrespective of the HLA class II profile; however, the more dramatic alteration of the lymphomononuclear phenotype profile was observed for patients possessing the HLA-DQB1*0201 allele. |
| 3643 | 15030582 | These patients exhibited decreased percentage of CD3(+), CD4(+), CD8(+), CD19(+) and CD14(+) cells bearing HLA-DQ molecules and decreased fluorescence intensity for HLA-DQ molecules on CD19(+) cells compared to patients without the DQB1*0201 allele. |
| 3644 | 15030582 | Although type 1 diabetes patients shared CD4/DQ or CD19/DR phenotype abnormalities, patients typed as DQB1*0201 presented additional abnormalities in terms of DQ expression and cell phenotypes bearing DQ molecules. |
| 3645 | 15030582 | The coexpression of HLA and CD3, CD4, CD8, CD19 and CD14 molecules was evaluated by flow cytometry. |
| 3646 | 15030582 | Patients presented decreased percentage of double-positive CD4(+)/DQ(+) cells and increased percentage of CD19(+)/DR(+) cells, irrespective of the HLA class II profile; however, the more dramatic alteration of the lymphomononuclear phenotype profile was observed for patients possessing the HLA-DQB1*0201 allele. |
| 3647 | 15030582 | These patients exhibited decreased percentage of CD3(+), CD4(+), CD8(+), CD19(+) and CD14(+) cells bearing HLA-DQ molecules and decreased fluorescence intensity for HLA-DQ molecules on CD19(+) cells compared to patients without the DQB1*0201 allele. |
| 3648 | 15030582 | Although type 1 diabetes patients shared CD4/DQ or CD19/DR phenotype abnormalities, patients typed as DQB1*0201 presented additional abnormalities in terms of DQ expression and cell phenotypes bearing DQ molecules. |
| 3649 | 15030582 | The coexpression of HLA and CD3, CD4, CD8, CD19 and CD14 molecules was evaluated by flow cytometry. |
| 3650 | 15030582 | Patients presented decreased percentage of double-positive CD4(+)/DQ(+) cells and increased percentage of CD19(+)/DR(+) cells, irrespective of the HLA class II profile; however, the more dramatic alteration of the lymphomononuclear phenotype profile was observed for patients possessing the HLA-DQB1*0201 allele. |
| 3651 | 15030582 | These patients exhibited decreased percentage of CD3(+), CD4(+), CD8(+), CD19(+) and CD14(+) cells bearing HLA-DQ molecules and decreased fluorescence intensity for HLA-DQ molecules on CD19(+) cells compared to patients without the DQB1*0201 allele. |
| 3652 | 15030582 | Although type 1 diabetes patients shared CD4/DQ or CD19/DR phenotype abnormalities, patients typed as DQB1*0201 presented additional abnormalities in terms of DQ expression and cell phenotypes bearing DQ molecules. |
| 3653 | 15030582 | The coexpression of HLA and CD3, CD4, CD8, CD19 and CD14 molecules was evaluated by flow cytometry. |
| 3654 | 15030582 | Patients presented decreased percentage of double-positive CD4(+)/DQ(+) cells and increased percentage of CD19(+)/DR(+) cells, irrespective of the HLA class II profile; however, the more dramatic alteration of the lymphomononuclear phenotype profile was observed for patients possessing the HLA-DQB1*0201 allele. |
| 3655 | 15030582 | These patients exhibited decreased percentage of CD3(+), CD4(+), CD8(+), CD19(+) and CD14(+) cells bearing HLA-DQ molecules and decreased fluorescence intensity for HLA-DQ molecules on CD19(+) cells compared to patients without the DQB1*0201 allele. |
| 3656 | 15030582 | Although type 1 diabetes patients shared CD4/DQ or CD19/DR phenotype abnormalities, patients typed as DQB1*0201 presented additional abnormalities in terms of DQ expression and cell phenotypes bearing DQ molecules. |
| 3657 | 15034081 | Using tetramer staining, TdT(-/-) and TdT(+/+) NOD mice showed similar frequencies of the diabetogenic BDC 2.5 CD4(+) T cells. |
| 3658 | 15034081 | We found no increase in CD4(+)CD25(+) regulatory T cells in NOD TdT(-/-) mice. |
| 3659 | 15034081 | Using tetramer staining, TdT(-/-) and TdT(+/+) NOD mice showed similar frequencies of the diabetogenic BDC 2.5 CD4(+) T cells. |
| 3660 | 15034081 | We found no increase in CD4(+)CD25(+) regulatory T cells in NOD TdT(-/-) mice. |
| 3661 | 15035967 | Autoreactive CD4(+) T helper cells and CD8(+) cytotoxic T lymphocytes (CTLs) recognize b-cell-derived peptides in the context of major histocompatibility complex class II and I molecules, respectively, in a process that terminates in b-cell death. |
| 3662 | 15047612 | The activation requirements of autoreactive CD4(+) T-cells were investigated in GAD65-specific HLA-DR0401-restricted clones derived from a diabetic patient using major histocompatibility complex (MHC) class II tetramers (TMrs) as stimulating agents. |
| 3663 | 15047612 | These signals ranged from the early steps of phospholipase C (PLC)-gamma(1) phosphorylation and Ca(2+) mobilization to more complex events, such as CD69 upregulation, cytokine mRNA transcription and secretion, and proliferation. |
| 3664 | 15048713 | Granulocyte-macrophage colony-stimulating factor (GM-CSF) is frequently used in preclinical and clinical protocols to modulate autoimmune responses, bone marrow transplants, and recovery from immune ablative therapies. |
| 3665 | 15048713 | In vivo transfer of CD8(+) and CD4(+) T cells demonstrate that autoreactive T cells undergo extensive division in pancreatic lymph nodes of GM-CSF-transgenic mice compared with wild-type NOD male mice. |
| 3666 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3667 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3668 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3669 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3670 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3671 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3672 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3673 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3674 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3675 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3676 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3677 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3678 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3679 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3680 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3681 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3682 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3683 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3684 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3685 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3686 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3687 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3688 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3689 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3690 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3691 | 15096540 | T-bet controls autoaggressive CD8 lymphocyte responses in type 1 diabetes. |
| 3692 | 15096540 | The T-box transcription factor T-bet is known to control lineage commitment and interferon-gamma production by T helper 1 (Th1) CD4 lymphocytes. |
| 3693 | 15096540 | We report here that T-bet is essential for development of CD8 lymphocyte-dependent autoimmune diabetes (type 1 diabetes [T1D]) in the rat insulin promoter-lymphocytic choriomeningitis virus (LCMV) transgenic model for virally induced T1D. |
| 3694 | 15096540 | In the absence of T-bet, autoaggressive (anti-LCMV) CD8 lymphocytes were reduced in number and produced less IFN-gamma, but increased IL-2 compared with controls. |
| 3695 | 15096540 | Further analysis showed that T-bet intrinsically controls the generation, but not apoptosis, maintenance, or secondary expansion of antiviral effector/memory CD8 lymphocytes. |
| 3696 | 15100283 | Injection of naive OVA-specific CD8 T cells into transgenic mice expressing OVA in the pancreas only resulted in islet destruction when activated CD4 Th cells were coinjected. |
| 3697 | 15100283 | This requirement for activated CD4 T cell help for induction of primary CD8 T cell-mediated immunity to tissue Ags contrasts recent reports suggesting that help is only important for CTL memory. |
| 3698 | 15100283 | Our findings show that signaling of CD40 on the dendritic cell presenting to CD8 T cells is important, but not sufficient, for induction of diabetes. |
| 3699 | 15100283 | Injection of naive OVA-specific CD8 T cells into transgenic mice expressing OVA in the pancreas only resulted in islet destruction when activated CD4 Th cells were coinjected. |
| 3700 | 15100283 | This requirement for activated CD4 T cell help for induction of primary CD8 T cell-mediated immunity to tissue Ags contrasts recent reports suggesting that help is only important for CTL memory. |
| 3701 | 15100283 | Our findings show that signaling of CD40 on the dendritic cell presenting to CD8 T cells is important, but not sufficient, for induction of diabetes. |
| 3702 | 15114683 | We previously demonstrated that peripheral CD4(lo)CD40(+) T cells give rise to pathogenic T cells in the non-obese diabetic (NOD) model. |
| 3703 | 15114683 | Here we show that peripheral CD4(+)CD40(+) T cells from diabetic or pre-diabetic NOD mice induce insulin-dependent diabetes mellitus. |
| 3704 | 15114683 | Consistent with breach of peripheral tolerance, CD4(lo)CD40(+) T cells expand with age in NOD mice but not in MHC-matched non-obese resistant (NOR) or BALB/c controls. |
| 3705 | 15114683 | Suggestive of a causal role for CD40 in autoimmunity, blocking CD40-CD154 interactions early during NOD development prevents autoaggressive T cell expansion while promoting increases in CD4(+)CD25(+) regulatory T cells. |
| 3706 | 15114683 | We previously demonstrated that peripheral CD4(lo)CD40(+) T cells give rise to pathogenic T cells in the non-obese diabetic (NOD) model. |
| 3707 | 15114683 | Here we show that peripheral CD4(+)CD40(+) T cells from diabetic or pre-diabetic NOD mice induce insulin-dependent diabetes mellitus. |
| 3708 | 15114683 | Consistent with breach of peripheral tolerance, CD4(lo)CD40(+) T cells expand with age in NOD mice but not in MHC-matched non-obese resistant (NOR) or BALB/c controls. |
| 3709 | 15114683 | Suggestive of a causal role for CD40 in autoimmunity, blocking CD40-CD154 interactions early during NOD development prevents autoaggressive T cell expansion while promoting increases in CD4(+)CD25(+) regulatory T cells. |
| 3710 | 15114683 | We previously demonstrated that peripheral CD4(lo)CD40(+) T cells give rise to pathogenic T cells in the non-obese diabetic (NOD) model. |
| 3711 | 15114683 | Here we show that peripheral CD4(+)CD40(+) T cells from diabetic or pre-diabetic NOD mice induce insulin-dependent diabetes mellitus. |
| 3712 | 15114683 | Consistent with breach of peripheral tolerance, CD4(lo)CD40(+) T cells expand with age in NOD mice but not in MHC-matched non-obese resistant (NOR) or BALB/c controls. |
| 3713 | 15114683 | Suggestive of a causal role for CD40 in autoimmunity, blocking CD40-CD154 interactions early during NOD development prevents autoaggressive T cell expansion while promoting increases in CD4(+)CD25(+) regulatory T cells. |
| 3714 | 15114683 | We previously demonstrated that peripheral CD4(lo)CD40(+) T cells give rise to pathogenic T cells in the non-obese diabetic (NOD) model. |
| 3715 | 15114683 | Here we show that peripheral CD4(+)CD40(+) T cells from diabetic or pre-diabetic NOD mice induce insulin-dependent diabetes mellitus. |
| 3716 | 15114683 | Consistent with breach of peripheral tolerance, CD4(lo)CD40(+) T cells expand with age in NOD mice but not in MHC-matched non-obese resistant (NOR) or BALB/c controls. |
| 3717 | 15114683 | Suggestive of a causal role for CD40 in autoimmunity, blocking CD40-CD154 interactions early during NOD development prevents autoaggressive T cell expansion while promoting increases in CD4(+)CD25(+) regulatory T cells. |
| 3718 | 15117972 | Defective suppressor function of human CD4+ CD25+ regulatory T cells in autoimmune polyglandular syndrome type II. |
| 3719 | 15117972 | However, in several murine models, depletion of CD4(+) CD25(+) regulatory T cells (T(regs)) causes a syndrome resembling human APS-II with multiple endocrinopathies. |
| 3720 | 15117972 | Defective suppressor function of human CD4+ CD25+ regulatory T cells in autoimmune polyglandular syndrome type II. |
| 3721 | 15117972 | However, in several murine models, depletion of CD4(+) CD25(+) regulatory T cells (T(regs)) causes a syndrome resembling human APS-II with multiple endocrinopathies. |
| 3722 | 15127321 | In this study we initially evaluated 43 patients with recent-onset Type 1 diabetes (disease duration <or= 6 months, 29 ICA positive) with regard to beta-cell secretion stimulation test with glucagon and immunologic parameters, including CD4 +, CD8 +, CD4 + CD25 +, CD8 + CD25 + lymphocyte subsets. |
| 3723 | 15127321 | The percentage of CD4 + cells was 42 +/- 9,4 % (healthy controls 44 +/- 7.3 %, p nonsig.) and percentage of CD8 + was 33 +/- 8.6 % (healthy control 31 +/- 8.3 %, p nonsig.). |
| 3724 | 15127321 | Relative size of CD4 + CD25 + subpopulation was 7 +/- 5.4 % (healthy control 2 +/- 2 %, p < 0.001). |
| 3725 | 15127321 | The change in the excursion of C-peptide between baseline and follow-up visit (C-peptide6min (6month-baseline)) showed mild, negative correlation with relative size of the CD8 + CD25 + subpopulation (r = - 0.511, p = 0.025), which may indicate that the size of this cell subpopulation has predictive value in assessing future functional beta-cell changes. |
| 3726 | 15127321 | In this study we initially evaluated 43 patients with recent-onset Type 1 diabetes (disease duration <or= 6 months, 29 ICA positive) with regard to beta-cell secretion stimulation test with glucagon and immunologic parameters, including CD4 +, CD8 +, CD4 + CD25 +, CD8 + CD25 + lymphocyte subsets. |
| 3727 | 15127321 | The percentage of CD4 + cells was 42 +/- 9,4 % (healthy controls 44 +/- 7.3 %, p nonsig.) and percentage of CD8 + was 33 +/- 8.6 % (healthy control 31 +/- 8.3 %, p nonsig.). |
| 3728 | 15127321 | Relative size of CD4 + CD25 + subpopulation was 7 +/- 5.4 % (healthy control 2 +/- 2 %, p < 0.001). |
| 3729 | 15127321 | The change in the excursion of C-peptide between baseline and follow-up visit (C-peptide6min (6month-baseline)) showed mild, negative correlation with relative size of the CD8 + CD25 + subpopulation (r = - 0.511, p = 0.025), which may indicate that the size of this cell subpopulation has predictive value in assessing future functional beta-cell changes. |
| 3730 | 15127321 | In this study we initially evaluated 43 patients with recent-onset Type 1 diabetes (disease duration <or= 6 months, 29 ICA positive) with regard to beta-cell secretion stimulation test with glucagon and immunologic parameters, including CD4 +, CD8 +, CD4 + CD25 +, CD8 + CD25 + lymphocyte subsets. |
| 3731 | 15127321 | The percentage of CD4 + cells was 42 +/- 9,4 % (healthy controls 44 +/- 7.3 %, p nonsig.) and percentage of CD8 + was 33 +/- 8.6 % (healthy control 31 +/- 8.3 %, p nonsig.). |
| 3732 | 15127321 | Relative size of CD4 + CD25 + subpopulation was 7 +/- 5.4 % (healthy control 2 +/- 2 %, p < 0.001). |
| 3733 | 15127321 | The change in the excursion of C-peptide between baseline and follow-up visit (C-peptide6min (6month-baseline)) showed mild, negative correlation with relative size of the CD8 + CD25 + subpopulation (r = - 0.511, p = 0.025), which may indicate that the size of this cell subpopulation has predictive value in assessing future functional beta-cell changes. |
| 3734 | 15128778 | The presence of autoreactive CD4(+) T cells in the peripheral blood of healthy human subjects was investigated after removal of CD4(+)CD25(+) regulatory T cells (Treg). |
| 3735 | 15128778 | CD4(+) T cells that were directed against the type 1 diabetes-associated autoantigen glutamic acid decarboxylase 65, the melanocyte differentiation Ag tyrosinase, and the cancer/testis tumor Ag NY-ESO-1 were readily derived from PBMC of healthy individuals. |
| 3736 | 15128778 | Addition of CD4(+)CD25(+) Treg back to the CD4(+)CD25(-) population suppressed the expansion of the autoreactive T cells. |
| 3737 | 15128778 | The presence of autoreactive CD4(+) T cells in the peripheral blood of healthy human subjects was investigated after removal of CD4(+)CD25(+) regulatory T cells (Treg). |
| 3738 | 15128778 | CD4(+) T cells that were directed against the type 1 diabetes-associated autoantigen glutamic acid decarboxylase 65, the melanocyte differentiation Ag tyrosinase, and the cancer/testis tumor Ag NY-ESO-1 were readily derived from PBMC of healthy individuals. |
| 3739 | 15128778 | Addition of CD4(+)CD25(+) Treg back to the CD4(+)CD25(-) population suppressed the expansion of the autoreactive T cells. |
| 3740 | 15128778 | The presence of autoreactive CD4(+) T cells in the peripheral blood of healthy human subjects was investigated after removal of CD4(+)CD25(+) regulatory T cells (Treg). |
| 3741 | 15128778 | CD4(+) T cells that were directed against the type 1 diabetes-associated autoantigen glutamic acid decarboxylase 65, the melanocyte differentiation Ag tyrosinase, and the cancer/testis tumor Ag NY-ESO-1 were readily derived from PBMC of healthy individuals. |
| 3742 | 15128778 | Addition of CD4(+)CD25(+) Treg back to the CD4(+)CD25(-) population suppressed the expansion of the autoreactive T cells. |
| 3743 | 15133294 | The results showed that the radon and thermal therapy enhanced the antioxidation functions, such as the activities of superoxide dismutase (SOD) and catalase, which inhibit lipid peroxidation and total cholesterol produced in the body. |
| 3744 | 15133294 | Moreover the therapy enhanced concanavalin A (ConA)-induced mitogen response and increased the percentage of CD4 positive cells, which is the marker of helper T cells, and decreased the percentage of CD8 positive cells, which is the common marker of killer T cells and suppressor T cells, in the white blood cell differentiation antigen (CD8/CD4) assay. |
| 3745 | 15133294 | Furthermore, the therapy increased the levels of alpha atrial natriuretic polypeptide (alpha ANP), beta endorphin, adrenocorticotropic hormone (ACTH), insulin and glucose-6-phosphate dehydrogenase (G-6-PDH), and it decreased the vasopression level. |
| 3746 | 15147359 | We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. |
| 3747 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 3748 | 15147359 | Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4(+)CD8(+) lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. |
| 3749 | 15147359 | In the whole study group, we found a correlation (multiple R 0.5, P < 0.001) of CD23(+)CD25(+) cells with blood counts of monocytes, CD4(+)CD8(+) cells, CD25(+) cells, basal haemolysis and plasma levels of thiols. |
| 3750 | 15147359 | In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0.6, P = 0.01) positively with sIL-6R, negatively with duration of diabetes and CD23(+)CD25(+) counts; plasma creatinine correlated positively (multiple R 0.6, P < 0.001) with both sIL-2R and tumour necrosis factor (TNF)-alpha concentration. |
| 3751 | 15147359 | Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4(+)CD8(+), CD23(+)CD25(+) and CD25(+) phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. |
| 3752 | 15147359 | We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. |
| 3753 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 3754 | 15147359 | Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4(+)CD8(+) lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. |
| 3755 | 15147359 | In the whole study group, we found a correlation (multiple R 0.5, P < 0.001) of CD23(+)CD25(+) cells with blood counts of monocytes, CD4(+)CD8(+) cells, CD25(+) cells, basal haemolysis and plasma levels of thiols. |
| 3756 | 15147359 | In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0.6, P = 0.01) positively with sIL-6R, negatively with duration of diabetes and CD23(+)CD25(+) counts; plasma creatinine correlated positively (multiple R 0.6, P < 0.001) with both sIL-2R and tumour necrosis factor (TNF)-alpha concentration. |
| 3757 | 15147359 | Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4(+)CD8(+), CD23(+)CD25(+) and CD25(+) phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. |
| 3758 | 15147359 | We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. |
| 3759 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 3760 | 15147359 | Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4(+)CD8(+) lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. |
| 3761 | 15147359 | In the whole study group, we found a correlation (multiple R 0.5, P < 0.001) of CD23(+)CD25(+) cells with blood counts of monocytes, CD4(+)CD8(+) cells, CD25(+) cells, basal haemolysis and plasma levels of thiols. |
| 3762 | 15147359 | In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0.6, P = 0.01) positively with sIL-6R, negatively with duration of diabetes and CD23(+)CD25(+) counts; plasma creatinine correlated positively (multiple R 0.6, P < 0.001) with both sIL-2R and tumour necrosis factor (TNF)-alpha concentration. |
| 3763 | 15147359 | Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4(+)CD8(+), CD23(+)CD25(+) and CD25(+) phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. |
| 3764 | 15147359 | We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. |
| 3765 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 3766 | 15147359 | Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4(+)CD8(+) lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. |
| 3767 | 15147359 | In the whole study group, we found a correlation (multiple R 0.5, P < 0.001) of CD23(+)CD25(+) cells with blood counts of monocytes, CD4(+)CD8(+) cells, CD25(+) cells, basal haemolysis and plasma levels of thiols. |
| 3768 | 15147359 | In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0.6, P = 0.01) positively with sIL-6R, negatively with duration of diabetes and CD23(+)CD25(+) counts; plasma creatinine correlated positively (multiple R 0.6, P < 0.001) with both sIL-2R and tumour necrosis factor (TNF)-alpha concentration. |
| 3769 | 15147359 | Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4(+)CD8(+), CD23(+)CD25(+) and CD25(+) phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. |
| 3770 | 15184499 | The low number of CD4+ CD25+ regulatory T cells (Tregs), their anergic phenotype, and diverse antigen specificity present major challenges to harnessing this potent tolerogenic population to treat autoimmunity and transplant rejection. |
| 3771 | 15184499 | Purified CD4+ CD25+ Tregs were expanded up to 200-fold in less than 2 wk in vitro using a combination of anti-CD3, anti-CD28, and interleukin 2. |
| 3772 | 15184499 | The low number of CD4+ CD25+ regulatory T cells (Tregs), their anergic phenotype, and diverse antigen specificity present major challenges to harnessing this potent tolerogenic population to treat autoimmunity and transplant rejection. |
| 3773 | 15184499 | Purified CD4+ CD25+ Tregs were expanded up to 200-fold in less than 2 wk in vitro using a combination of anti-CD3, anti-CD28, and interleukin 2. |
| 3774 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3775 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3776 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3777 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3778 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3779 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3780 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3781 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3782 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3783 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3784 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3785 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3786 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3787 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3788 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3789 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3790 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3791 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3792 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3793 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3794 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3795 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3796 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3797 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3798 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3799 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3800 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3801 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3802 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3803 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3804 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3805 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3806 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3807 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3808 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3809 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3810 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3811 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3812 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3813 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3814 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3815 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3816 | 15184500 | CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. |
| 3817 | 15184500 | To silence autoimmunity, we used dendritic cells (DCs) from NOD mice to expand CD25+ CD4+ suppressor T cells from BDC2.5 mice, which are specific for a single islet autoantigen. |
| 3818 | 15184500 | The expanded T cells were more suppressive in vitro than their freshly isolated counterparts, indicating that DCs from autoimmune mice can increase the number and function of antigen-specific, CD25+ CD4+ regulatory T cells. |
| 3819 | 15184500 | Importantly, only 5,000 expanded CD25+ CD4+ BDC2.5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclonal, CD25+ CD4+ T cells from NOD mice were inactive. |
| 3820 | 15184500 | The expanded CD25+ CD4+ BDC2.5 T cells were effective even if administered 14 d after the diabetogenic T cells. |
| 3821 | 15184500 | Our data indicate that DCs can generate CD25+ CD4+ T cells that suppress autoimmune disease in vivo. |
| 3822 | 15184500 | This might be harnessed as a new avenue for immunotherapy, especially because CD25+ CD4+ regulatory cells responsive to a single autoantigen can inhibit diabetes mediated by reactivity to multiple antigens. |
| 3823 | 15184501 | CD4+CD25+ T regulatory cells dependent on ICOS promote regulation of effector cells in the prediabetic lesion. |
| 3824 | 15184501 | CD4+CD25+ T regulatory cells (Tregs) prevent autoimmune disease, yet little is known about precisely where they exert their influence naturally in a spontaneous autoimmune disorder. |
| 3825 | 15184501 | We find that BDC2.5 T cell receptor transgenic animals contain a small subset of FoxP3 positive CD4+CD25+CD69- cells in the pancreas, actively turning over, expressing the clonotypic receptor, and containing functional regulatory activity. |
| 3826 | 15184501 | Gene expression profiling confirms that the CD4+CD25+CD69- cells in pancreatic tissue express transcripts diagnostic of regulatory cells, but with significantly higher levels of interleukin 10 and inducible costimulator (ICOS) than their lymph node counterparts. |
| 3827 | 15184501 | Thus, CD4+CD25+69- Tregs operate directly in the autoimmune lesion and are dependent on ICOS to keep it in a nondestructive state. |
| 3828 | 15184501 | CD4+CD25+ T regulatory cells dependent on ICOS promote regulation of effector cells in the prediabetic lesion. |
| 3829 | 15184501 | CD4+CD25+ T regulatory cells (Tregs) prevent autoimmune disease, yet little is known about precisely where they exert their influence naturally in a spontaneous autoimmune disorder. |
| 3830 | 15184501 | We find that BDC2.5 T cell receptor transgenic animals contain a small subset of FoxP3 positive CD4+CD25+CD69- cells in the pancreas, actively turning over, expressing the clonotypic receptor, and containing functional regulatory activity. |
| 3831 | 15184501 | Gene expression profiling confirms that the CD4+CD25+CD69- cells in pancreatic tissue express transcripts diagnostic of regulatory cells, but with significantly higher levels of interleukin 10 and inducible costimulator (ICOS) than their lymph node counterparts. |
| 3832 | 15184501 | Thus, CD4+CD25+69- Tregs operate directly in the autoimmune lesion and are dependent on ICOS to keep it in a nondestructive state. |
| 3833 | 15184501 | CD4+CD25+ T regulatory cells dependent on ICOS promote regulation of effector cells in the prediabetic lesion. |
| 3834 | 15184501 | CD4+CD25+ T regulatory cells (Tregs) prevent autoimmune disease, yet little is known about precisely where they exert their influence naturally in a spontaneous autoimmune disorder. |
| 3835 | 15184501 | We find that BDC2.5 T cell receptor transgenic animals contain a small subset of FoxP3 positive CD4+CD25+CD69- cells in the pancreas, actively turning over, expressing the clonotypic receptor, and containing functional regulatory activity. |
| 3836 | 15184501 | Gene expression profiling confirms that the CD4+CD25+CD69- cells in pancreatic tissue express transcripts diagnostic of regulatory cells, but with significantly higher levels of interleukin 10 and inducible costimulator (ICOS) than their lymph node counterparts. |
| 3837 | 15184501 | Thus, CD4+CD25+69- Tregs operate directly in the autoimmune lesion and are dependent on ICOS to keep it in a nondestructive state. |
| 3838 | 15184501 | CD4+CD25+ T regulatory cells dependent on ICOS promote regulation of effector cells in the prediabetic lesion. |
| 3839 | 15184501 | CD4+CD25+ T regulatory cells (Tregs) prevent autoimmune disease, yet little is known about precisely where they exert their influence naturally in a spontaneous autoimmune disorder. |
| 3840 | 15184501 | We find that BDC2.5 T cell receptor transgenic animals contain a small subset of FoxP3 positive CD4+CD25+CD69- cells in the pancreas, actively turning over, expressing the clonotypic receptor, and containing functional regulatory activity. |
| 3841 | 15184501 | Gene expression profiling confirms that the CD4+CD25+CD69- cells in pancreatic tissue express transcripts diagnostic of regulatory cells, but with significantly higher levels of interleukin 10 and inducible costimulator (ICOS) than their lymph node counterparts. |
| 3842 | 15184501 | Thus, CD4+CD25+69- Tregs operate directly in the autoimmune lesion and are dependent on ICOS to keep it in a nondestructive state. |
| 3843 | 15184501 | CD4+CD25+ T regulatory cells dependent on ICOS promote regulation of effector cells in the prediabetic lesion. |
| 3844 | 15184501 | CD4+CD25+ T regulatory cells (Tregs) prevent autoimmune disease, yet little is known about precisely where they exert their influence naturally in a spontaneous autoimmune disorder. |
| 3845 | 15184501 | We find that BDC2.5 T cell receptor transgenic animals contain a small subset of FoxP3 positive CD4+CD25+CD69- cells in the pancreas, actively turning over, expressing the clonotypic receptor, and containing functional regulatory activity. |
| 3846 | 15184501 | Gene expression profiling confirms that the CD4+CD25+CD69- cells in pancreatic tissue express transcripts diagnostic of regulatory cells, but with significantly higher levels of interleukin 10 and inducible costimulator (ICOS) than their lymph node counterparts. |
| 3847 | 15184501 | Thus, CD4+CD25+69- Tregs operate directly in the autoimmune lesion and are dependent on ICOS to keep it in a nondestructive state. |
| 3848 | 15192149 | CD154 is a negative regulator of autoaggressive CD8+ T cells in type 1 diabetes. |
| 3849 | 15192149 | TNF/CD80 mice, a CD8(+) T cell-mediated model for type 1 diabetes, transgenically express tumor necrosis factor alpha (TNF-alpha) and the costimulatory molecule CD80 in their pancreatic islets. |
| 3850 | 15192149 | TNF/CD80 CD154-deficient mice rapidly develop diabetes, whereas CD154-sufficient mice do not. |
| 3851 | 15192149 | This finding correlates with the decreased numbers of CD4(+)CD25(+) T regulatory (T(R)) cells in the islets and pancreatic lymph nodes, in comparison to disease-protected CD154-sufficient mice. |
| 3852 | 15192149 | Adoptive transfer studies show that CD8(+) T cells from TNF/CD80 CD154-deficient, but not CD154-sufficient, mice are resistant to regulation in vivo. |
| 3853 | 15192149 | This study provides evidence that CD40-transduced signals initiate T(R) cell increase in vivo and that CD154-transduced signals sensitize autoaggressive CD8(+) T cells to suppression. |
| 3854 | 15194776 | After four immunizations over an 8-month period, all animals developed HCV-specific humoral and cellular immune responses including antibodies to HCV structural proteins and gamma interferon(+) (IFN-gamma(+))CD4(+) and IFN-gamma(+)CD8(+) T-cell responses. |
| 3855 | 15214031 | This resistance was associated with lower production of proinflammatory cytokines and a decreased expansion of PLP(139-151)-specific CD4(+) T cells after immunization and restimulation with PLP peptide in vitro. |
| 3856 | 15220188 | In addition, antidiabetic peroxisome proliferator-activated receptor gamma-activating thiazolidinediones inhibited C-peptide-induced CD4(+) cell chemotaxis as well as PI 3-Kgamma activation. |
| 3857 | 15220219 | Mutations of the forkhead/winged helix transcription factor FOXP3 gene on chromosome Xp11.23 cause a rare recessive monogenic disorder called IPEX (immune dysregulation, polyendocrinopathy, including type 1 diabetes, enteropathy, and X-linked syndrome). |
| 3858 | 15220219 | FOXP3 is necessary for the differentiation of a key immune suppressive subset of T-cells, the CD4+CD25+ regulatory T-cells. |
| 3859 | 15229381 | KRV causes autoimmune type 1 diabetes in diabetes resistant-BioBreeding rats by breakdown of immune balance, including the preferential activation of effector T cells, such as Th1-like CD45RC+CD4+ T cells and CD8+ T cells, and down-regulation of Th2-like CD45RC-CD4+ and CD4+CD25+ T cells, rather than by direct infection of pancreatic beta cells. |
| 3860 | 15238071 | As compared with normal animals, NOD thymocytes (including the CD4+CD25+ regulatory T cells) exhibit a decrease in the membrane expression of alpha5beta1, resulting in a functional impairment of fibronectin-mediated interactions, including cell migration. |
| 3861 | 15239090 | The total CD4(+) and CD8(+) cell response was analyzed with 600 overlapping HCV peptides and 6 proteins by ex vivo enzyme-linked immunospot (ELISpot), intracellular cytokine staining, and proliferation assays. |
| 3862 | 15240736 | RAGE expression was detected on CD4(+), CD8(+), and B cells from diabetic mice and transferred to NOD/scid recipients. |
| 3863 | 15240736 | RAGE blockade was associated with increased expression of IL-10 and TGF-beta in the islets from protected mice. |
| 3864 | 15270841 | However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. |
| 3865 | 15270841 | Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). |
| 3866 | 15270841 | Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). |
| 3867 | 15270841 | Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). |
| 3868 | 15270841 | However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. |
| 3869 | 15270841 | Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). |
| 3870 | 15270841 | Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). |
| 3871 | 15270841 | Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). |
| 3872 | 15270855 | We performed flow cytometry for lymphocyte subtypes and for activation markers (HLA-DR, CD25, and CD69 or CD71). |
| 3873 | 15270855 | The ratios of both T to B cells and CD4+ to CD8+ cells were elevated at birth, but CD4+ cells were not activated. |
| 3874 | 15277377 | GAD65-specific CD4+ T-cells with high antigen avidity are prevalent in peripheral blood of patients with type 1 diabetes. |
| 3875 | 15277378 | Strikingly, treatment of NOD mice with Flt3-ligand significantly decreased insulitis and progression to diabetes and was associated with a significant increase in myeloid dendritic cells and in vivo induction of CD4+/CD25+ cells in the pancreatic lymph node. |
| 3876 | 15294969 | CD8(+) T cells are essential for the destruction of the insulin-producing pancreatic beta cells characterizing this disease. |
| 3877 | 15294969 | AI4 is a pathogenic CD8(+) T cell clone, isolated from the islets of a 5-wk-old female NOD mouse, which is capable of mediating overt diabetes in the absence of CD4(+) T cell help. |
| 3878 | 15296648 | Intracellular IFN-gamma production and IL-12 serum levels in latent autoimmune diabetes of adults (LADA) and in type 2 diabetes. |
| 3879 | 15296648 | Th1 cytokines, such as interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), and Th1-inducing cytokines, such as IL-12, are involved in the pathogenesis of various organ-specific autoimmune diseases, including autoimmune diabetes. |
| 3880 | 15296648 | In this study, we investigated intracellular IFN-gamma release by T lymphocytes and IL-12 serum levels in 48 type 2 and 36 latent autoimmune diabetes of adults (LADA) diabetics and 25 control subjects in an attempt to evaluate their role in the pathogenesis of these clinical entities. |
| 3881 | 15296648 | In all study groups, IFN-gamma content of CD4(+) and CD8(+) lymphocytes was significantly upregulated by stimulation. |
| 3882 | 15296648 | Furthermore, it was observed that CD4(+) and CD8(+) lymphocytes from type 2 diabetics produced significantly lower levels of IFN-gamma compared with LADA patients and controls. |
| 3883 | 15296648 | However, the percentages of CD4(+)/IFN-gamma(+) and CD8(+)/IFN-gamma(+) cells from type 2 diabetics were significantly higher compared with controls. |
| 3884 | 15296648 | In contrast, the low IFN-gamma levels observed in type 2 diabetics in combination with the low IL-12 serum levels might be a contributing factor in the frequently observed chronic complications in these patients. |
| 3885 | 15296648 | Intracellular IFN-gamma production and IL-12 serum levels in latent autoimmune diabetes of adults (LADA) and in type 2 diabetes. |
| 3886 | 15296648 | Th1 cytokines, such as interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), and Th1-inducing cytokines, such as IL-12, are involved in the pathogenesis of various organ-specific autoimmune diseases, including autoimmune diabetes. |
| 3887 | 15296648 | In this study, we investigated intracellular IFN-gamma release by T lymphocytes and IL-12 serum levels in 48 type 2 and 36 latent autoimmune diabetes of adults (LADA) diabetics and 25 control subjects in an attempt to evaluate their role in the pathogenesis of these clinical entities. |
| 3888 | 15296648 | In all study groups, IFN-gamma content of CD4(+) and CD8(+) lymphocytes was significantly upregulated by stimulation. |
| 3889 | 15296648 | Furthermore, it was observed that CD4(+) and CD8(+) lymphocytes from type 2 diabetics produced significantly lower levels of IFN-gamma compared with LADA patients and controls. |
| 3890 | 15296648 | However, the percentages of CD4(+)/IFN-gamma(+) and CD8(+)/IFN-gamma(+) cells from type 2 diabetics were significantly higher compared with controls. |
| 3891 | 15296648 | In contrast, the low IFN-gamma levels observed in type 2 diabetics in combination with the low IL-12 serum levels might be a contributing factor in the frequently observed chronic complications in these patients. |
| 3892 | 15296648 | Intracellular IFN-gamma production and IL-12 serum levels in latent autoimmune diabetes of adults (LADA) and in type 2 diabetes. |
| 3893 | 15296648 | Th1 cytokines, such as interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), and Th1-inducing cytokines, such as IL-12, are involved in the pathogenesis of various organ-specific autoimmune diseases, including autoimmune diabetes. |
| 3894 | 15296648 | In this study, we investigated intracellular IFN-gamma release by T lymphocytes and IL-12 serum levels in 48 type 2 and 36 latent autoimmune diabetes of adults (LADA) diabetics and 25 control subjects in an attempt to evaluate their role in the pathogenesis of these clinical entities. |
| 3895 | 15296648 | In all study groups, IFN-gamma content of CD4(+) and CD8(+) lymphocytes was significantly upregulated by stimulation. |
| 3896 | 15296648 | Furthermore, it was observed that CD4(+) and CD8(+) lymphocytes from type 2 diabetics produced significantly lower levels of IFN-gamma compared with LADA patients and controls. |
| 3897 | 15296648 | However, the percentages of CD4(+)/IFN-gamma(+) and CD8(+)/IFN-gamma(+) cells from type 2 diabetics were significantly higher compared with controls. |
| 3898 | 15296648 | In contrast, the low IFN-gamma levels observed in type 2 diabetics in combination with the low IL-12 serum levels might be a contributing factor in the frequently observed chronic complications in these patients. |
| 3899 | 15302166 | Compared to controls, patients presented increased fluorescence intensity of HLA class I molecules on CD3+, CD4+ and CD8+ cells. |
| 3900 | 15313430 | These teratogenic effects were accompanied by a decreased percentage of cells expressing Mac-1, Thy-1.2, CD4 or CD8 in the spleen and inguinal as well as paraaortic lymph nodes, except for Mac-1 expression by splenocytes, which increased significantly in the beginning of pregnancy and decreased later. |
| 3901 | 15322272 | Therapeutic vaccination using CD4+CD25+ antigen-specific regulatory T cells. |
| 3902 | 15322272 | In this review, we summarize current efforts to induce and maintain tolerance in the autoimmune diabetes setting by using therapeutic vaccination with CD4(+)CD25(+) regulatory T cells. |
| 3903 | 15322272 | Therapeutic vaccination using CD4+CD25+ antigen-specific regulatory T cells. |
| 3904 | 15322272 | In this review, we summarize current efforts to induce and maintain tolerance in the autoimmune diabetes setting by using therapeutic vaccination with CD4(+)CD25(+) regulatory T cells. |
| 3905 | 15324933 | This was followed by an imbalance between CD4(+)CD25(+) and CD4(+)CD69(+) T cells in the pancreas that was mirrored in the phenotype of autoreactive T cells in the blood. |
| 3906 | 15324933 | Waves of activated CD4(+)CD69(+) T cells in blood preceded the disease onset suggesting that the autoimmune attack on pancreas is a discontinuous "hit-and-run" rather than a continuous process. |
| 3907 | 15324933 | This was followed by an imbalance between CD4(+)CD25(+) and CD4(+)CD69(+) T cells in the pancreas that was mirrored in the phenotype of autoreactive T cells in the blood. |
| 3908 | 15324933 | Waves of activated CD4(+)CD69(+) T cells in blood preceded the disease onset suggesting that the autoimmune attack on pancreas is a discontinuous "hit-and-run" rather than a continuous process. |
| 3909 | 15340148 | Unique role of CD4+CD62L+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice. |
| 3910 | 15340148 | We first show that diabetes onset is prevented in such mice by infusion of polyclonal CD4(+) T cells expressing L-selectin (CD62L) but not prevented or only marginally prevented by CD4(+)CD25(+) T cells. |
| 3911 | 15340148 | Similarly, we found with a cotransfer model that CD4(+)CD62L(+) T cells but not CD4(+)CD25(+) T cells inhibited diabetes transfer into NOD SCID recipients by transgenic NOD BDC2.5 SCID cells. |
| 3912 | 15340148 | Data are presented arguing for the role of CD4(+)CD62L(+) T cells present within the polyclonal diabetogenic population in mediating this apparently paradoxical effect. |
| 3913 | 15340148 | Collectively, these data confirm the central role of CD4(+)CD62L(+) regulatory T cells in controlling disease onset in a well defined transgenic model of autoimmune diabetes and suggest the intervention of homeostatic mechanisms as part of their mode of action. |
| 3914 | 15340148 | Unique role of CD4+CD62L+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice. |
| 3915 | 15340148 | We first show that diabetes onset is prevented in such mice by infusion of polyclonal CD4(+) T cells expressing L-selectin (CD62L) but not prevented or only marginally prevented by CD4(+)CD25(+) T cells. |
| 3916 | 15340148 | Similarly, we found with a cotransfer model that CD4(+)CD62L(+) T cells but not CD4(+)CD25(+) T cells inhibited diabetes transfer into NOD SCID recipients by transgenic NOD BDC2.5 SCID cells. |
| 3917 | 15340148 | Data are presented arguing for the role of CD4(+)CD62L(+) T cells present within the polyclonal diabetogenic population in mediating this apparently paradoxical effect. |
| 3918 | 15340148 | Collectively, these data confirm the central role of CD4(+)CD62L(+) regulatory T cells in controlling disease onset in a well defined transgenic model of autoimmune diabetes and suggest the intervention of homeostatic mechanisms as part of their mode of action. |
| 3919 | 15340148 | Unique role of CD4+CD62L+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice. |
| 3920 | 15340148 | We first show that diabetes onset is prevented in such mice by infusion of polyclonal CD4(+) T cells expressing L-selectin (CD62L) but not prevented or only marginally prevented by CD4(+)CD25(+) T cells. |
| 3921 | 15340148 | Similarly, we found with a cotransfer model that CD4(+)CD62L(+) T cells but not CD4(+)CD25(+) T cells inhibited diabetes transfer into NOD SCID recipients by transgenic NOD BDC2.5 SCID cells. |
| 3922 | 15340148 | Data are presented arguing for the role of CD4(+)CD62L(+) T cells present within the polyclonal diabetogenic population in mediating this apparently paradoxical effect. |
| 3923 | 15340148 | Collectively, these data confirm the central role of CD4(+)CD62L(+) regulatory T cells in controlling disease onset in a well defined transgenic model of autoimmune diabetes and suggest the intervention of homeostatic mechanisms as part of their mode of action. |
| 3924 | 15340148 | Unique role of CD4+CD62L+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice. |
| 3925 | 15340148 | We first show that diabetes onset is prevented in such mice by infusion of polyclonal CD4(+) T cells expressing L-selectin (CD62L) but not prevented or only marginally prevented by CD4(+)CD25(+) T cells. |
| 3926 | 15340148 | Similarly, we found with a cotransfer model that CD4(+)CD62L(+) T cells but not CD4(+)CD25(+) T cells inhibited diabetes transfer into NOD SCID recipients by transgenic NOD BDC2.5 SCID cells. |
| 3927 | 15340148 | Data are presented arguing for the role of CD4(+)CD62L(+) T cells present within the polyclonal diabetogenic population in mediating this apparently paradoxical effect. |
| 3928 | 15340148 | Collectively, these data confirm the central role of CD4(+)CD62L(+) regulatory T cells in controlling disease onset in a well defined transgenic model of autoimmune diabetes and suggest the intervention of homeostatic mechanisms as part of their mode of action. |
| 3929 | 15340148 | Unique role of CD4+CD62L+ regulatory T cells in the control of autoimmune diabetes in T cell receptor transgenic mice. |
| 3930 | 15340148 | We first show that diabetes onset is prevented in such mice by infusion of polyclonal CD4(+) T cells expressing L-selectin (CD62L) but not prevented or only marginally prevented by CD4(+)CD25(+) T cells. |
| 3931 | 15340148 | Similarly, we found with a cotransfer model that CD4(+)CD62L(+) T cells but not CD4(+)CD25(+) T cells inhibited diabetes transfer into NOD SCID recipients by transgenic NOD BDC2.5 SCID cells. |
| 3932 | 15340148 | Data are presented arguing for the role of CD4(+)CD62L(+) T cells present within the polyclonal diabetogenic population in mediating this apparently paradoxical effect. |
| 3933 | 15340148 | Collectively, these data confirm the central role of CD4(+)CD62L(+) regulatory T cells in controlling disease onset in a well defined transgenic model of autoimmune diabetes and suggest the intervention of homeostatic mechanisms as part of their mode of action. |
| 3934 | 15343360 | Parallel with disease protection, we observed a prolonged increase of the numbers of CD4+CD25+ T cells in the periphery of GAD-IgG-treated mice, compared to those treated with a control IgG vector, both in the prediabetic period and persisting even 8 months after gene therapy. |
| 3935 | 15343360 | Moreover, CD4+CD25+ T cells induced by GAD-IgG fusion construct were capable of suppressing the proliferative response of CD4+CD25- T cells in vitro; and ablation of the activity of CD4+CD25+ T cells by blocking antibody against CD25 could reverse GAD-specific T-cell hyporesponsiveness. |
| 3936 | 15343360 | These results suggested that CD4+CD25+ T-cell subset induced in GAD-IgG-treated NOD mice represented the regulatory or suppressive CD4+CD25+ T cells (Treg) and might play an important role in the induction and maintenance of tolerance in NOD mice. |
| 3937 | 15343360 | Furthermore, the numbers of splenic CD4+CD62L+ regulatory T cells in GAD-IgG-treated mice during the prediabetic period and serum TGF-beta levels in 34-38-week-old GAD-IgG-protected mice were also increased, compared to control IgG-treated ones. |
| 3938 | 15343360 | Parallel with disease protection, we observed a prolonged increase of the numbers of CD4+CD25+ T cells in the periphery of GAD-IgG-treated mice, compared to those treated with a control IgG vector, both in the prediabetic period and persisting even 8 months after gene therapy. |
| 3939 | 15343360 | Moreover, CD4+CD25+ T cells induced by GAD-IgG fusion construct were capable of suppressing the proliferative response of CD4+CD25- T cells in vitro; and ablation of the activity of CD4+CD25+ T cells by blocking antibody against CD25 could reverse GAD-specific T-cell hyporesponsiveness. |
| 3940 | 15343360 | These results suggested that CD4+CD25+ T-cell subset induced in GAD-IgG-treated NOD mice represented the regulatory or suppressive CD4+CD25+ T cells (Treg) and might play an important role in the induction and maintenance of tolerance in NOD mice. |
| 3941 | 15343360 | Furthermore, the numbers of splenic CD4+CD62L+ regulatory T cells in GAD-IgG-treated mice during the prediabetic period and serum TGF-beta levels in 34-38-week-old GAD-IgG-protected mice were also increased, compared to control IgG-treated ones. |
| 3942 | 15343360 | Parallel with disease protection, we observed a prolonged increase of the numbers of CD4+CD25+ T cells in the periphery of GAD-IgG-treated mice, compared to those treated with a control IgG vector, both in the prediabetic period and persisting even 8 months after gene therapy. |
| 3943 | 15343360 | Moreover, CD4+CD25+ T cells induced by GAD-IgG fusion construct were capable of suppressing the proliferative response of CD4+CD25- T cells in vitro; and ablation of the activity of CD4+CD25+ T cells by blocking antibody against CD25 could reverse GAD-specific T-cell hyporesponsiveness. |
| 3944 | 15343360 | These results suggested that CD4+CD25+ T-cell subset induced in GAD-IgG-treated NOD mice represented the regulatory or suppressive CD4+CD25+ T cells (Treg) and might play an important role in the induction and maintenance of tolerance in NOD mice. |
| 3945 | 15343360 | Furthermore, the numbers of splenic CD4+CD62L+ regulatory T cells in GAD-IgG-treated mice during the prediabetic period and serum TGF-beta levels in 34-38-week-old GAD-IgG-protected mice were also increased, compared to control IgG-treated ones. |
| 3946 | 15343360 | Parallel with disease protection, we observed a prolonged increase of the numbers of CD4+CD25+ T cells in the periphery of GAD-IgG-treated mice, compared to those treated with a control IgG vector, both in the prediabetic period and persisting even 8 months after gene therapy. |
| 3947 | 15343360 | Moreover, CD4+CD25+ T cells induced by GAD-IgG fusion construct were capable of suppressing the proliferative response of CD4+CD25- T cells in vitro; and ablation of the activity of CD4+CD25+ T cells by blocking antibody against CD25 could reverse GAD-specific T-cell hyporesponsiveness. |
| 3948 | 15343360 | These results suggested that CD4+CD25+ T-cell subset induced in GAD-IgG-treated NOD mice represented the regulatory or suppressive CD4+CD25+ T cells (Treg) and might play an important role in the induction and maintenance of tolerance in NOD mice. |
| 3949 | 15343360 | Furthermore, the numbers of splenic CD4+CD62L+ regulatory T cells in GAD-IgG-treated mice during the prediabetic period and serum TGF-beta levels in 34-38-week-old GAD-IgG-protected mice were also increased, compared to control IgG-treated ones. |
| 3950 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3951 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3952 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3953 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3954 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3955 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3956 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3957 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3958 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3959 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3960 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3961 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3962 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3963 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3964 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3965 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3966 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3967 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3968 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3969 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3970 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3971 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3972 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3973 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3974 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3975 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3976 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3977 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3978 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3979 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3980 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3981 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3982 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3983 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3984 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3985 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3986 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3987 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3988 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3989 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3990 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3991 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3992 | 15356107 | B7-2 (CD86) controls the priming of autoreactive CD4 T cell response against pancreatic islets. |
| 3993 | 15356107 | We investigated the role played by B7-2 in influencing pathogenic autoimmunity from islet-reactive CD4 T cells in B7-2 knockout (KO) NOD mice which are protected from type 1 diabetes. |
| 3994 | 15356107 | B7-2 deficiency caused a profound diminishment in the generation of spontaneously activated CD4 T cells and islet-specific CD4 T cell expansion. |
| 3995 | 15356107 | CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation led to defective activation and failure to induce disease in NODscid recipients. |
| 3996 | 15356107 | Furthermore, CD4 T cells exhibited enhanced death in the absence of B7-2. |
| 3997 | 15356107 | Interestingly, we found that B7-2 is required to achieve normal levels of CD4+CD25+CD62L+ T regulatory cells because a significant reduction of these T regulatory cells was observed in the thymus but not in the peripheral compartments of B7-2KO mice. |
| 3998 | 15356107 | Taken together these results clearly indicate that B7-2 plays a critical role in priming islet-reactive CD4 T cells, suggesting a simplified, two-cell model for the impact of this costimulatory molecule in autoimmunity against islets. |
| 3999 | 15358643 | In the placebo group, an increase in the number of subsets with the activated phenotype in both the CD4(CD29+) and the CD8 (CD11a+) compartments was noted during the course of the study. |
| 4000 | 15358643 | However, in the placebo group the proportions of activated CD4 and CD8 cells increased over time. |
| 4001 | 15358643 | In the placebo group, an increase in the number of subsets with the activated phenotype in both the CD4(CD29+) and the CD8 (CD11a+) compartments was noted during the course of the study. |
| 4002 | 15358643 | However, in the placebo group the proportions of activated CD4 and CD8 cells increased over time. |
| 4003 | 15368274 | In NOD mice, CD28/B7 and CD40/CD40 ligand (L) interactions control the onset of diabetes from 2 to 4 weeks of age, but blocking these molecules has little effect after this time. |
| 4004 | 15368274 | We now show that OX40 is expressed on CD4 and CD8 T cells several weeks prior to islet destruction, which is initiated around weeks 12-14, and that OX40L is present on dendritic cells in both secondary lymphoid organs and the pancreas from 11 to 13 weeks of age. |
| 4005 | 15368281 | While CD4(+) T cells from NOD mice secreted IFN-gamma, IL-4, IL-5 and IL-10 in response to LACK, those from LACK-expressing Tg mice secreted reduced levels of cytokines. |
| 4006 | 15380036 | Three forms of these regulatory T cells have been described: those that function via the production of the cytokine IL-10 (T regulatory 1 cells), transforming growth factor beta (Th3 cells), and a population of T cells that suppresses proliferation via a cell-contact-dependent mechanism (CD4+CD25+ TR cells). |
| 4007 | 15383562 | Phenotypically "immature" dendritic cells (DCs), defined by low cell surface CD40, CD80, and CD86 can elicit host immune suppression in allotransplantation and autoimmunity. |
| 4008 | 15383562 | CD40, CD80, and CD86 cell surface molecules were specifically down-regulated by treating NOD DCs ex vivo with a mixture of antisense oligonucleotides targeting the CD40, CD80, and CD86 primary transcripts. |
| 4009 | 15383562 | Engineered DC promoted an increased prevalence of CD4(+)CD25(+) T cells in NOD recipients at all ages examined and diabetes-free recipients exhibited significantly greater numbers of CD4(+)CD25(+) T cells compared with untreated NOD mice. |
| 4010 | 15383571 | Treatment of NOD mice with a mitogenic anti-CD3 depletes CD4(+)CD25(-)CD62L(+) but not CD4(+)CD25(+)CD62L(+) T cells, thereby resulting in an increase of the latter subset in the spleen. |
| 4011 | 15383571 | These results demonstrate that the capacity of anti-CD3 to protect NOD mice from T1D correlates with its ability to perturb T cell homeostasis by inducing CD8(+) T cell AICD and increasing the number of CD4(+)CD25(+)CD62L(+) T cells in the periphery. |
| 4012 | 15383571 | Treatment of NOD mice with a mitogenic anti-CD3 depletes CD4(+)CD25(-)CD62L(+) but not CD4(+)CD25(+)CD62L(+) T cells, thereby resulting in an increase of the latter subset in the spleen. |
| 4013 | 15383571 | These results demonstrate that the capacity of anti-CD3 to protect NOD mice from T1D correlates with its ability to perturb T cell homeostasis by inducing CD8(+) T cell AICD and increasing the number of CD4(+)CD25(+)CD62L(+) T cells in the periphery. |
| 4014 | 15386802 | This review will concentrate on two different types of regulatory T-cells, the naturally occurring ('professional') CD4+CD25+ T-cells and antigen-induced ('adaptive') CD4+ Th2-like regulatory T-cells. |
| 4015 | 15460904 | Donor-specific tolerance induced by simultaneous allogeneic islet transplantation with CD4+CD25+ T-cells into hepatic parenchyma in mice. |
| 4016 | 15467837 | CD28-B7 and CD40 ligand-CD40 (CD40L-CD40) costimulatory pathways affect the development of disease and are promising therapeutic targets. |
| 4017 | 15467837 | Moreover, the residual proliferation of the autoreactive cells was effectively controlled by CD28-dependent CD4+CD25+ regulatory T cells (Treg's), as depletion of Treg's partially restored proliferation of autoreactive T cells and resulted in diabetes in an adoptive-transfer model. |
| 4018 | 15468055 | Distinct roles of CTLA-4 and TGF-beta in CD4+CD25+ regulatory T cell function. |
| 4019 | 15468055 | Both CTLA-4 and TGF-beta have been implicated in suppression by CD4+CD25+ regulatory T cells (Treg). |
| 4020 | 15468055 | In this study, the relationship between CTLA-4 and TGF-beta in Treg function was examined. |
| 4021 | 15468055 | These CTLA-4-deficient Treg expressed increased levels of the suppressive cytokines IL-10 and TGF-beta, and in vitro suppression mediated by CTLA-4(-/-) Treg was markedly reduced by neutralizing TGF-beta, suggesting that CTLA-4-deficient Treg develop a compensatory suppressive mechanism through CTLA-4-independent production of TGF-beta. |
| 4022 | 15468055 | Distinct roles of CTLA-4 and TGF-beta in CD4+CD25+ regulatory T cell function. |
| 4023 | 15468055 | Both CTLA-4 and TGF-beta have been implicated in suppression by CD4+CD25+ regulatory T cells (Treg). |
| 4024 | 15468055 | In this study, the relationship between CTLA-4 and TGF-beta in Treg function was examined. |
| 4025 | 15468055 | These CTLA-4-deficient Treg expressed increased levels of the suppressive cytokines IL-10 and TGF-beta, and in vitro suppression mediated by CTLA-4(-/-) Treg was markedly reduced by neutralizing TGF-beta, suggesting that CTLA-4-deficient Treg develop a compensatory suppressive mechanism through CTLA-4-independent production of TGF-beta. |
| 4026 | 15470032 | Insulin-dependent diabetes mellitus (IDDM) and Sjogren's syndrome (SS) are highly regulated autoimmune diseases that develop spontaneously in NOD mice. |
| 4027 | 15470032 | The aim of the present in vivo study was to explore the functional importance of the E2f1 molecule in IDDM and SS, in the context of whole animal physiology and pathophysiology, using E2f1-deficient NOD mice. |
| 4028 | 15470032 | These mice also exhibited a defect in T lymphocyte development, leading to excessive numbers of mature T cells (CD4+ and CD8+), due to a maturation stage-specific defect in the apoptosis of thymocytes and peripheral T cells. |
| 4029 | 15470032 | Furthermore, E2f1-deficient mice showed a profound decrease of immunoregulatory CD4+CD25+ T cells, while the spleen cells of NOD mice lacking E2f1 showed a significant increase of the proinflammatory cytokine IFN-gamma following antigenic stimulation in vitro. |
| 4030 | 15470032 | Consistent with these observations, E2f1 homozygous mutant NOD mice were highly predisposed to the development of IDDM and SS. |
| 4031 | 15470032 | Insulin-dependent diabetes mellitus (IDDM) and Sjogren's syndrome (SS) are highly regulated autoimmune diseases that develop spontaneously in NOD mice. |
| 4032 | 15470032 | The aim of the present in vivo study was to explore the functional importance of the E2f1 molecule in IDDM and SS, in the context of whole animal physiology and pathophysiology, using E2f1-deficient NOD mice. |
| 4033 | 15470032 | These mice also exhibited a defect in T lymphocyte development, leading to excessive numbers of mature T cells (CD4+ and CD8+), due to a maturation stage-specific defect in the apoptosis of thymocytes and peripheral T cells. |
| 4034 | 15470032 | Furthermore, E2f1-deficient mice showed a profound decrease of immunoregulatory CD4+CD25+ T cells, while the spleen cells of NOD mice lacking E2f1 showed a significant increase of the proinflammatory cytokine IFN-gamma following antigenic stimulation in vitro. |
| 4035 | 15470032 | Consistent with these observations, E2f1 homozygous mutant NOD mice were highly predisposed to the development of IDDM and SS. |
| 4036 | 15474483 | Transcriptome and proteome expression in activated human CD4 and CD8 T-lymphocytes. |
| 4037 | 15474483 | T-lymphocytes (T-cells) are unique in that unlike monocytes, they have no insulin receptors, and are insulin insensitive, but upon activation with antigens develop insulin, IGF-1, and IL-2 receptors, and become insulin sensitive tissues. |
| 4038 | 15474483 | We analyzed the genomics and proteomics of activated and non-activated CD4+ and CD8+ T-cells of normal subjects using Affymetrix microarray gene chips and proteomes by SELDI-TOF mass spectrometry analysis. |
| 4039 | 15474483 | Genes for IL-2, insulin, and IGF-1 receptors were increased at least 2-fold in activated vs non-activated T-cells. |
| 4040 | 15474483 | Among activated ontologies were signal transduction pathways such as IRS-1, IRS-2, Akt, and glycolytic pathways. |
| 4041 | 15474483 | Transcriptome and proteome expression in activated human CD4 and CD8 T-lymphocytes. |
| 4042 | 15474483 | T-lymphocytes (T-cells) are unique in that unlike monocytes, they have no insulin receptors, and are insulin insensitive, but upon activation with antigens develop insulin, IGF-1, and IL-2 receptors, and become insulin sensitive tissues. |
| 4043 | 15474483 | We analyzed the genomics and proteomics of activated and non-activated CD4+ and CD8+ T-cells of normal subjects using Affymetrix microarray gene chips and proteomes by SELDI-TOF mass spectrometry analysis. |
| 4044 | 15474483 | Genes for IL-2, insulin, and IGF-1 receptors were increased at least 2-fold in activated vs non-activated T-cells. |
| 4045 | 15474483 | Among activated ontologies were signal transduction pathways such as IRS-1, IRS-2, Akt, and glycolytic pathways. |
| 4046 | 15476470 | Additional signaling pathways and molecules, such as the Janus kinase pathway and vascular endothelial growth factor have been added to those recognized as important in pharmacologic immunosuppression, and the concepts of regulation, once polarized between CD8+ and CD4+ camps, have begun to converge upon a recognition that there are many phenotypes of regulatory cells. |
| 4047 | 15492124 | Loss of one copy of Aire diminished thymic expression of the endogenous insulin gene and the transgene, resulting in a 300% increase in islet-reactive CD4 T cells escaping thymic deletion in T cell receptor transgenic mice, and dramatically increased progression to diabetes. |
| 4048 | 15492124 | Thymic deletion induced by antigen under control of the thyroglobulin promoter was abolished in Aire homozygotes and less efficient in heterozygotes, providing an explanation for thyroid autoimmunity in APS1. |
| 4049 | 15494484 | At 5-8 wk of age, even in the absence of TCRbeta expression, CD4+ and CD4+CD8+ blasts appear spontaneously. |
| 4050 | 15494484 | They mimic normal beta selection by up-regulating germline TCR-Calpha transcripts, CD2, and Bcl-xL and down-regulating Bcl-2. |
| 4051 | 15494484 | However, they fail to down-regulate transcription factors HEB-alt and Hes1 and initially express aberrantly high levels of Spi-B, c-kit (CD117), and IL-7Ralpha. |
| 4052 | 15494540 | CD4 T cells play an important role in hepatitis B virus (HBV) infection by secretion of Th1 cytokines that down-regulate HBV replication, and by promoting CD8 T cell and B cell responses. |
| 4053 | 15494540 | All 10 epitopes bound with high affinity to the most prevalent HLA-DR Ags, were conserved among HBV genomes, and induced IFN-gamma responses from HBV-specific CD4+ T cells. |
| 4054 | 15494540 | Several epitopes contained nested MHC class I motifs and stimulated HBV-specific IFN-gamma production and cytotoxicity of CD8+ T cells. |
| 4055 | 15494540 | CD4 T cells play an important role in hepatitis B virus (HBV) infection by secretion of Th1 cytokines that down-regulate HBV replication, and by promoting CD8 T cell and B cell responses. |
| 4056 | 15494540 | All 10 epitopes bound with high affinity to the most prevalent HLA-DR Ags, were conserved among HBV genomes, and induced IFN-gamma responses from HBV-specific CD4+ T cells. |
| 4057 | 15494540 | Several epitopes contained nested MHC class I motifs and stimulated HBV-specific IFN-gamma production and cytotoxicity of CD8+ T cells. |
| 4058 | 15534371 | It has been reported that the differentiation of CD4+CD25+ regulatory T cells (T reg cells) can be induced by agonist peptide/major histocompatibility complex ligands in the thymus. |
| 4059 | 15534371 | However, CD4+CD25+ thymocytes were much less sensitive than their CD4+CD25- companions, by two to three orders of magnitude, to agonist-induced clonal deletion, such that their proportion increased, giving the false impression of induced differentiation. |
| 4060 | 15534371 | To account for these and prior observations, one can propose that differentiation along the CD4+CD25+ pathway is induced by cues other than recognition of self-agonist cues, which are poorly read by thymocytes, whose T cell receptors are conducive to selection toward the conventional CD4+CD25- lineage. |
| 4061 | 15534371 | It has been reported that the differentiation of CD4+CD25+ regulatory T cells (T reg cells) can be induced by agonist peptide/major histocompatibility complex ligands in the thymus. |
| 4062 | 15534371 | However, CD4+CD25+ thymocytes were much less sensitive than their CD4+CD25- companions, by two to three orders of magnitude, to agonist-induced clonal deletion, such that their proportion increased, giving the false impression of induced differentiation. |
| 4063 | 15534371 | To account for these and prior observations, one can propose that differentiation along the CD4+CD25+ pathway is induced by cues other than recognition of self-agonist cues, which are poorly read by thymocytes, whose T cell receptors are conducive to selection toward the conventional CD4+CD25- lineage. |
| 4064 | 15534371 | It has been reported that the differentiation of CD4+CD25+ regulatory T cells (T reg cells) can be induced by agonist peptide/major histocompatibility complex ligands in the thymus. |
| 4065 | 15534371 | However, CD4+CD25+ thymocytes were much less sensitive than their CD4+CD25- companions, by two to three orders of magnitude, to agonist-induced clonal deletion, such that their proportion increased, giving the false impression of induced differentiation. |
| 4066 | 15534371 | To account for these and prior observations, one can propose that differentiation along the CD4+CD25+ pathway is induced by cues other than recognition of self-agonist cues, which are poorly read by thymocytes, whose T cell receptors are conducive to selection toward the conventional CD4+CD25- lineage. |
| 4067 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4068 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4069 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4070 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4071 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4072 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4073 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4074 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4075 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4076 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4077 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4078 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4079 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4080 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4081 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4082 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4083 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4084 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4085 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4086 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4087 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4088 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4089 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4090 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4091 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4092 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4093 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4094 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4095 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4096 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4097 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4098 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4099 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4100 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4101 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4102 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4103 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4104 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4105 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4106 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4107 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4108 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4109 | 15539509 | Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody. |
| 4110 | 15539509 | CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. |
| 4111 | 15539509 | Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. |
| 4112 | 15539509 | Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. |
| 4113 | 15539509 | When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. |
| 4114 | 15539509 | When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. |
| 4115 | 15539509 | These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi. |
| 4116 | 15542454 | Nonspecific in vitro stimulation induced more CD-4+/IL-4+ cells in Brussels maintained. |
| 4117 | 15542454 | TSHR stimulation produced a significant increase in IL-4 secretion in six of nine local but one of seven Brussels mice. |
| 4118 | 15549775 | Inhibition of altered peptide ligand-mediated antagonism of human GAD65-responsive CD4+ T cells by non-antagonizable T cells. |
| 4119 | 15549775 | In this study we identified several altered peptide ligands derived from the type 1 diabetes-associated autoantigen human glutamic acid decarboxylase 65 (hGAD65) epitope that were capable of antagonizing a subset of a panel of human CD4(+) GAD65 (555-567)-responsive T cell clones derived from a diabetic individual. |
| 4120 | 15549775 | Inhibition of altered peptide ligand-mediated antagonism of human GAD65-responsive CD4+ T cells by non-antagonizable T cells. |
| 4121 | 15549775 | In this study we identified several altered peptide ligands derived from the type 1 diabetes-associated autoantigen human glutamic acid decarboxylase 65 (hGAD65) epitope that were capable of antagonizing a subset of a panel of human CD4(+) GAD65 (555-567)-responsive T cell clones derived from a diabetic individual. |
| 4122 | 15557155 | CTLA-4, a homologue of CD28, is a negative regulator of T cell activation in the periphery and is transiently expressed on the cell surface after T cell activation. |
| 4123 | 15557155 | This investigation was initiated to determine the role of CTLA-4 in the activation of CD4(+)CD8(+) double-positive (DP) and CD4(+)CD8(-) and CD4(-)CD8(+) single-positive (SP) thymocytes using fetal thymic organ cultures (FTOC) of MHC class II-restricted, OVA(323-339)-restricted TCR transgenic mice (DO11.10). |
| 4124 | 15557155 | In addition, anti-CTLA-4 Ab treatment inhibited OVA(323-339)-induced expression of the early activation marker, CD69, in DP thymocytes, but increased CD69 in SP thymocytes. |
| 4125 | 15557165 | Individual nonobese diabetic mice exhibit unique patterns of CD8+ T cell reactivity to three islet antigens, including the newly identified widely expressed dystrophia myotonica kinase. |
| 4126 | 15557165 | Spontaneous autoimmune diabetes development in NOD mice requires both CD8(+) and CD4(+) T cells. |
| 4127 | 15557165 | Although the Ags for G9C8 and 8.3 are known to be insulin and islet-specific glucose-6-phosphatase catalytic subunit-related protein, respectively, only mimotope peptides had previously been identified for AI4. |
| 4128 | 15557165 | Screening of a combinatorial peptide library in positional scanning format led to the identification of a peptide derived from dystrophia myotonica kinase (DMK) that is recognized by AI4-like T cells. |
| 4129 | 15557171 | Immunization of NOD mice with autoantigens such as glutamic acid decarboxylase (GAD) 221-235 peptide (p221) can induce Ag-specific CD4(+) T regulatory (Tr) cells. |
| 4130 | 15557171 | The N221(+) T cells produced IFN-gamma and IL-10, but very little IL-4, in response to p221 stimulation. |
| 4131 | 15557171 | This suppressive activity was cell contact-independent and was abrogated by Abs to IL-10 or IL-10R. |
| 4132 | 15557171 | Interestingly, IL-2 produced by other T cells present in the cell culture induced unactivated N221(+) T cells to exhibit regulatory activities involving production of IL-10. |
| 4133 | 15578422 | The CD4+/CD8+ ratio was low during the initial follow up stages (3 and 7 days) in untreated diabetic rats, yet an increased ratio corresponding to areas around the polymer remains was noted in the animals treated with copolymer loaded with the growth hormone. |
| 4134 | 15585854 | Autoimmunity presumably manifests as a consequence of a shortfall in the maintenance of peripheral tolerance by CD4(+)CD25(+) T regulatory cells (Tregs). |
| 4135 | 15591438 | CD4(+)CD25(+) T-cells can be used to interfere with spontaneous autoimmune diseases such as type 1 diabetes. |
| 4136 | 15616013 | Treatment with granulocyte colony-stimulating factor prevents diabetes in NOD mice by recruiting plasmacytoid dendritic cells and functional CD4(+)CD25(+) regulatory T-cells. |
| 4137 | 15616013 | Accumulating evidence that granulocyte colony-stimulating factor (G-CSF), the key hematopoietic growth factor of the myeloid lineage, not only represents a major component of the endogenous response to infections, but also affects adaptive immune responses, prompted us to investigate the therapeutic potential of G-CSF in autoimmune type 1 diabetes. |
| 4138 | 15616013 | G-CSF recipients further displayed accumulation of functional CD4(+)CD25(+) regulatory T-cells that produce transforming growth factor-beta1 (TGF-beta1) and actively suppressed diabetes transfer by diabetogenic effector cells in secondary NOD-SCID recipients. |
| 4139 | 15616013 | G-CSF's ability to promote key tolerogenic interactions between DCs and regulatory T-cells was demonstrated by enhanced recruitment of TGF-beta1-expressing CD4(+)CD25(+) cells after adoptive transfer of DCs isolated from G-CSF- relative to vehicle-treated mice into naive NOD recipients. |
| 4140 | 15616013 | Treatment with granulocyte colony-stimulating factor prevents diabetes in NOD mice by recruiting plasmacytoid dendritic cells and functional CD4(+)CD25(+) regulatory T-cells. |
| 4141 | 15616013 | Accumulating evidence that granulocyte colony-stimulating factor (G-CSF), the key hematopoietic growth factor of the myeloid lineage, not only represents a major component of the endogenous response to infections, but also affects adaptive immune responses, prompted us to investigate the therapeutic potential of G-CSF in autoimmune type 1 diabetes. |
| 4142 | 15616013 | G-CSF recipients further displayed accumulation of functional CD4(+)CD25(+) regulatory T-cells that produce transforming growth factor-beta1 (TGF-beta1) and actively suppressed diabetes transfer by diabetogenic effector cells in secondary NOD-SCID recipients. |
| 4143 | 15616013 | G-CSF's ability to promote key tolerogenic interactions between DCs and regulatory T-cells was demonstrated by enhanced recruitment of TGF-beta1-expressing CD4(+)CD25(+) cells after adoptive transfer of DCs isolated from G-CSF- relative to vehicle-treated mice into naive NOD recipients. |
| 4144 | 15616013 | Treatment with granulocyte colony-stimulating factor prevents diabetes in NOD mice by recruiting plasmacytoid dendritic cells and functional CD4(+)CD25(+) regulatory T-cells. |
| 4145 | 15616013 | Accumulating evidence that granulocyte colony-stimulating factor (G-CSF), the key hematopoietic growth factor of the myeloid lineage, not only represents a major component of the endogenous response to infections, but also affects adaptive immune responses, prompted us to investigate the therapeutic potential of G-CSF in autoimmune type 1 diabetes. |
| 4146 | 15616013 | G-CSF recipients further displayed accumulation of functional CD4(+)CD25(+) regulatory T-cells that produce transforming growth factor-beta1 (TGF-beta1) and actively suppressed diabetes transfer by diabetogenic effector cells in secondary NOD-SCID recipients. |
| 4147 | 15616013 | G-CSF's ability to promote key tolerogenic interactions between DCs and regulatory T-cells was demonstrated by enhanced recruitment of TGF-beta1-expressing CD4(+)CD25(+) cells after adoptive transfer of DCs isolated from G-CSF- relative to vehicle-treated mice into naive NOD recipients. |
| 4148 | 15616015 | Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes. |
| 4149 | 15616015 | The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4(+)CD25(+) T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. |
| 4150 | 15616015 | We hypothesized that a deficiency in the CD4(+)CD25(+) Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. |
| 4151 | 15616015 | We show that although levels of CD4(+)CD25(+) T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). |
| 4152 | 15616015 | Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-gamma (P = 0.005) and decreased interleukin-10 production (P = 0.03). |
| 4153 | 15616015 | These deficiencies may reflect a disturbance in the balance of the CD4(+)CD25(+) population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). |
| 4154 | 15616015 | These data demonstrate deficiency in function of the CD4(+)CD25(+) Treg population that may influence the pathogenesis of type 1 diabetes. |
| 4155 | 15616015 | Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes. |
| 4156 | 15616015 | The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4(+)CD25(+) T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. |
| 4157 | 15616015 | We hypothesized that a deficiency in the CD4(+)CD25(+) Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. |
| 4158 | 15616015 | We show that although levels of CD4(+)CD25(+) T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). |
| 4159 | 15616015 | Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-gamma (P = 0.005) and decreased interleukin-10 production (P = 0.03). |
| 4160 | 15616015 | These deficiencies may reflect a disturbance in the balance of the CD4(+)CD25(+) population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). |
| 4161 | 15616015 | These data demonstrate deficiency in function of the CD4(+)CD25(+) Treg population that may influence the pathogenesis of type 1 diabetes. |
| 4162 | 15616015 | Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes. |
| 4163 | 15616015 | The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4(+)CD25(+) T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. |
| 4164 | 15616015 | We hypothesized that a deficiency in the CD4(+)CD25(+) Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. |
| 4165 | 15616015 | We show that although levels of CD4(+)CD25(+) T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). |
| 4166 | 15616015 | Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-gamma (P = 0.005) and decreased interleukin-10 production (P = 0.03). |
| 4167 | 15616015 | These deficiencies may reflect a disturbance in the balance of the CD4(+)CD25(+) population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). |
| 4168 | 15616015 | These data demonstrate deficiency in function of the CD4(+)CD25(+) Treg population that may influence the pathogenesis of type 1 diabetes. |
| 4169 | 15616015 | Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes. |
| 4170 | 15616015 | The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4(+)CD25(+) T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. |
| 4171 | 15616015 | We hypothesized that a deficiency in the CD4(+)CD25(+) Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. |
| 4172 | 15616015 | We show that although levels of CD4(+)CD25(+) T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). |
| 4173 | 15616015 | Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-gamma (P = 0.005) and decreased interleukin-10 production (P = 0.03). |
| 4174 | 15616015 | These deficiencies may reflect a disturbance in the balance of the CD4(+)CD25(+) population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). |
| 4175 | 15616015 | These data demonstrate deficiency in function of the CD4(+)CD25(+) Treg population that may influence the pathogenesis of type 1 diabetes. |
| 4176 | 15616015 | Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes. |
| 4177 | 15616015 | The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4(+)CD25(+) T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. |
| 4178 | 15616015 | We hypothesized that a deficiency in the CD4(+)CD25(+) Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. |
| 4179 | 15616015 | We show that although levels of CD4(+)CD25(+) T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). |
| 4180 | 15616015 | Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-gamma (P = 0.005) and decreased interleukin-10 production (P = 0.03). |
| 4181 | 15616015 | These deficiencies may reflect a disturbance in the balance of the CD4(+)CD25(+) population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). |
| 4182 | 15616015 | These data demonstrate deficiency in function of the CD4(+)CD25(+) Treg population that may influence the pathogenesis of type 1 diabetes. |
| 4183 | 15616015 | Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes. |
| 4184 | 15616015 | The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4(+)CD25(+) T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. |
| 4185 | 15616015 | We hypothesized that a deficiency in the CD4(+)CD25(+) Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. |
| 4186 | 15616015 | We show that although levels of CD4(+)CD25(+) T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). |
| 4187 | 15616015 | Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-gamma (P = 0.005) and decreased interleukin-10 production (P = 0.03). |
| 4188 | 15616015 | These deficiencies may reflect a disturbance in the balance of the CD4(+)CD25(+) population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). |
| 4189 | 15616015 | These data demonstrate deficiency in function of the CD4(+)CD25(+) Treg population that may influence the pathogenesis of type 1 diabetes. |
| 4190 | 15622961 | It is clear that beta cell destruction is mediated primarily byT cells with both CD4+ and CD8+ T cells playing an important role. |
| 4191 | 15624122 | Increased levels of SST were also found in antigen-presenting cells and are associated with a significant increase of CD8 expression levels on CD4(+)/CD8(+) immature thymocytes. |
| 4192 | 15634886 | An age-dependent differential expression of B7-1 and B7-2 was associated with the development of insulitis and CD4(+)CD25(+) T cell deficiency in autoimmune disease-prone mice. |
| 4193 | 15634886 | Whereas BCR and LPS stimulation increased B7-2 expression on B cells from autoimmune disease-prone and nonautoimmune disease-prone mice, LPS-induced B7-1 expression was higher on NOD than C57BL/6 B cells. |
| 4194 | 15634886 | B7 blockade of BCR-stimulated NOD B cells by anti-B7-1 and anti-B7-2 mAbs during coadoptive transfer with diabetogenic T cells into NOD.scid mice protected these recipients from T1D. |
| 4195 | 15650365 | This revealed an association between peripheral blood cell numbers of specific lymphocyte subpopulations (CD4(+), CD3(+)CD25(+), and naïve T-cells) and serum levels of markers for AITD (free thyroxine [T(4)] and thyroid-stimulating immunoglobulin). |
| 4196 | 15667574 | Aberrant regulation of interleukin-12 receptor beta2 chain on type 1 cytokine-stimulated T lymphocytes in type 1 diabetes. |
| 4197 | 15667574 | We studied, in T1D, type 1 and 2 cytokine-induced expression of the interleukin-12 receptor beta2 chain (IL-12Rbeta2 chain), which plays a critical role in regulating T-cell polarization. |
| 4198 | 15667574 | Peripheral blood lymphocytes from children with newly diagnosed T1D (n=10; mean age 10 years), from children with longstanding T1D (n=8; mean age 12.9 years) and from healthy children (n=15; mean age 11.5 years) were stimulated with phytohaemagglutinin (PHA) in a type 1 (IL-12 and anti-IL-4) or a type 2 (IL-4 and anti-IL-12) cytokine environment. |
| 4199 | 15667574 | Secretion of interferon-gamma (IFN-gamma), IL-5 and IL-13, as detected by enzyme-linked immunosorbent assay (ELISA), and expression of the IL-12Rbeta2 chain on CD4 and CD8 cells by flow cytometry, were analysed. |
| 4200 | 15667574 | Children with newly diagnosed and longstanding T1D had lower expression levels of the IL-12Rbeta2 chain on IL-12Rbeta2 chain-positive CD4 T cells (for a type 1 or a type 2 cytokine environment: P=0.01 and P=0.002 or P=0.02 and P=0.01, respectively) and on IL-12Rbeta2 chain-positive CD8 T cells (for a type 1 or a type 2 cytokine environment: P=0.007 and P=0.0007 or P=0.003 and P=0.01, respectively) when compared to healthy children. |
| 4201 | 15667574 | A decreased percentage of IL-12Rbeta2 chain-expressing CD4 T cells (P=0.07 and P=0.03) and CD8 T cells (P=0.004 and P=0.01) and increased secretion of IL-13 (P=0.006 and P=0.04) in a type 1 cytokine environment was seen in both groups of patients. |
| 4202 | 15667574 | Aberrant regulation of interleukin-12 receptor beta2 chain on type 1 cytokine-stimulated T lymphocytes in type 1 diabetes. |
| 4203 | 15667574 | We studied, in T1D, type 1 and 2 cytokine-induced expression of the interleukin-12 receptor beta2 chain (IL-12Rbeta2 chain), which plays a critical role in regulating T-cell polarization. |
| 4204 | 15667574 | Peripheral blood lymphocytes from children with newly diagnosed T1D (n=10; mean age 10 years), from children with longstanding T1D (n=8; mean age 12.9 years) and from healthy children (n=15; mean age 11.5 years) were stimulated with phytohaemagglutinin (PHA) in a type 1 (IL-12 and anti-IL-4) or a type 2 (IL-4 and anti-IL-12) cytokine environment. |
| 4205 | 15667574 | Secretion of interferon-gamma (IFN-gamma), IL-5 and IL-13, as detected by enzyme-linked immunosorbent assay (ELISA), and expression of the IL-12Rbeta2 chain on CD4 and CD8 cells by flow cytometry, were analysed. |
| 4206 | 15667574 | Children with newly diagnosed and longstanding T1D had lower expression levels of the IL-12Rbeta2 chain on IL-12Rbeta2 chain-positive CD4 T cells (for a type 1 or a type 2 cytokine environment: P=0.01 and P=0.002 or P=0.02 and P=0.01, respectively) and on IL-12Rbeta2 chain-positive CD8 T cells (for a type 1 or a type 2 cytokine environment: P=0.007 and P=0.0007 or P=0.003 and P=0.01, respectively) when compared to healthy children. |
| 4207 | 15667574 | A decreased percentage of IL-12Rbeta2 chain-expressing CD4 T cells (P=0.07 and P=0.03) and CD8 T cells (P=0.004 and P=0.01) and increased secretion of IL-13 (P=0.006 and P=0.04) in a type 1 cytokine environment was seen in both groups of patients. |
| 4208 | 15667574 | Aberrant regulation of interleukin-12 receptor beta2 chain on type 1 cytokine-stimulated T lymphocytes in type 1 diabetes. |
| 4209 | 15667574 | We studied, in T1D, type 1 and 2 cytokine-induced expression of the interleukin-12 receptor beta2 chain (IL-12Rbeta2 chain), which plays a critical role in regulating T-cell polarization. |
| 4210 | 15667574 | Peripheral blood lymphocytes from children with newly diagnosed T1D (n=10; mean age 10 years), from children with longstanding T1D (n=8; mean age 12.9 years) and from healthy children (n=15; mean age 11.5 years) were stimulated with phytohaemagglutinin (PHA) in a type 1 (IL-12 and anti-IL-4) or a type 2 (IL-4 and anti-IL-12) cytokine environment. |
| 4211 | 15667574 | Secretion of interferon-gamma (IFN-gamma), IL-5 and IL-13, as detected by enzyme-linked immunosorbent assay (ELISA), and expression of the IL-12Rbeta2 chain on CD4 and CD8 cells by flow cytometry, were analysed. |
| 4212 | 15667574 | Children with newly diagnosed and longstanding T1D had lower expression levels of the IL-12Rbeta2 chain on IL-12Rbeta2 chain-positive CD4 T cells (for a type 1 or a type 2 cytokine environment: P=0.01 and P=0.002 or P=0.02 and P=0.01, respectively) and on IL-12Rbeta2 chain-positive CD8 T cells (for a type 1 or a type 2 cytokine environment: P=0.007 and P=0.0007 or P=0.003 and P=0.01, respectively) when compared to healthy children. |
| 4213 | 15667574 | A decreased percentage of IL-12Rbeta2 chain-expressing CD4 T cells (P=0.07 and P=0.03) and CD8 T cells (P=0.004 and P=0.01) and increased secretion of IL-13 (P=0.006 and P=0.04) in a type 1 cytokine environment was seen in both groups of patients. |
| 4214 | 15699486 | Based on these and other preclinical data, we have carried out a Phase I/II trial of the humanized FcR non-binding anti-CD3 mAb hOKT3gamma1(Ala-Ala) in patients with new-onset type 1 diabetes. mAb treatment prevented the loss of insulin production over the first two years of the disease with reduced hemoglobin A1c levels and insulin usage. |
| 4215 | 15699486 | CD4(+)IL-10(+) T cells can be found in patients after treatment; in addition, the CD8(+) T cells are induced by the mAb, and these cells may regulate antigen- specific responses. |
| 4216 | 15699488 | CD4+ T cell proliferation in response to GAD and proinsulin in healthy, pre-diabetic, and diabetic donors. |
| 4217 | 15699488 | However, peripheral blood cells from healthy, pre-diabetic and diabetic donors exhibited overlap in responses to glutamic acid decarboxylase (GAD65) and proinsulin (PI). |
| 4218 | 15699491 | In each HLA type group, GAD-reactive IFN-gamma-producing CD4(+) cells were assessed by means of intracellular cytokine staining for flow cytometry. |
| 4219 | 15699491 | Type 1 diabetic patients with HLA DR9/X had significantly higher numbers of GAD-reactive IFN-gamma-producing CD4(+) cells as compared to type 1 diabetic patients with DR4/X or DR4/9 (P < 0.05) and all type 2 diabetic patients. |
| 4220 | 15699491 | There was no significant difference in the number of GAD-reactive IFN-gamma-producing CD4(+) cells between type 1 diabetic and type 2 diabetic patients belonging to the DR4/X and DR4/9 groups. |
| 4221 | 15699491 | In each HLA type group, GAD-reactive IFN-gamma-producing CD4(+) cells were assessed by means of intracellular cytokine staining for flow cytometry. |
| 4222 | 15699491 | Type 1 diabetic patients with HLA DR9/X had significantly higher numbers of GAD-reactive IFN-gamma-producing CD4(+) cells as compared to type 1 diabetic patients with DR4/X or DR4/9 (P < 0.05) and all type 2 diabetic patients. |
| 4223 | 15699491 | There was no significant difference in the number of GAD-reactive IFN-gamma-producing CD4(+) cells between type 1 diabetic and type 2 diabetic patients belonging to the DR4/X and DR4/9 groups. |
| 4224 | 15699491 | In each HLA type group, GAD-reactive IFN-gamma-producing CD4(+) cells were assessed by means of intracellular cytokine staining for flow cytometry. |
| 4225 | 15699491 | Type 1 diabetic patients with HLA DR9/X had significantly higher numbers of GAD-reactive IFN-gamma-producing CD4(+) cells as compared to type 1 diabetic patients with DR4/X or DR4/9 (P < 0.05) and all type 2 diabetic patients. |
| 4226 | 15699491 | There was no significant difference in the number of GAD-reactive IFN-gamma-producing CD4(+) cells between type 1 diabetic and type 2 diabetic patients belonging to the DR4/X and DR4/9 groups. |
| 4227 | 15699519 | Based on these findings we have developed experimental autoimmune diabetes (EAD), a new mouse model characterized by (1) CD4(+)/CD8(+) insulitis, induced by (2) (prepro)insulin DNA vaccination, leading to (3) beta cell damage and insulin deficiency in (4) RIP-B7.1 transgenic mice (H-2(b)). |
| 4228 | 15707400 | Naive T cells and T cells with potential regulatory function (CD4+CD25+) were not prevalent following aggressive depletion. |
| 4229 | 15724624 | The patients felt better, their quality of life improved, CD3+, CD4+, CD5+ cells and granule-contained lymphocytes content normalized. |
| 4230 | 15725572 | We found that immature NOD CD4+CD8+ DP thymocytes have a lower activation threshold than C57BL/6 and Balb/c thymocytes. |
| 4231 | 15725572 | This was confirmed by showing that NOD DP thymocytes have a higher level of ERK and JNK phosphorylation. |
| 4232 | 15725577 | In mouse models, CD4+CD25+ T cells are involved in maintenance of peripheral tolerance. |
| 4233 | 15725577 | In humans, a subset of CD4+CD25+ T cells expressing high levels of CD25 (CD4+CD25high) with characteristics identical to murine CD4+CD25+ was recently described. |
| 4234 | 15725577 | In contrast to a previous report, we found no difference in the number of CD4+CD25high and CD4+CD25+ T cells between T1D and NC. |
| 4235 | 15725577 | In mouse models, CD4+CD25+ T cells are involved in maintenance of peripheral tolerance. |
| 4236 | 15725577 | In humans, a subset of CD4+CD25+ T cells expressing high levels of CD25 (CD4+CD25high) with characteristics identical to murine CD4+CD25+ was recently described. |
| 4237 | 15725577 | In contrast to a previous report, we found no difference in the number of CD4+CD25high and CD4+CD25+ T cells between T1D and NC. |
| 4238 | 15725577 | In mouse models, CD4+CD25+ T cells are involved in maintenance of peripheral tolerance. |
| 4239 | 15725577 | In humans, a subset of CD4+CD25+ T cells expressing high levels of CD25 (CD4+CD25high) with characteristics identical to murine CD4+CD25+ was recently described. |
| 4240 | 15725577 | In contrast to a previous report, we found no difference in the number of CD4+CD25high and CD4+CD25+ T cells between T1D and NC. |
| 4241 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 4242 | 15753206 | Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. |
| 4243 | 15753206 | IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. |
| 4244 | 15753206 | In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. |
| 4245 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 4246 | 15753206 | The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. |
| 4247 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 4248 | 15753206 | Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. |
| 4249 | 15753206 | IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. |
| 4250 | 15753206 | In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. |
| 4251 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 4252 | 15753206 | The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. |
| 4253 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 4254 | 15753206 | Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. |
| 4255 | 15753206 | IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. |
| 4256 | 15753206 | In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. |
| 4257 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 4258 | 15753206 | The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. |
| 4259 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 4260 | 15753206 | Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. |
| 4261 | 15753206 | IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. |
| 4262 | 15753206 | In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. |
| 4263 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 4264 | 15753206 | The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. |
| 4265 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 4266 | 15753206 | Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. |
| 4267 | 15753206 | IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. |
| 4268 | 15753206 | In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. |
| 4269 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 4270 | 15753206 | The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. |
| 4271 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 4272 | 15753206 | Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. |
| 4273 | 15753206 | IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. |
| 4274 | 15753206 | In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. |
| 4275 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 4276 | 15753206 | The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. |
| 4277 | 15753318 | De novo generation of antigen-specific CD4+CD25+ regulatory T cells from human CD4+CD25- cells. |
| 4278 | 15753318 | CD4+CD25+FOXP3+ regulatory T cells (T(R)) also require activation through the T cell receptor for function. |
| 4279 | 15753318 | De novo generation of antigen-specific CD4+CD25+ regulatory T cells from human CD4+CD25- cells. |
| 4280 | 15753318 | CD4+CD25+FOXP3+ regulatory T cells (T(R)) also require activation through the T cell receptor for function. |
| 4281 | 15753402 | Although nonresponsive toward the HPV16 E7 oncoprotein in the CD8+ T-cell compartment by virtue of MHC haplotype, the mice were capable of mounting an induced CD4+ T-cell response against E7, and in addition developed spontaneous anti-E7 antibodies. |
| 4282 | 15763918 | Selection of aberrant class II restricted CD8+ T cells in NOD mice expressing a glutamic acid decarboxylase (GAD)65-specific T cell receptor transgene. |
| 4283 | 15763918 | Interestingly, the CD8+ tetramer(-) T cells that are expressing endogenous TCR can delay diabetes induction in a transfer model, as we previously showed for CD4+ tetramer+ T cells in these mice. |
| 4284 | 15763918 | The MHC mismatched CD8+ cells appear to be positively selected in an atypical fashion, in that they do not upregulate CD69 or reexpress CD44, and they escape negative selection. |
| 4285 | 15771578 | The strength of this mouse strain is that it develops spontaneous autoimmune diabetes, which shares many similarities to autoimmune or type 1a diabetes (T1D) in human subjects, including the presence of pancreas-specific autoantibodies, autoreactive CD4+ and CD8+ T cells, and genetic linkage to disease syntenic to that found in humans. |
| 4286 | 15778350 | Simultaneous induction of CD4 T cell tolerance and CD8 T cell immunity by semimature dendritic cells. |
| 4287 | 15778350 | This protection was mediated by IL-10-producing CD4 T cells specific for the self Ag. |
| 4288 | 15778350 | Double-peptide-loaded semimature DC also induced simultaneously in the same animal partially activated CD8 T cells with cytolytic function as well as protection from MOG-induced autoimmune encephalomyelitis. |
| 4289 | 15778350 | Simultaneous induction of CD4 T cell tolerance and CD8 T cell immunity by semimature dendritic cells. |
| 4290 | 15778350 | This protection was mediated by IL-10-producing CD4 T cells specific for the self Ag. |
| 4291 | 15778350 | Double-peptide-loaded semimature DC also induced simultaneously in the same animal partially activated CD8 T cells with cytolytic function as well as protection from MOG-induced autoimmune encephalomyelitis. |
| 4292 | 15789355 | CD4(+)CD25(+)) were induced. |
| 4293 | 15790360 | A search for peripheral T cells that might exert dominant inhibitory effects on autoreactivity has implicated a subpopulation of CD4(+)CD25(+) T cells called regulatory T cells (Tregs). |
| 4294 | 15790360 | We restrict our comments to the suppression mediated by cells within the CD4 lineage; the impact of the cells within the CD8 lineage that may suppress via engagement of Qa-1 on effector T cells is not addressed in this review. |
| 4295 | 15790360 | A search for peripheral T cells that might exert dominant inhibitory effects on autoreactivity has implicated a subpopulation of CD4(+)CD25(+) T cells called regulatory T cells (Tregs). |
| 4296 | 15790360 | We restrict our comments to the suppression mediated by cells within the CD4 lineage; the impact of the cells within the CD8 lineage that may suppress via engagement of Qa-1 on effector T cells is not addressed in this review. |
| 4297 | 15790363 | Both the CD4(+) and the CD8(+) T-cell subsets are required for T1D development. |
| 4298 | 15790363 | This finding led to enormous interest in the CD4(+) T cells participating in the development of T1D, while the CD8(+) subset was relatively ignored. |
| 4299 | 15790363 | However, the isolation of beta-cell-autoreactive CD8(+) T-cell clones from the islets of NOD mice helped to generate interest in the pathogenic role of this subset, as has accumulating evidence that certain class I MHC alleles are additional risk factors for T1D development in humans. |
| 4300 | 15790363 | Both the CD4(+) and the CD8(+) T-cell subsets are required for T1D development. |
| 4301 | 15790363 | This finding led to enormous interest in the CD4(+) T cells participating in the development of T1D, while the CD8(+) subset was relatively ignored. |
| 4302 | 15790363 | However, the isolation of beta-cell-autoreactive CD8(+) T-cell clones from the islets of NOD mice helped to generate interest in the pathogenic role of this subset, as has accumulating evidence that certain class I MHC alleles are additional risk factors for T1D development in humans. |
| 4303 | 15806729 | Early studies suggested that CD8(+) "suppressor" T cells were important, but it is now accepted that it may involve either anergy/deletion of CD4(+) T cells, or the induction of regulatory CD4(+) T cells that produce IL-10 and/or TGFbeta. |
| 4304 | 15806729 | There may also be a role for CD4(+) CD25(+) T(reg), but how and when all these different mechanisms operate is still unclear. |
| 4305 | 15806729 | Early studies suggested that CD8(+) "suppressor" T cells were important, but it is now accepted that it may involve either anergy/deletion of CD4(+) T cells, or the induction of regulatory CD4(+) T cells that produce IL-10 and/or TGFbeta. |
| 4306 | 15806729 | There may also be a role for CD4(+) CD25(+) T(reg), but how and when all these different mechanisms operate is still unclear. |
| 4307 | 15816002 | Our data show that human NKT cells also undergo early stages of development in the thymus, forming a CD4(+)CD161(-/low) population that predominates neonatal thymic and blood NKT cell pools. |
| 4308 | 15816002 | CD4(-) and CD161(+) NKT cells accumulate with age in the blood, but not thymus, to the point that they dominate the NKT cell compartment in adult blood. |
| 4309 | 15816002 | This is consistent with the post-thymic maturation of NKT cells exported from the thymus at the putatively immature CD4(+)CD161(-/low) stage. |
| 4310 | 15816002 | Our data show that human NKT cells also undergo early stages of development in the thymus, forming a CD4(+)CD161(-/low) population that predominates neonatal thymic and blood NKT cell pools. |
| 4311 | 15816002 | CD4(-) and CD161(+) NKT cells accumulate with age in the blood, but not thymus, to the point that they dominate the NKT cell compartment in adult blood. |
| 4312 | 15816002 | This is consistent with the post-thymic maturation of NKT cells exported from the thymus at the putatively immature CD4(+)CD161(-/low) stage. |
| 4313 | 15816002 | Our data show that human NKT cells also undergo early stages of development in the thymus, forming a CD4(+)CD161(-/low) population that predominates neonatal thymic and blood NKT cell pools. |
| 4314 | 15816002 | CD4(-) and CD161(+) NKT cells accumulate with age in the blood, but not thymus, to the point that they dominate the NKT cell compartment in adult blood. |
| 4315 | 15816002 | This is consistent with the post-thymic maturation of NKT cells exported from the thymus at the putatively immature CD4(+)CD161(-/low) stage. |
| 4316 | 15829405 | It selectively prevented the loss of the immunoregulatory T cells expressing the CD4(+)CD25+ phenotype that also stained CD62L+ in peripancreatic lymph nodes and promoted their expansion in the spleen. |
| 4317 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4318 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4319 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4320 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4321 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4322 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4323 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4324 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4325 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4326 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4327 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4328 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4329 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4330 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4331 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4332 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4333 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4334 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4335 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4336 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4337 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4338 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4339 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4340 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4341 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4342 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4343 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4344 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4345 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4346 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4347 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4348 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4349 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4350 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4351 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4352 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4353 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4354 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4355 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4356 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4357 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4358 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4359 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4360 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4361 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4362 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4363 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4364 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4365 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4366 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4367 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4368 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4369 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4370 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4371 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4372 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4373 | 15837817 | Single cell analysis shows decreasing FoxP3 and TGFbeta1 coexpressing CD4+CD25+ regulatory T cells during autoimmune diabetes. |
| 4374 | 15837817 | Natural CD4(+)CD25(+) regulatory T (CD4(+)CD25(+) T reg) cells play a key role in the immunoregulation of autoimmunity. |
| 4375 | 15837817 | However, little is known about the interactions between CD4(+)CD25(+) T reg cells and autoreactive T cells. |
| 4376 | 15837817 | This is due, in part, to the difficulty of using cell surface markers to identify CD4(+)CD25(+) T reg cells accurately. |
| 4377 | 15837817 | Using a novel real-time PCR assay, mRNA copy number of FoxP3, TGFbeta1, and interleukin (IL)-10 was measured in single cells to characterize and quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D). |
| 4378 | 15837817 | The suppressor function of CD4(+)CD25(+)CD62L(hi) T cells, mediated by TGFbeta, declined in an age-dependent manner. |
| 4379 | 15837817 | This loss of function coincided with a temporal decrease in the percentage of FoxP3 and TGFbeta1 coexpressing T cells within pancreatic lymph node and islet infiltrating CD4(+)CD25(+)CD62L(hi) T cells, and was detected in female NOD mice but not in NOD male mice, or NOR or C57BL/6 female mice. |
| 4380 | 15837817 | These results demonstrate that the majority of FoxP3-positive CD4(+)CD25(+) T reg cells in NOD mice express TGFbeta1 but not IL-10, and that a defect in the maintenance and/or expansion of this pool of immunoregulatory effectors is associated with the progression of T1D. |
| 4381 | 15843527 | Identification of CD4+ T cell-specific epitopes of islet-specific glucose-6-phosphatase catalytic subunit-related protein: a novel beta cell autoantigen in type 1 diabetes. |
| 4382 | 15843527 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) has been identified as a novel CD8(+) T cell-specific autoantigen in NOD mice. |
| 4383 | 15843527 | This study was undertaken to identify MHC class II-specific CD4(+) T cell epitopes of IGRP. |
| 4384 | 15843527 | Experiments using purified CD4(+) and CD8(+) T cells from IGRP peptide-primed mice also showed a predominant CD4(+) T cell response with no significant activation of CD8(+) T cells. |
| 4385 | 15843527 | T cells from P1-, P3-, and P7-primed mice secreted both IFN-gamma and IL-10 cytokines, whereas P2-primed cells secreted only IFN-gamma. |
| 4386 | 15843527 | In summary, we have identified two I-A(g7)-restricted CD4(+) T cell epitopes of IGRP that can modulate and prevent the development of diabetes in NOD mice. |
| 4387 | 15843527 | These results provide the first evidence on the role of IGRP-specific, MHC class II-restricted CD4(+) T cells in disease protection and may help in the development of novel therapies for type 1 diabetes. |
| 4388 | 15843527 | Identification of CD4+ T cell-specific epitopes of islet-specific glucose-6-phosphatase catalytic subunit-related protein: a novel beta cell autoantigen in type 1 diabetes. |
| 4389 | 15843527 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) has been identified as a novel CD8(+) T cell-specific autoantigen in NOD mice. |
| 4390 | 15843527 | This study was undertaken to identify MHC class II-specific CD4(+) T cell epitopes of IGRP. |
| 4391 | 15843527 | Experiments using purified CD4(+) and CD8(+) T cells from IGRP peptide-primed mice also showed a predominant CD4(+) T cell response with no significant activation of CD8(+) T cells. |
| 4392 | 15843527 | T cells from P1-, P3-, and P7-primed mice secreted both IFN-gamma and IL-10 cytokines, whereas P2-primed cells secreted only IFN-gamma. |
| 4393 | 15843527 | In summary, we have identified two I-A(g7)-restricted CD4(+) T cell epitopes of IGRP that can modulate and prevent the development of diabetes in NOD mice. |
| 4394 | 15843527 | These results provide the first evidence on the role of IGRP-specific, MHC class II-restricted CD4(+) T cells in disease protection and may help in the development of novel therapies for type 1 diabetes. |
| 4395 | 15843527 | Identification of CD4+ T cell-specific epitopes of islet-specific glucose-6-phosphatase catalytic subunit-related protein: a novel beta cell autoantigen in type 1 diabetes. |
| 4396 | 15843527 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) has been identified as a novel CD8(+) T cell-specific autoantigen in NOD mice. |
| 4397 | 15843527 | This study was undertaken to identify MHC class II-specific CD4(+) T cell epitopes of IGRP. |
| 4398 | 15843527 | Experiments using purified CD4(+) and CD8(+) T cells from IGRP peptide-primed mice also showed a predominant CD4(+) T cell response with no significant activation of CD8(+) T cells. |
| 4399 | 15843527 | T cells from P1-, P3-, and P7-primed mice secreted both IFN-gamma and IL-10 cytokines, whereas P2-primed cells secreted only IFN-gamma. |
| 4400 | 15843527 | In summary, we have identified two I-A(g7)-restricted CD4(+) T cell epitopes of IGRP that can modulate and prevent the development of diabetes in NOD mice. |
| 4401 | 15843527 | These results provide the first evidence on the role of IGRP-specific, MHC class II-restricted CD4(+) T cells in disease protection and may help in the development of novel therapies for type 1 diabetes. |
| 4402 | 15843527 | Identification of CD4+ T cell-specific epitopes of islet-specific glucose-6-phosphatase catalytic subunit-related protein: a novel beta cell autoantigen in type 1 diabetes. |
| 4403 | 15843527 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) has been identified as a novel CD8(+) T cell-specific autoantigen in NOD mice. |
| 4404 | 15843527 | This study was undertaken to identify MHC class II-specific CD4(+) T cell epitopes of IGRP. |
| 4405 | 15843527 | Experiments using purified CD4(+) and CD8(+) T cells from IGRP peptide-primed mice also showed a predominant CD4(+) T cell response with no significant activation of CD8(+) T cells. |
| 4406 | 15843527 | T cells from P1-, P3-, and P7-primed mice secreted both IFN-gamma and IL-10 cytokines, whereas P2-primed cells secreted only IFN-gamma. |
| 4407 | 15843527 | In summary, we have identified two I-A(g7)-restricted CD4(+) T cell epitopes of IGRP that can modulate and prevent the development of diabetes in NOD mice. |
| 4408 | 15843527 | These results provide the first evidence on the role of IGRP-specific, MHC class II-restricted CD4(+) T cells in disease protection and may help in the development of novel therapies for type 1 diabetes. |
| 4409 | 15843527 | Identification of CD4+ T cell-specific epitopes of islet-specific glucose-6-phosphatase catalytic subunit-related protein: a novel beta cell autoantigen in type 1 diabetes. |
| 4410 | 15843527 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) has been identified as a novel CD8(+) T cell-specific autoantigen in NOD mice. |
| 4411 | 15843527 | This study was undertaken to identify MHC class II-specific CD4(+) T cell epitopes of IGRP. |
| 4412 | 15843527 | Experiments using purified CD4(+) and CD8(+) T cells from IGRP peptide-primed mice also showed a predominant CD4(+) T cell response with no significant activation of CD8(+) T cells. |
| 4413 | 15843527 | T cells from P1-, P3-, and P7-primed mice secreted both IFN-gamma and IL-10 cytokines, whereas P2-primed cells secreted only IFN-gamma. |
| 4414 | 15843527 | In summary, we have identified two I-A(g7)-restricted CD4(+) T cell epitopes of IGRP that can modulate and prevent the development of diabetes in NOD mice. |
| 4415 | 15843527 | These results provide the first evidence on the role of IGRP-specific, MHC class II-restricted CD4(+) T cells in disease protection and may help in the development of novel therapies for type 1 diabetes. |
| 4416 | 15847799 | Media supplemented with IL-2+IL-4 supported growth of the largest number of antigen-specific clones. |
| 4417 | 15847799 | Based on these findings, IL-2+IL-4, anti-CD3 and round-bottom plates were used to clone FACS-sorted autoantigen-specific CFSE-labelled CD4+ T cells. |
| 4418 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4419 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4420 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4421 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4422 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4423 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4424 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4425 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4426 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4427 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4428 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4429 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4430 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4431 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4432 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4433 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4434 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4435 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4436 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4437 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4438 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4439 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4440 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4441 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4442 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4443 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4444 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4445 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4446 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4447 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4448 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4449 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4450 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4451 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4452 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4453 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4454 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4455 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4456 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4457 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4458 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4459 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4460 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4461 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4462 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4463 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4464 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4465 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4466 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4467 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4468 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4469 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4470 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4471 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4472 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4473 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4474 | 15855328 | The delay in diabetes appearance is explained by the presence of regulatory CD4+ CD25+ T-cells that control diabetogenic effectors and that are, in our hands, transforming growth factor (TGF)-beta-dependent. |
| 4475 | 15855336 | When diabetic mice are treated with the RANKL antagonist osteoprotegerin (OPG), there is a significant reversal of alveolar bone loss, as well as reduced RANKL expression in A. actinomycetemcomitans-reactive CD4+ T-cells. |
| 4476 | 15855336 | Thus, microorganism-reactive CD4+ T-cells and the RANKL-OPG axis provide the molecular basis of the advanced periodontal breakdown in diabetes and, therefore, OPG may hold therapeutic potential for treating bone loss in diabetic subjects at high risk. |
| 4477 | 15855336 | When diabetic mice are treated with the RANKL antagonist osteoprotegerin (OPG), there is a significant reversal of alveolar bone loss, as well as reduced RANKL expression in A. actinomycetemcomitans-reactive CD4+ T-cells. |
| 4478 | 15855336 | Thus, microorganism-reactive CD4+ T-cells and the RANKL-OPG axis provide the molecular basis of the advanced periodontal breakdown in diabetes and, therefore, OPG may hold therapeutic potential for treating bone loss in diabetic subjects at high risk. |
| 4479 | 15867147 | The c-Jun NH(2)-terminal kinase isoform (JNK) 1 is implicated in type 2 diabetes. |
| 4480 | 15867147 | Here, we demonstrate that JNK2 may play an important role in type 1 (insulin-dependent) diabetes that is caused by autoimmune destruction of beta cells. |
| 4481 | 15867147 | CD4(+) T cells from JNK2-deficient nonobese diabetic mice produced less IFN-gamma but significantly increased amounts of IL-4 and IL-5, indicating polarization toward the Th2 phenotype. |
| 4482 | 15867147 | We conclude that JNK protein kinases may have important roles in diabetes, including functions of JNK1 in type 2 diabetes and JNK2 in type 1 diabetes. |
| 4483 | 15870014 | In vitro expanded human CD4+CD25+ regulatory T cells suppress effector T cell proliferation. |
| 4484 | 15870014 | We isolated CD4+CD25 hi cells from human peripheral blood and expanded them in vitro in the presence of anti-CD3 and anti-CD28 magnetic Xcyte Dynabeads and high concentrations of exogenous Interleukin (IL)-2. |
| 4485 | 15870014 | Tregs were effectively expanded up to 200-fold while maintaining surface expression of CD25 and other markers of Tregs: CD62L, HLA-DR, CCR6, and FOXP3. |
| 4486 | 15870014 | In vitro expanded human CD4+CD25+ regulatory T cells suppress effector T cell proliferation. |
| 4487 | 15870014 | We isolated CD4+CD25 hi cells from human peripheral blood and expanded them in vitro in the presence of anti-CD3 and anti-CD28 magnetic Xcyte Dynabeads and high concentrations of exogenous Interleukin (IL)-2. |
| 4488 | 15870014 | Tregs were effectively expanded up to 200-fold while maintaining surface expression of CD25 and other markers of Tregs: CD62L, HLA-DR, CCR6, and FOXP3. |
| 4489 | 15881418 | Administration of protoporphyrins to the recipients of allogeneic islets also resulted in transient powerful immunosuppression with reduced lymphocyte proliferative responses, increased proportion of regulatory cells (CD4+CD25+), decreased mononuclear cell infiltrating the graft, paralleled by a systemic upregulation of HO-1 expression. |
| 4490 | 15897273 | This previously unrecognized feature of a CD4(+) T cell response contrasts with the proliferative behavior of CD8(+) T cells that has been documented, and it implies that the two T cell subsets might require different strategies for efficient vaccination. |
| 4491 | 15905517 | We report in this study that this deficiency develops after the CD4(+)CD8(+) double-positive stage of thymic T cell development and is due to a lineage-specific depletion of CD4(-)CD8(-) double-negative alphabeta T cells and iNKT cells from the thymus between embryonic day 18 and day 1 after birth. |
| 4492 | 15935691 | Correlation between intracellular interferon-gamma (IFN-gamma) production by CD4+ and CD8+ lymphocytes and IFN-gamma gene polymorphism in patients with type 2 diabetes mellitus and latent autoimmune diabetes of adults (LADA). |
| 4493 | 15935691 | Subsequently, an attempt was made to correlate the presence of this mutation with the ability of CD4+ or CD8+ lymphocytes from these individuals to release IFN-gamma following mitogenic stimulation. |
| 4494 | 15935691 | CD4+ and CD8+ cells obtained from type 2 diabetics released significantly lower amounts of IFN-gamma in the intracellular space, compared to those released by cells obtained from LADA patients and healthy volunteers. |
| 4495 | 15935691 | Furthermore, even CD4+ and CD8+ from type 2 diabetics bearing the TT genotype (high producers) released significantly lower amounts of IFN-gamma than LADA patients carrying the same genotype, probably due to the activity of molecules directly or indirectly inhibiting IFN-gamma production. |
| 4496 | 15935691 | Correlation between intracellular interferon-gamma (IFN-gamma) production by CD4+ and CD8+ lymphocytes and IFN-gamma gene polymorphism in patients with type 2 diabetes mellitus and latent autoimmune diabetes of adults (LADA). |
| 4497 | 15935691 | Subsequently, an attempt was made to correlate the presence of this mutation with the ability of CD4+ or CD8+ lymphocytes from these individuals to release IFN-gamma following mitogenic stimulation. |
| 4498 | 15935691 | CD4+ and CD8+ cells obtained from type 2 diabetics released significantly lower amounts of IFN-gamma in the intracellular space, compared to those released by cells obtained from LADA patients and healthy volunteers. |
| 4499 | 15935691 | Furthermore, even CD4+ and CD8+ from type 2 diabetics bearing the TT genotype (high producers) released significantly lower amounts of IFN-gamma than LADA patients carrying the same genotype, probably due to the activity of molecules directly or indirectly inhibiting IFN-gamma production. |
| 4500 | 15935691 | Correlation between intracellular interferon-gamma (IFN-gamma) production by CD4+ and CD8+ lymphocytes and IFN-gamma gene polymorphism in patients with type 2 diabetes mellitus and latent autoimmune diabetes of adults (LADA). |
| 4501 | 15935691 | Subsequently, an attempt was made to correlate the presence of this mutation with the ability of CD4+ or CD8+ lymphocytes from these individuals to release IFN-gamma following mitogenic stimulation. |
| 4502 | 15935691 | CD4+ and CD8+ cells obtained from type 2 diabetics released significantly lower amounts of IFN-gamma in the intracellular space, compared to those released by cells obtained from LADA patients and healthy volunteers. |
| 4503 | 15935691 | Furthermore, even CD4+ and CD8+ from type 2 diabetics bearing the TT genotype (high producers) released significantly lower amounts of IFN-gamma than LADA patients carrying the same genotype, probably due to the activity of molecules directly or indirectly inhibiting IFN-gamma production. |
| 4504 | 15935691 | Correlation between intracellular interferon-gamma (IFN-gamma) production by CD4+ and CD8+ lymphocytes and IFN-gamma gene polymorphism in patients with type 2 diabetes mellitus and latent autoimmune diabetes of adults (LADA). |
| 4505 | 15935691 | Subsequently, an attempt was made to correlate the presence of this mutation with the ability of CD4+ or CD8+ lymphocytes from these individuals to release IFN-gamma following mitogenic stimulation. |
| 4506 | 15935691 | CD4+ and CD8+ cells obtained from type 2 diabetics released significantly lower amounts of IFN-gamma in the intracellular space, compared to those released by cells obtained from LADA patients and healthy volunteers. |
| 4507 | 15935691 | Furthermore, even CD4+ and CD8+ from type 2 diabetics bearing the TT genotype (high producers) released significantly lower amounts of IFN-gamma than LADA patients carrying the same genotype, probably due to the activity of molecules directly or indirectly inhibiting IFN-gamma production. |
| 4508 | 15942943 | RAD51L1 is a tumor-suppressor gene belonging to the RAD51 family, already implicated in many tumors (uterine leiomyomas, pseudo-Meigs syndromes, pulmonary chondroid hamartomas) and involved in recombinational repair of DNA double-strand breaks. |
| 4509 | 15942943 | BMP2 belongs to the TGFbeta superfamily, and the BMP2-BMP4 genes are involved in thymocyte differentiation by blocking progression from CD4-CD8- to CD4+CD8+ while maintaining a sufficient pool of immature precursors. |
| 4510 | 15975818 | Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). |
| 4511 | 15975818 | Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. |
| 4512 | 15975818 | Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. |
| 4513 | 15975818 | Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. |
| 4514 | 15975818 | Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease. |
| 4515 | 15975818 | Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). |
| 4516 | 15975818 | Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. |
| 4517 | 15975818 | Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. |
| 4518 | 15975818 | Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. |
| 4519 | 15975818 | Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease. |
| 4520 | 15975818 | Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). |
| 4521 | 15975818 | Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. |
| 4522 | 15975818 | Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. |
| 4523 | 15975818 | Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. |
| 4524 | 15975818 | Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease. |
| 4525 | 15977097 | At T1DM onset we observed significantly lower percentage of peripheral CD4 + and CD8 + cells producing IFN-gamma in patients compared to controls and subjects at risk. |
| 4526 | 15977097 | The 15-month follow-up patients showed significantly lower percentage of CD4 + and CD8 + cells producing IFN-gamma compared to the other groups. |
| 4527 | 15977097 | At T1DM onset we observed significantly lower percentage of peripheral CD4 + and CD8 + cells producing IFN-gamma in patients compared to controls and subjects at risk. |
| 4528 | 15977097 | The 15-month follow-up patients showed significantly lower percentage of CD4 + and CD8 + cells producing IFN-gamma compared to the other groups. |
| 4529 | 15979891 | In 62 GDM patients and 74 women with normal glucose tolerance (NGT), and their babies, we assessed total lymphocytes, T lymphocyte subsets CD3 and CD8 expressing T cell receptor (TCR) alpha/beta or gamma/delta, CD16 and CD19, pancreatic autoantibodies and cytokines (IL-5, IL-2, soluble receptor IL-2). |
| 4530 | 15979891 | Insulin-treated GDM mothers had lower CD4 and CD4/CD8 ratios, and higher CD8 and IL-5 than diet-treated GDM or controls. |
| 4531 | 15979891 | Five women were positive for pancreatic autoantibodies, with lower CD4 (p<0.01) and CD4/CD8 ratios (p<0.05), and higher CD8 (p<0.03) and CD19 than GDM and control mothers negative for autoantibodies. |
| 4532 | 15979891 | GDM newborn had higher CD8 gamma/delta and lower CD16 than NGT babies. |
| 4533 | 15979891 | In 62 GDM patients and 74 women with normal glucose tolerance (NGT), and their babies, we assessed total lymphocytes, T lymphocyte subsets CD3 and CD8 expressing T cell receptor (TCR) alpha/beta or gamma/delta, CD16 and CD19, pancreatic autoantibodies and cytokines (IL-5, IL-2, soluble receptor IL-2). |
| 4534 | 15979891 | Insulin-treated GDM mothers had lower CD4 and CD4/CD8 ratios, and higher CD8 and IL-5 than diet-treated GDM or controls. |
| 4535 | 15979891 | Five women were positive for pancreatic autoantibodies, with lower CD4 (p<0.01) and CD4/CD8 ratios (p<0.05), and higher CD8 (p<0.03) and CD19 than GDM and control mothers negative for autoantibodies. |
| 4536 | 15979891 | GDM newborn had higher CD8 gamma/delta and lower CD16 than NGT babies. |
| 4537 | 15993359 | The (CD4+)(CD25+)/(CD4+)(CD25-) cell ratio increased (P=.0128) at 24 weeks in the 20 microg group. |
| 4538 | 16005609 | DEF dimer protection relied on induction of anergy of diabetogenic CD4 T-cells in spleen, and stimulation of IL-10-secreting T regulatory type 1 cells in pancreas. |
| 4539 | 16034108 | CD8+ T cell tolerance in nonobese diabetic mice is restored by insulin-dependent diabetes resistance alleles. |
| 4540 | 16034108 | In the current study we have used NOD-InsHA transgenic mice that express the influenza hemagglutinin (HA) as an islet Ag to compare the fate of HA-specific CD8+ T cells in diabetes susceptible NOD-InsHA mice with that observed in diabetes-resistant congenic mice having protective alleles at insulin-dependent diabetes (Idd) 3, Idd5.1, and Idd5.2 (Idd3/5 strain) or at Idd9.1, Idd9.2, and Idd9.3 (Idd9 strain). |
| 4541 | 16034108 | However, by following the fate of naive, CFSE-labeled, islet Ag-specific CD8+ (HA-specific clone-4) or CD4+ (BDC2.5) T cells, we observed that tolerance is achieved differently in each protected strain. |
| 4542 | 16034108 | In Idd3/5 mice, tolerance occurs during the initial activation of islet Ag-specific CD8+ and CD4+ T cells in the pancreatic lymph nodes where CD25+ regulatory T cells (Tregs) effectively prevent their accumulation. |
| 4543 | 16034108 | In contrast, resistance alleles in Idd9 mice do not prevent the accumulation of islet Ag-specific CD8+ and CD4+ T cells in the pancreatic lymph nodes, indicating that tolerance occurs at a later checkpoint. |
| 4544 | 16034108 | CD8+ T cell tolerance in nonobese diabetic mice is restored by insulin-dependent diabetes resistance alleles. |
| 4545 | 16034108 | In the current study we have used NOD-InsHA transgenic mice that express the influenza hemagglutinin (HA) as an islet Ag to compare the fate of HA-specific CD8+ T cells in diabetes susceptible NOD-InsHA mice with that observed in diabetes-resistant congenic mice having protective alleles at insulin-dependent diabetes (Idd) 3, Idd5.1, and Idd5.2 (Idd3/5 strain) or at Idd9.1, Idd9.2, and Idd9.3 (Idd9 strain). |
| 4546 | 16034108 | However, by following the fate of naive, CFSE-labeled, islet Ag-specific CD8+ (HA-specific clone-4) or CD4+ (BDC2.5) T cells, we observed that tolerance is achieved differently in each protected strain. |
| 4547 | 16034108 | In Idd3/5 mice, tolerance occurs during the initial activation of islet Ag-specific CD8+ and CD4+ T cells in the pancreatic lymph nodes where CD25+ regulatory T cells (Tregs) effectively prevent their accumulation. |
| 4548 | 16034108 | In contrast, resistance alleles in Idd9 mice do not prevent the accumulation of islet Ag-specific CD8+ and CD4+ T cells in the pancreatic lymph nodes, indicating that tolerance occurs at a later checkpoint. |
| 4549 | 16034108 | CD8+ T cell tolerance in nonobese diabetic mice is restored by insulin-dependent diabetes resistance alleles. |
| 4550 | 16034108 | In the current study we have used NOD-InsHA transgenic mice that express the influenza hemagglutinin (HA) as an islet Ag to compare the fate of HA-specific CD8+ T cells in diabetes susceptible NOD-InsHA mice with that observed in diabetes-resistant congenic mice having protective alleles at insulin-dependent diabetes (Idd) 3, Idd5.1, and Idd5.2 (Idd3/5 strain) or at Idd9.1, Idd9.2, and Idd9.3 (Idd9 strain). |
| 4551 | 16034108 | However, by following the fate of naive, CFSE-labeled, islet Ag-specific CD8+ (HA-specific clone-4) or CD4+ (BDC2.5) T cells, we observed that tolerance is achieved differently in each protected strain. |
| 4552 | 16034108 | In Idd3/5 mice, tolerance occurs during the initial activation of islet Ag-specific CD8+ and CD4+ T cells in the pancreatic lymph nodes where CD25+ regulatory T cells (Tregs) effectively prevent their accumulation. |
| 4553 | 16034108 | In contrast, resistance alleles in Idd9 mice do not prevent the accumulation of islet Ag-specific CD8+ and CD4+ T cells in the pancreatic lymph nodes, indicating that tolerance occurs at a later checkpoint. |
| 4554 | 16038020 | Cytokine interleukin-12 (IL-12) is one of the key factors in the differentiation of naïve CD4(+) T cells into Th1 cells. |
| 4555 | 16038020 | In this study we used 2-DE and MS to find and identify IL-12 regulated proteins in human CD4(+) T cells. |
| 4556 | 16038020 | Among the upregulated proteins there are a multifunctional cytokine macrophage migration inhibitory factor and a known IL-12 target gene Programmed cell death 4. |
| 4557 | 16038020 | Downregulated proteins include p21-activated kinase 2 and its upstream GTPase Cdc42. |
| 4558 | 16038020 | Compared to previous reports our analysis provides a new view on the IL-12 induced changes on CD4(+) T cells underscoring the importance of creating and combining the data generated at various levels to build a comprehensive view of a given biological process of the cell. |
| 4559 | 16038020 | Cytokine interleukin-12 (IL-12) is one of the key factors in the differentiation of naïve CD4(+) T cells into Th1 cells. |
| 4560 | 16038020 | In this study we used 2-DE and MS to find and identify IL-12 regulated proteins in human CD4(+) T cells. |
| 4561 | 16038020 | Among the upregulated proteins there are a multifunctional cytokine macrophage migration inhibitory factor and a known IL-12 target gene Programmed cell death 4. |
| 4562 | 16038020 | Downregulated proteins include p21-activated kinase 2 and its upstream GTPase Cdc42. |
| 4563 | 16038020 | Compared to previous reports our analysis provides a new view on the IL-12 induced changes on CD4(+) T cells underscoring the importance of creating and combining the data generated at various levels to build a comprehensive view of a given biological process of the cell. |
| 4564 | 16038020 | Cytokine interleukin-12 (IL-12) is one of the key factors in the differentiation of naïve CD4(+) T cells into Th1 cells. |
| 4565 | 16038020 | In this study we used 2-DE and MS to find and identify IL-12 regulated proteins in human CD4(+) T cells. |
| 4566 | 16038020 | Among the upregulated proteins there are a multifunctional cytokine macrophage migration inhibitory factor and a known IL-12 target gene Programmed cell death 4. |
| 4567 | 16038020 | Downregulated proteins include p21-activated kinase 2 and its upstream GTPase Cdc42. |
| 4568 | 16038020 | Compared to previous reports our analysis provides a new view on the IL-12 induced changes on CD4(+) T cells underscoring the importance of creating and combining the data generated at various levels to build a comprehensive view of a given biological process of the cell. |
| 4569 | 16048553 | Oral antigen induces T-helper 2 [interleukin (IL)-4/IL-10] and Th3 [transforming growth factor (TGF)-beta] T cells plus CD4+CD25+ regulatory cells and latency-associated peptide+ T cells. |
| 4570 | 16048553 | Induction of oral tolerance is enhanced by IL-4, IL-10, anti-IL-12, TGF-beta, cholera toxin B subunit, Flt-3 ligand, and anti-CD40 ligand. |
| 4571 | 16081026 | Much focus has been placed on thymically derived CD4(+)CD25(+) regulatory T cells, given that the depletion of this subset in murine models results in the spontaneous development of autoimmune diseases. |
| 4572 | 16106371 | Our results indicate that (1) autoreactive CD4 T cells to GAD65 autoantigen are commonly present in humans expressing diabetes-susceptible HLA-DR*0401 molecules; (2) these autoreactive T cells undergo avidity maturation upon encountering the self antigen early in life; (3) the disease is associated with an imbalance between autoreactive CD4+CD25+ and CD4+CD69+ T cells specific for GAD65. |
| 4573 | 16116193 | Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice. |
| 4574 | 16116193 | CD4+CD25+Foxp3+ regulatory T cells (T(reg)) are critical for controlling autoimmunity. |
| 4575 | 16116193 | Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice. |
| 4576 | 16116193 | CD4+CD25+Foxp3+ regulatory T cells (T(reg)) are critical for controlling autoimmunity. |
| 4577 | 16122720 | CD4+CD25+ regulatory T cells control the progression from periinsulitis to destructive insulitis in murine autoimmune diabetes. |
| 4578 | 16122720 | Consistent with this hypothesis, CD4+CD25+ cell-depleted spleen cells from NOR mice mediated islet cell destruction and overt diabetes in NOD SCID mice. |
| 4579 | 16122720 | Therefore, islet cell-specific effector cells in NOR mice appear to be under the control of CD4+CD25+ regulatory T cells, confirming the importance of regulatory cells in the control of autoimmune diabetes. |
| 4580 | 16122720 | CD4+CD25+ regulatory T cells control the progression from periinsulitis to destructive insulitis in murine autoimmune diabetes. |
| 4581 | 16122720 | Consistent with this hypothesis, CD4+CD25+ cell-depleted spleen cells from NOR mice mediated islet cell destruction and overt diabetes in NOD SCID mice. |
| 4582 | 16122720 | Therefore, islet cell-specific effector cells in NOR mice appear to be under the control of CD4+CD25+ regulatory T cells, confirming the importance of regulatory cells in the control of autoimmune diabetes. |
| 4583 | 16122720 | CD4+CD25+ regulatory T cells control the progression from periinsulitis to destructive insulitis in murine autoimmune diabetes. |
| 4584 | 16122720 | Consistent with this hypothesis, CD4+CD25+ cell-depleted spleen cells from NOR mice mediated islet cell destruction and overt diabetes in NOD SCID mice. |
| 4585 | 16122720 | Therefore, islet cell-specific effector cells in NOR mice appear to be under the control of CD4+CD25+ regulatory T cells, confirming the importance of regulatory cells in the control of autoimmune diabetes. |
| 4586 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4587 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4588 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4589 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4590 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4591 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4592 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4593 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4594 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4595 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4596 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4597 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4598 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4599 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4600 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4601 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4602 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4603 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4604 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4605 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4606 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4607 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4608 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4609 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4610 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4611 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4612 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4613 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4614 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4615 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4616 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4617 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4618 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4619 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4620 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4621 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4622 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4623 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4624 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4625 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4626 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4627 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4628 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4629 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4630 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4631 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4632 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4633 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4634 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4635 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4636 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4637 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4638 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4639 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4640 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4641 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4642 | 16126946 | Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice. |
| 4643 | 16126946 | Naturally occurring CD4(+)CD25(+) T(reg) (nT(reg)) cells, which typically display potent inhibitory effects on T cell functions in vitro and in vivo, may be defective at controlling autoimmunity in T1D. |
| 4644 | 16126946 | We have examined the relative contribution of CD4(+)CD25(+) nT(reg) cells in the immune regulation of T1D in the NOD mouse model. |
| 4645 | 16126946 | CD4(+)CD25(+) T cells represent 5-10% of CD4(+) thymocytes or peripheral T cells from prediabetic neonatal NOD mice, are anergic to TCR signals, and potently suppress activated T cells in a contact-dependent and cytokine-independent fashion in vitro. |
| 4646 | 16126946 | Unlike total CD4(+) T cells, prediabetic CD25(+)-depleted CD4(+) T cells are potently diabetogenic when transferred in immunodeficient NOD mice. |
| 4647 | 16126946 | Co-transfer of CD4(+)CD25(+) T cells from thymocytes or peripheral lymphoid tissues of neonatal NOD mice dramatically halts disease development and beta-islet cell lymphocytic infiltration, even when T1D is induced by CD4(+) T cells from BDC2.5 transgenic or diabetic NOD mice. |
| 4648 | 16126946 | Finally, we show that CD4(+)CD25(+) T(reg) preferentially accumulate in inflamed pancreatic environments, where they potently inhibit the antigen-specific expansion and cytokine effector functions of diabetogenic T cells. |
| 4649 | 16126946 | Thus, CD4(+)CD25(+) T cell-mediated regulation is operative in the prediabetic neonatal T cell repertoire and can suppress the diabetogenic process and control the onset of T1D. |
| 4650 | 16155578 | Although major histocompatibility complex (MHC) class II-restricted CD4 T cells are well appreciated for their contribution to peripheral tolerance to tissue allografts, little is known regarding MHC class I-dependent reactivity in this process. |
| 4651 | 16155578 | Here we show a crucial role for host MHC class I-dependent NK cell reactivity for allograft tolerance in mice induced through either costimulation blockade using CD154-specific antibody therapy or by targeting LFA-1 (also known as CD11a). |
| 4652 | 16155578 | Tolerance induction absolutely required host expression of MHC class I, but was independent of CD8 T cell-dependent immunity. |
| 4653 | 16178866 | Clots were analysed immunohistochemically for detection of platelets (CD41a), leucocytes/lymphocytes (CD11b), granulocytes (CD16, lysozyme), neutrophilic granulocytes (neutrophil elastase), eosinophilic granulocytes (NaCN + H(2)O(2)), macrophages (CD68), dendritic cells (CD209/DC-SIGN), B cells (CD20) and T cells (CD4, CD8). |
| 4654 | 16184198 | To determine whether specific lysosomal proteases might influence the outcome of a CD4+ T cell-dependent autoimmune response, we generated mice that lack cathepsin L (Cat L) on the autoimmune diabetes-prone NOD inbred background. |
| 4655 | 16203996 | Mice with a defect in Foxp3, required for the generation and activity of CD4(+)CD25(+) regulatory T cells, exhibit massive lymphoproliferation and severe inflammatory infiltration of multiple organs, in particular the lungs, liver, and skin. |
| 4656 | 16209918 | How do CD4+CD25+ regulatory T cells control autoimmunity? |
| 4657 | 16209918 | The CD4(+)CD25(+)Foxp3(+) Treg subset develops in the thymus, can be induced in the periphery during the course of normal immune responses and utilizes a T cell repertoire skewed towards autoantigens. |
| 4658 | 16209918 | How do CD4+CD25+ regulatory T cells control autoimmunity? |
| 4659 | 16209918 | The CD4(+)CD25(+)Foxp3(+) Treg subset develops in the thymus, can be induced in the periphery during the course of normal immune responses and utilizes a T cell repertoire skewed towards autoantigens. |
| 4660 | 16236123 | Particular interest has focused on the CVB4 non-structural protein P2C, which we previously showed to be a major target of the effector memory anti-CVB4 CD4 T-cell response, and which harbours a region of sequence similarity with the islet autoantigen, glutamic acid decarboxylase (GAD65). |
| 4661 | 16236123 | In the present study therefore we examined the affinity of 20-mer overlapping P2C peptides for soluble HLA-DR4, -DR3, -DQ2 and -DQ8. |
| 4662 | 16236123 | DR4 and DQ8, P =0.0076; DR3 and DQ2 P = 0.002). |
| 4663 | 16243487 | The gene product, Scurfin, is required for the development of CD4+CD25+ T regulatory cells. |
| 4664 | 16247001 | Moreover, neonatal treatment with TNF-alpha resulted in skewed development of a CD8alpha(+)CD11b(-)CD11c(+) DC subset such that TNF-alpha decreases the CD8alpha(+)CD11c(+) DC subset, increases the CD11c(+)CD11b(+) subset, and causes an increase in the expression of CD40 and CD54 on mature DCs capable of inducing immunity. |
| 4665 | 16247001 | Anti-TNF-alpha-treated mice had an increase in the CD8alpha(+)CD11c(+) DCs. |
| 4666 | 16247001 | Notably, adoptively transferred naïve CD4(+) T cells from BDC2.5 T cell receptor transgenic mice proliferated in the pancreatic lymph nodes in TNF-alpha-treated NOD mice but not in anti-TNF-alpha-treated mice. |
| 4667 | 16249070 | Comparative study of GAD65-specific CD4+ T cells in healthy and type 1 diabetic subjects. |
| 4668 | 16249070 | The prevalence of autoreactive CD4+ T cells towards the immunodominant GAD65(555-567) epitope in DR4 healthy and T1D subjects was investigated with class II tetramers. |
| 4669 | 16249070 | A slightly higher percentage of diabetic subjects had GAD65(555-567) tetramer-positive T cells upon GAD65(555-567) peptide stimulation on the total CD4+ T-cell populations compared to healthy subjects. |
| 4670 | 16249070 | In contrast, three quarters of subjects in both groups had tetramer-positive T cells resulting from stimulation of the CD4+CD25+ regulatory T-cell depleted CD4+ T cells. |
| 4671 | 16249070 | These findings suggested that there is no difference in thymic selection of DR4 restricted GAD-reactive T cells amongst healthy and T1D individuals but GAD65(555-567)-reactive T cells have been preferentially activated in diabetic patients. |
| 4672 | 16249070 | Comparative study of GAD65-specific CD4+ T cells in healthy and type 1 diabetic subjects. |
| 4673 | 16249070 | The prevalence of autoreactive CD4+ T cells towards the immunodominant GAD65(555-567) epitope in DR4 healthy and T1D subjects was investigated with class II tetramers. |
| 4674 | 16249070 | A slightly higher percentage of diabetic subjects had GAD65(555-567) tetramer-positive T cells upon GAD65(555-567) peptide stimulation on the total CD4+ T-cell populations compared to healthy subjects. |
| 4675 | 16249070 | In contrast, three quarters of subjects in both groups had tetramer-positive T cells resulting from stimulation of the CD4+CD25+ regulatory T-cell depleted CD4+ T cells. |
| 4676 | 16249070 | These findings suggested that there is no difference in thymic selection of DR4 restricted GAD-reactive T cells amongst healthy and T1D individuals but GAD65(555-567)-reactive T cells have been preferentially activated in diabetic patients. |
| 4677 | 16249070 | Comparative study of GAD65-specific CD4+ T cells in healthy and type 1 diabetic subjects. |
| 4678 | 16249070 | The prevalence of autoreactive CD4+ T cells towards the immunodominant GAD65(555-567) epitope in DR4 healthy and T1D subjects was investigated with class II tetramers. |
| 4679 | 16249070 | A slightly higher percentage of diabetic subjects had GAD65(555-567) tetramer-positive T cells upon GAD65(555-567) peptide stimulation on the total CD4+ T-cell populations compared to healthy subjects. |
| 4680 | 16249070 | In contrast, three quarters of subjects in both groups had tetramer-positive T cells resulting from stimulation of the CD4+CD25+ regulatory T-cell depleted CD4+ T cells. |
| 4681 | 16249070 | These findings suggested that there is no difference in thymic selection of DR4 restricted GAD-reactive T cells amongst healthy and T1D individuals but GAD65(555-567)-reactive T cells have been preferentially activated in diabetic patients. |
| 4682 | 16249070 | Comparative study of GAD65-specific CD4+ T cells in healthy and type 1 diabetic subjects. |
| 4683 | 16249070 | The prevalence of autoreactive CD4+ T cells towards the immunodominant GAD65(555-567) epitope in DR4 healthy and T1D subjects was investigated with class II tetramers. |
| 4684 | 16249070 | A slightly higher percentage of diabetic subjects had GAD65(555-567) tetramer-positive T cells upon GAD65(555-567) peptide stimulation on the total CD4+ T-cell populations compared to healthy subjects. |
| 4685 | 16249070 | In contrast, three quarters of subjects in both groups had tetramer-positive T cells resulting from stimulation of the CD4+CD25+ regulatory T-cell depleted CD4+ T cells. |
| 4686 | 16249070 | These findings suggested that there is no difference in thymic selection of DR4 restricted GAD-reactive T cells amongst healthy and T1D individuals but GAD65(555-567)-reactive T cells have been preferentially activated in diabetic patients. |
| 4687 | 16260488 | To investigate the specificity of proinsulin-specific T cells in T1D, we isolated human CD4(+) T cell clones to proinsulin from the blood of a donor who had T1D. |
| 4688 | 16260488 | CD4(+) T cell clones that recognized this epitope were isolated from an HLA DR4(+) child with autoantibodies to insulin, and therefore, at risk for T1D, but not from two healthy HLA DR4(+) donors. |
| 4689 | 16260488 | To investigate the specificity of proinsulin-specific T cells in T1D, we isolated human CD4(+) T cell clones to proinsulin from the blood of a donor who had T1D. |
| 4690 | 16260488 | CD4(+) T cell clones that recognized this epitope were isolated from an HLA DR4(+) child with autoantibodies to insulin, and therefore, at risk for T1D, but not from two healthy HLA DR4(+) donors. |
| 4691 | 16263129 | Supernatant samples were analysed by ELISA for TNFalpha, IFNgamma and IL-10 production. |
| 4692 | 16263129 | Plastic adhesion decreased the macrophage numbers by approximately 30% and CD4(+)CD25(+) cells by about 60%. |
| 4693 | 16263129 | This was accompanied by increased medium levels of TNFalpha, IFNgamma and IL-10, which suggest that either CD4(+)CD25(+) cells, macrophages, or both, down-regulate production of both Th1 and certain Th2 cytokines. |
| 4694 | 16263129 | Supernatant samples were analysed by ELISA for TNFalpha, IFNgamma and IL-10 production. |
| 4695 | 16263129 | Plastic adhesion decreased the macrophage numbers by approximately 30% and CD4(+)CD25(+) cells by about 60%. |
| 4696 | 16263129 | This was accompanied by increased medium levels of TNFalpha, IFNgamma and IL-10, which suggest that either CD4(+)CD25(+) cells, macrophages, or both, down-regulate production of both Th1 and certain Th2 cytokines. |
| 4697 | 16263242 | GAD65- and proinsulin-specific CD4+ T-cells detected by MHC class II tetramers in peripheral blood of type 1 diabetes patients and at-risk subjects. |
| 4698 | 16263242 | In this study we have analyzed the prevalence of glutamate decarboxylase 65 (GAD65)- and proinsulin-specific CD4(+) T-cells in type 1 diabetes patients, at-risk subjects and in HLA-matched control children. |
| 4699 | 16263242 | Peripheral blood mononuclear cells were cultured in the presence of two different GAD65 peptides (555-567, 557I and 274-286) or with a proinsulin (B24-C36) peptide for 10-11days. |
| 4700 | 16263242 | Our results show that 11 of 18 (61%) type 1 diabetes patients and 7 of the 20 (35%) at-risk subjects were positive for one of the three GAD65 or proinsulin-containing tetramers, whereas only 2 of 21 (9.5%) controls had tetramer binding cells (p = 0.0007 type 1 diabetes vs. controls and p = 0.0488 at-risk subjects vs. controls, Chi-square test). |
| 4701 | 16263242 | In conclusion, type 1 diabetes patients and at-risk subjects have a significantly higher prevalence of GAD65- and proinsulin-specific CD4(+) T-cells than the control subjects. |
| 4702 | 16263242 | GAD65- and proinsulin-specific CD4+ T-cells detected by MHC class II tetramers in peripheral blood of type 1 diabetes patients and at-risk subjects. |
| 4703 | 16263242 | In this study we have analyzed the prevalence of glutamate decarboxylase 65 (GAD65)- and proinsulin-specific CD4(+) T-cells in type 1 diabetes patients, at-risk subjects and in HLA-matched control children. |
| 4704 | 16263242 | Peripheral blood mononuclear cells were cultured in the presence of two different GAD65 peptides (555-567, 557I and 274-286) or with a proinsulin (B24-C36) peptide for 10-11days. |
| 4705 | 16263242 | Our results show that 11 of 18 (61%) type 1 diabetes patients and 7 of the 20 (35%) at-risk subjects were positive for one of the three GAD65 or proinsulin-containing tetramers, whereas only 2 of 21 (9.5%) controls had tetramer binding cells (p = 0.0007 type 1 diabetes vs. controls and p = 0.0488 at-risk subjects vs. controls, Chi-square test). |
| 4706 | 16263242 | In conclusion, type 1 diabetes patients and at-risk subjects have a significantly higher prevalence of GAD65- and proinsulin-specific CD4(+) T-cells than the control subjects. |
| 4707 | 16263242 | GAD65- and proinsulin-specific CD4+ T-cells detected by MHC class II tetramers in peripheral blood of type 1 diabetes patients and at-risk subjects. |
| 4708 | 16263242 | In this study we have analyzed the prevalence of glutamate decarboxylase 65 (GAD65)- and proinsulin-specific CD4(+) T-cells in type 1 diabetes patients, at-risk subjects and in HLA-matched control children. |
| 4709 | 16263242 | Peripheral blood mononuclear cells were cultured in the presence of two different GAD65 peptides (555-567, 557I and 274-286) or with a proinsulin (B24-C36) peptide for 10-11days. |
| 4710 | 16263242 | Our results show that 11 of 18 (61%) type 1 diabetes patients and 7 of the 20 (35%) at-risk subjects were positive for one of the three GAD65 or proinsulin-containing tetramers, whereas only 2 of 21 (9.5%) controls had tetramer binding cells (p = 0.0007 type 1 diabetes vs. controls and p = 0.0488 at-risk subjects vs. controls, Chi-square test). |
| 4711 | 16263242 | In conclusion, type 1 diabetes patients and at-risk subjects have a significantly higher prevalence of GAD65- and proinsulin-specific CD4(+) T-cells than the control subjects. |
| 4712 | 16263243 | CD4(+)hCD90(+) cells had a higher capacity to secret IFN-gamma than CD4(+)hCD90(-) cells in an autoantigen-specific manner. |
| 4713 | 16280647 | Fluorochrome-labeled recombinant MHC class II-peptide reagents function as soluble mimetics of this interaction, bind to their specific TCR, and allow for detection of antigen-specific CD4+ T cells. |
| 4714 | 16280647 | Several issues are currently being addressed to improve the performance of these T cell assays: enrichment steps for better sensitivity, multiplexing of several islet epitopes, simultaneous monitoring of CD4+ and CD8+ responses, detection of low avidity T cells, combination of quantitative (number of positive cells) and qualitative (cytokine secretion, naive/memory phenotype) readouts. |
| 4715 | 16280647 | CD4+ T cells are key effectors of autoimmunity, and these MHC class II peptide reagents, through their signaling properties, might also provide therapeutics to block the autoimmune process at its onset, analogous to the use of OKT3gammao1(AlaAla) anti-CD3 antibody but in an antigen-specific fashion. |
| 4716 | 16280647 | Fluorochrome-labeled recombinant MHC class II-peptide reagents function as soluble mimetics of this interaction, bind to their specific TCR, and allow for detection of antigen-specific CD4+ T cells. |
| 4717 | 16280647 | Several issues are currently being addressed to improve the performance of these T cell assays: enrichment steps for better sensitivity, multiplexing of several islet epitopes, simultaneous monitoring of CD4+ and CD8+ responses, detection of low avidity T cells, combination of quantitative (number of positive cells) and qualitative (cytokine secretion, naive/memory phenotype) readouts. |
| 4718 | 16280647 | CD4+ T cells are key effectors of autoimmunity, and these MHC class II peptide reagents, through their signaling properties, might also provide therapeutics to block the autoimmune process at its onset, analogous to the use of OKT3gammao1(AlaAla) anti-CD3 antibody but in an antigen-specific fashion. |
| 4719 | 16280647 | Fluorochrome-labeled recombinant MHC class II-peptide reagents function as soluble mimetics of this interaction, bind to their specific TCR, and allow for detection of antigen-specific CD4+ T cells. |
| 4720 | 16280647 | Several issues are currently being addressed to improve the performance of these T cell assays: enrichment steps for better sensitivity, multiplexing of several islet epitopes, simultaneous monitoring of CD4+ and CD8+ responses, detection of low avidity T cells, combination of quantitative (number of positive cells) and qualitative (cytokine secretion, naive/memory phenotype) readouts. |
| 4721 | 16280647 | CD4+ T cells are key effectors of autoimmunity, and these MHC class II peptide reagents, through their signaling properties, might also provide therapeutics to block the autoimmune process at its onset, analogous to the use of OKT3gammao1(AlaAla) anti-CD3 antibody but in an antigen-specific fashion. |
| 4722 | 16280652 | While this process takes place, beta cell antigen-specific CD8+ T cells are activated by IL-2 produced by the activated TH1 CD4+ T cells, differentiate into cytotoxic T cells and are recruited into the pancreatic islets. |
| 4723 | 16280652 | These activated TH1 CD4+ T cells and CD8+ cytotoxic T cells are involved in the destruction of beta cells. |
| 4724 | 16280652 | Thus, activated macrophages, TH1 CD4+ T cells, and beta cell-cytotoxic CD8+ T cells act synergistically to destroy beta cells, resulting in autoimmune type 1 diabetes. |
| 4725 | 16280652 | While this process takes place, beta cell antigen-specific CD8+ T cells are activated by IL-2 produced by the activated TH1 CD4+ T cells, differentiate into cytotoxic T cells and are recruited into the pancreatic islets. |
| 4726 | 16280652 | These activated TH1 CD4+ T cells and CD8+ cytotoxic T cells are involved in the destruction of beta cells. |
| 4727 | 16280652 | Thus, activated macrophages, TH1 CD4+ T cells, and beta cell-cytotoxic CD8+ T cells act synergistically to destroy beta cells, resulting in autoimmune type 1 diabetes. |
| 4728 | 16280652 | While this process takes place, beta cell antigen-specific CD8+ T cells are activated by IL-2 produced by the activated TH1 CD4+ T cells, differentiate into cytotoxic T cells and are recruited into the pancreatic islets. |
| 4729 | 16280652 | These activated TH1 CD4+ T cells and CD8+ cytotoxic T cells are involved in the destruction of beta cells. |
| 4730 | 16280652 | Thus, activated macrophages, TH1 CD4+ T cells, and beta cell-cytotoxic CD8+ T cells act synergistically to destroy beta cells, resulting in autoimmune type 1 diabetes. |
| 4731 | 16301684 | Effector function of diabetogenic CD4 Th1 T cell clones: a central role for TNF-alpha. |
| 4732 | 16301684 | We have investigated cytokine production both in vitro and in vivo in a panel of diabetogenic CD4 Th1 T cell clones derived from the NOD mouse. |
| 4733 | 16301684 | Ex vivo intracellular cytokine staining demonstrated that two important inflammatory cytokines, IFN-gamma and TNF-alpha, were being made by these T cells recovered from the pancreas 6 days following adoptive transfer. |
| 4734 | 16301684 | Similar analyses in other models demonstrated that disease induced by CD4 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells are required. |
| 4735 | 16301684 | Effector function of diabetogenic CD4 Th1 T cell clones: a central role for TNF-alpha. |
| 4736 | 16301684 | We have investigated cytokine production both in vitro and in vivo in a panel of diabetogenic CD4 Th1 T cell clones derived from the NOD mouse. |
| 4737 | 16301684 | Ex vivo intracellular cytokine staining demonstrated that two important inflammatory cytokines, IFN-gamma and TNF-alpha, were being made by these T cells recovered from the pancreas 6 days following adoptive transfer. |
| 4738 | 16301684 | Similar analyses in other models demonstrated that disease induced by CD4 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells are required. |
| 4739 | 16301684 | Effector function of diabetogenic CD4 Th1 T cell clones: a central role for TNF-alpha. |
| 4740 | 16301684 | We have investigated cytokine production both in vitro and in vivo in a panel of diabetogenic CD4 Th1 T cell clones derived from the NOD mouse. |
| 4741 | 16301684 | Ex vivo intracellular cytokine staining demonstrated that two important inflammatory cytokines, IFN-gamma and TNF-alpha, were being made by these T cells recovered from the pancreas 6 days following adoptive transfer. |
| 4742 | 16301684 | Similar analyses in other models demonstrated that disease induced by CD4 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells are required. |
| 4743 | 16301745 | Where CD4+CD25+ T reg cells impinge on autoimmune diabetes. |
| 4744 | 16301745 | Foxp3 is required for the generation and activity of CD4(+)CD25(+) regulatory T (T reg) cells, which are important controllers of autoimmunity, including type-1 diabetes. |
| 4745 | 16301745 | Where CD4+CD25+ T reg cells impinge on autoimmune diabetes. |
| 4746 | 16301745 | Foxp3 is required for the generation and activity of CD4(+)CD25(+) regulatory T (T reg) cells, which are important controllers of autoimmunity, including type-1 diabetes. |
| 4747 | 16304639 | We investigated whether iNKT activation with alpha-GalCer was protective in collagen-induced arthritis (CIA) in DBA/1 mice, a standard model of rheumatoid arthritis. |
| 4748 | 16304639 | Here, we have shown that in vivo iNKT cell function was altered in DBA/1 mice since stimulation with alpha-GalCer led to decreased IL-4 and IFN-gamma levels in sera, as compared with C57BL/6 mice. alpha-GalCer induced a clear-cut diminution of clinical and histological arthritides. |
| 4749 | 16304639 | An anti-IL-10 receptor antibody abrogated the protective effect of alpha-GalCer, suggesting a key role for IL-10 in the protection against CIA by activated iNKT cells. |
| 4750 | 16304639 | Confirming these data, disease protection conferred by alpha-GalCer correlated with the ability of LN CD4+ cells to secrete larger amounts of IL-10. |
| 4751 | 16306354 | Moreover, HA-specific CD4+ T-cells from anti-DEC-HA-treated INS-HA/TCR-HA mice exhibited increased expression of Foxp3, cytotoxic T-lymphocyte-associated antigen-4, and the immunosuppressive cytokines interleukin-10 and transforming growth factor-beta. |
| 4752 | 16311599 | Islet antigen-specific CD4(+)CD25(-) T helper cells (T(H) cells) and T(reg) cells swarmed and arrested in the presence of autoantigens. |
| 4753 | 16313366 | The NOD-derived islet-reactive CD4(+) T cell clone, BDC-2.5, is able to transfer diabetes to neonatal non-obese diabetic (NOD) mice but is unable to transfer disease to either adult NOD or NOD scid recipients. |
| 4754 | 16318983 | TGF-beta dependent and independent mechanisms have been described involving CD4(+) as well as CD8(+) T cells. |
| 4755 | 16318984 | This autoimmune disease is characterized by the selective loss of the insulin-producing beta cells via the cumulative effects of autoantigen-specific CD4(+) and CD8(+) T cells, autoantibodies, and activated antigen-presenting cells. |
| 4756 | 16329191 | Specific antiviral (self) CD8 T cells are mandatory for disease, but CD4 T cells are not. |
| 4757 | 16329191 | In this instance, diabetes can occur in the absence of infection if interferon gamma or B7.1 molecules are also expressed in the islets but not when IL-2, IL-4, IL-10, or IL-12 is similarly expressed. |
| 4758 | 16329191 | In contrast, both CD8 and CD4 antiviral (self) specific T cells are required when the self "viral" transgene is expressed concomitantly in beta cells and in the thymus. |
| 4759 | 16329191 | Specific antiviral (self) CD8 T cells are mandatory for disease, but CD4 T cells are not. |
| 4760 | 16329191 | In this instance, diabetes can occur in the absence of infection if interferon gamma or B7.1 molecules are also expressed in the islets but not when IL-2, IL-4, IL-10, or IL-12 is similarly expressed. |
| 4761 | 16329191 | In contrast, both CD8 and CD4 antiviral (self) specific T cells are required when the self "viral" transgene is expressed concomitantly in beta cells and in the thymus. |
| 4762 | 16352552 | Following virus infection, we profiled primary, memory, and secondary CD8+ and CD4+ T-cell responses directed against eight different viral epitopes. |
| 4763 | 16380473 | Costimulation blockade of both inducible costimulator and CD40 ligand induces dominant tolerance to islet allografts and prevents spontaneous autoimmune diabetes in the NOD mouse. |
| 4764 | 16380473 | Using a fully allogeneic mouse model, we tested the effectiveness of the combined blockade of the CD40 ligand and the inducible costimulator (ICOS) on islet allograft survival and in the prevention of autoimmune diabetes in the NOD mouse. |
| 4765 | 16380473 | Recipients treated with blocking monoclonal antibodies (mAbs) to ICOS and the CD40 ligand had significant prolongation of graft survival, with 26 of 28 functioning for >200 days. |
| 4766 | 16380473 | The immunohistology of tolerant grafts demonstrated the presence of CD4(+)CD25(+) T-cells expressing Foxp3, and islet/kidney composite grafts from tolerant mice, but not from mice lacking lymphocytes, were accepted indefinitely when transplanted into naïve B6 mice, suggesting that recipient T-cells were necessary to generate dominant tolerance. |
| 4767 | 16380473 | These data demonstrate that the blockade of CD40 ligand and ICOS signaling induces islet allograft tolerance involving a dominant mechanism associated with intragraft regulatory cells and prevents autoimmune diabetes in NOD mice. |
| 4768 | 16380475 | CD4(+) T-cells from rapamycin plus IL-10-treated mice transferred antigen-specific tolerance in mice that received new transplants. |
| 4769 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4770 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4771 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4772 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4773 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4774 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4775 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4776 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4777 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4778 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4779 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4780 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4781 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4782 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4783 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4784 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4785 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4786 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4787 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4788 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4789 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4790 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4791 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4792 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4793 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4794 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4795 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4796 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4797 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4798 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4799 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4800 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4801 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4802 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4803 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4804 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4805 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4806 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4807 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4808 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4809 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4810 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4811 | 16380489 | Interleukin-7 is a survival factor for CD4+ CD25+ T-cells and is expressed by diabetes-suppressive dendritic cells. |
| 4812 | 16380489 | Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). |
| 4813 | 16380489 | Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. |
| 4814 | 16380489 | Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. |
| 4815 | 16380489 | In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. |
| 4816 | 16380489 | In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. |
| 4817 | 16380489 | Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. |
| 4818 | 16380490 | No significant differences in plasma corticosterone, splenic CD4(+) or CD8(+) T-cell percentages, or functions of CD3(+) T-cells in vitro distinguished NOD wild-type from mutant mice. |
| 4819 | 16380490 | This correlated with significantly reduced (P < 0.01) frequencies of insulin and islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD8(+) T-effector clonotypes in mutant mice. |
| 4820 | 16380490 | In conclusion, metabolic disturbances elicited by a type 2 diabetes syndrome (insulin and/or leptin resistance, but not hypercorticism) appear to suppress type 1 diabetes development in NOD-Lepr(db-5J)/Lt by inhibiting activation of T-effector cells. |
| 4821 | 16380492 | The diabetes type 1 locus Idd6 modulates activity of CD4+CD25+ regulatory T-cells. |
| 4822 | 16380492 | Our transfer experiments using total splenocytes and purified T-cells demonstrated that the locus specifically controls the efficiency of disease protection mediated by the regulatory CD4(+)CD25(+) T-cell subset. |
| 4823 | 16380492 | The diabetes type 1 locus Idd6 modulates activity of CD4+CD25+ regulatory T-cells. |
| 4824 | 16380492 | Our transfer experiments using total splenocytes and purified T-cells demonstrated that the locus specifically controls the efficiency of disease protection mediated by the regulatory CD4(+)CD25(+) T-cell subset. |
| 4825 | 16387141 | We analyzed the immunological parameters of CD4/CD8 T lymphocyte ratios; islet cell antibodies (ICAs) and insulin antibodies (IAs). |
| 4826 | 16387141 | We observed that the CD4+/CD8+ T-cell ratio increased, peaking on day 90, in similar fashion in both groups: day -1: A = 1.18 +/- 0.03 versus B = 1.19 +/- 0.04; on day 90: A = 1.79 +/- 0.09, versus B = 1.75 +/- 0.08 (P = NS) immediately before the decrease in C-peptide levels. |
| 4827 | 16387141 | The CD4/CD8 ratio increased as the C-peptide level decreased, peaking on day 90 at the time of a decrease in C-peptide. |
| 4828 | 16387141 | We analyzed the immunological parameters of CD4/CD8 T lymphocyte ratios; islet cell antibodies (ICAs) and insulin antibodies (IAs). |
| 4829 | 16387141 | We observed that the CD4+/CD8+ T-cell ratio increased, peaking on day 90, in similar fashion in both groups: day -1: A = 1.18 +/- 0.03 versus B = 1.19 +/- 0.04; on day 90: A = 1.79 +/- 0.09, versus B = 1.75 +/- 0.08 (P = NS) immediately before the decrease in C-peptide levels. |
| 4830 | 16387141 | The CD4/CD8 ratio increased as the C-peptide level decreased, peaking on day 90 at the time of a decrease in C-peptide. |
| 4831 | 16387141 | We analyzed the immunological parameters of CD4/CD8 T lymphocyte ratios; islet cell antibodies (ICAs) and insulin antibodies (IAs). |
| 4832 | 16387141 | We observed that the CD4+/CD8+ T-cell ratio increased, peaking on day 90, in similar fashion in both groups: day -1: A = 1.18 +/- 0.03 versus B = 1.19 +/- 0.04; on day 90: A = 1.79 +/- 0.09, versus B = 1.75 +/- 0.08 (P = NS) immediately before the decrease in C-peptide levels. |
| 4833 | 16387141 | The CD4/CD8 ratio increased as the C-peptide level decreased, peaking on day 90 at the time of a decrease in C-peptide. |
| 4834 | 16393560 | [CD4 + CD25 + regulatory T cells and their importance to human illnesses]. |
| 4835 | 16409156 | Cd4+Cd25+ regulatory T cells and their therapeutic potential. |
| 4836 | 16409156 | A recently characterized subset of T cells, identified by their cell surface expression of CD4 and CD25, is critical in regulating the function of other immune cells and preventing potentially harmful autoimmune responses. |
| 4837 | 16409156 | Cd4+Cd25+ regulatory T cells and their therapeutic potential. |
| 4838 | 16409156 | A recently characterized subset of T cells, identified by their cell surface expression of CD4 and CD25, is critical in regulating the function of other immune cells and preventing potentially harmful autoimmune responses. |
| 4839 | 16415097 | Moreover, no significant differences were detected in lymphocyte sub-populations and mitogen-induced CD4(+) and CD8(+) proliferative responses between control and treatment groups. |
| 4840 | 16437243 | We analyzed, in a cross-sectional pilot study, HIV-antigen-stimulated IL-10 and tumor necrosis factor alpha (TNFalpha) production, and intracellular concentration (ICC), as well as B7-H1 expression, a marker preferentially presented by IL-10-producing cells, in 20 ARV-treated individuals in whom diabetes did (n=10; diabetes mellitus, DM) or did not (n=10; controls) develop. |
| 4841 | 16437243 | Results showed that: (1) IL-10 production was lower; (2) IL-10 ICC was reduced; (3) B7-H1-expressing CD19(+) cells were diminished; and (4) TNFalpha production and ICC by CD4(+) T cells was augmented in DM patients. |
| 4842 | 16458533 | CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) are critical for the regulation of tolerance and have shown enormous potential in suppressing pathological immune responses in autoimmune disease, transplantation, and graft-versus-host disease (GVHD). |
| 4843 | 16469503 | Dendritic cells (DCs) are important for several aspects of the development and function of CD4(+) CD25(+) regulatory T cells (Tregs), which are critical for maintaining peripheral tolerance and preventing autoimmunity. |
| 4844 | 16469503 | In cultures from human thymus, dendritic cells (DCs) conditioned with thymic stromal lymphopoietin (TSLP) mediate the production of Tregs from CD4(+) CD25(-) thymocytes. |
| 4845 | 16469503 | Dendritic cells (DCs) are important for several aspects of the development and function of CD4(+) CD25(+) regulatory T cells (Tregs), which are critical for maintaining peripheral tolerance and preventing autoimmunity. |
| 4846 | 16469503 | In cultures from human thymus, dendritic cells (DCs) conditioned with thymic stromal lymphopoietin (TSLP) mediate the production of Tregs from CD4(+) CD25(-) thymocytes. |
| 4847 | 16476010 | Elimination of CD4+ CD25+ regulatory T cells breaks down reovirus type 2-triggered and CpG ODN-induced prolonged mild autoimmune insulitis in DBA/1 mice. |
| 4848 | 16476010 | Compared with the control mice, newborn mice treated with monoclonal antibody (MoAb) against mouse CD25(+) CD4(+) T cells together with Reo-2 and CpG ODN greatly reduced the absolute number of splenic CD25(+) T cells and resulted in the development of severe insulitis, leading to an overt early diabetes. |
| 4849 | 16476010 | Moreover, the treatment of the MoAb increased production of interferon-gamma (IFN-gamma) and decreased that of interleukin-4 (IL-4) and transforming growth factor-beta1 (TGF-beta1) and developed high titre of autoantibodies against pancreatic islet cells. |
| 4850 | 16476010 | These evidences suggest that CD4(+) CD25(+) T cell may, at least in part, maintain tolerance to Reo-2-triggered and CpG ODN-induced prolonged mild Th1-dependent autoimmune insulitis, leading to the overt disease. |
| 4851 | 16476010 | Elimination of CD4+ CD25+ regulatory T cells breaks down reovirus type 2-triggered and CpG ODN-induced prolonged mild autoimmune insulitis in DBA/1 mice. |
| 4852 | 16476010 | Compared with the control mice, newborn mice treated with monoclonal antibody (MoAb) against mouse CD25(+) CD4(+) T cells together with Reo-2 and CpG ODN greatly reduced the absolute number of splenic CD25(+) T cells and resulted in the development of severe insulitis, leading to an overt early diabetes. |
| 4853 | 16476010 | Moreover, the treatment of the MoAb increased production of interferon-gamma (IFN-gamma) and decreased that of interleukin-4 (IL-4) and transforming growth factor-beta1 (TGF-beta1) and developed high titre of autoantibodies against pancreatic islet cells. |
| 4854 | 16476010 | These evidences suggest that CD4(+) CD25(+) T cell may, at least in part, maintain tolerance to Reo-2-triggered and CpG ODN-induced prolonged mild Th1-dependent autoimmune insulitis, leading to the overt disease. |
| 4855 | 16476010 | Elimination of CD4+ CD25+ regulatory T cells breaks down reovirus type 2-triggered and CpG ODN-induced prolonged mild autoimmune insulitis in DBA/1 mice. |
| 4856 | 16476010 | Compared with the control mice, newborn mice treated with monoclonal antibody (MoAb) against mouse CD25(+) CD4(+) T cells together with Reo-2 and CpG ODN greatly reduced the absolute number of splenic CD25(+) T cells and resulted in the development of severe insulitis, leading to an overt early diabetes. |
| 4857 | 16476010 | Moreover, the treatment of the MoAb increased production of interferon-gamma (IFN-gamma) and decreased that of interleukin-4 (IL-4) and transforming growth factor-beta1 (TGF-beta1) and developed high titre of autoantibodies against pancreatic islet cells. |
| 4858 | 16476010 | These evidences suggest that CD4(+) CD25(+) T cell may, at least in part, maintain tolerance to Reo-2-triggered and CpG ODN-induced prolonged mild Th1-dependent autoimmune insulitis, leading to the overt disease. |
| 4859 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 4860 | 16478885 | CD4(+)CD25(+) T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN-gamma production by HCV-specific T cells. |
| 4861 | 16478885 | Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3(+)CD4(+)CD25(+) regulatory T cells (T(Regs)) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. |
| 4862 | 16478885 | Foxp3(+)CD4(+)CD25(+) T(Regs) suppressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. |
| 4863 | 16478885 | However, Foxp3(+)CD4(+)CD25(+) T(Reg) cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3(+)CD4(+)CD25(+)T(Reg) cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. |
| 4864 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 4865 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 4866 | 16478885 | CD4(+)CD25(+) T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN-gamma production by HCV-specific T cells. |
| 4867 | 16478885 | Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3(+)CD4(+)CD25(+) regulatory T cells (T(Regs)) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. |
| 4868 | 16478885 | Foxp3(+)CD4(+)CD25(+) T(Regs) suppressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. |
| 4869 | 16478885 | However, Foxp3(+)CD4(+)CD25(+) T(Reg) cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3(+)CD4(+)CD25(+)T(Reg) cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. |
| 4870 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 4871 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 4872 | 16478885 | CD4(+)CD25(+) T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN-gamma production by HCV-specific T cells. |
| 4873 | 16478885 | Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3(+)CD4(+)CD25(+) regulatory T cells (T(Regs)) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. |
| 4874 | 16478885 | Foxp3(+)CD4(+)CD25(+) T(Regs) suppressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. |
| 4875 | 16478885 | However, Foxp3(+)CD4(+)CD25(+) T(Reg) cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3(+)CD4(+)CD25(+)T(Reg) cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. |
| 4876 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 4877 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 4878 | 16478885 | CD4(+)CD25(+) T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN-gamma production by HCV-specific T cells. |
| 4879 | 16478885 | Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3(+)CD4(+)CD25(+) regulatory T cells (T(Regs)) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. |
| 4880 | 16478885 | Foxp3(+)CD4(+)CD25(+) T(Regs) suppressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. |
| 4881 | 16478885 | However, Foxp3(+)CD4(+)CD25(+) T(Reg) cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3(+)CD4(+)CD25(+)T(Reg) cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. |
| 4882 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 4883 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 4884 | 16478885 | CD4(+)CD25(+) T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN-gamma production by HCV-specific T cells. |
| 4885 | 16478885 | Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3(+)CD4(+)CD25(+) regulatory T cells (T(Regs)) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. |
| 4886 | 16478885 | Foxp3(+)CD4(+)CD25(+) T(Regs) suppressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. |
| 4887 | 16478885 | However, Foxp3(+)CD4(+)CD25(+) T(Reg) cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3(+)CD4(+)CD25(+)T(Reg) cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. |
| 4888 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 4889 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 4890 | 16478885 | CD4(+)CD25(+) T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN-gamma production by HCV-specific T cells. |
| 4891 | 16478885 | Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3(+)CD4(+)CD25(+) regulatory T cells (T(Regs)) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. |
| 4892 | 16478885 | Foxp3(+)CD4(+)CD25(+) T(Regs) suppressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. |
| 4893 | 16478885 | However, Foxp3(+)CD4(+)CD25(+) T(Reg) cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3(+)CD4(+)CD25(+)T(Reg) cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. |
| 4894 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 4895 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD4+ T cells in human subjects. |
| 4896 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is recognized as a major autoantigen for autoimmune type 1 diabetes (T1D) in the NOD mouse model. |
| 4897 | 16493034 | This study was undertaken to examine CD4+ T cell responses toward IGRP in human subjects. |
| 4898 | 16493034 | The tetramer-guided epitope mapping approach was used to identify IGRP-specific CD4+ T cell epitopes. |
| 4899 | 16493034 | More than 80% of subjects with either DRB1*0401 or DRB1*0301 haplotype have IGRP-specific CD4+ T cell responses for at least one IGRP epitope. |
| 4900 | 16493034 | IGRP-specific T cells from both healthy and T1D groups produce both gamma-IFN and IL-10. |
| 4901 | 16493034 | DRA1*0101/DRB1*0401 IGRP(247-259)-restricted T cells also show cross-reactivity to an epitope derived from liver/kidney glucose-6-phosphatase. |
| 4902 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD4+ T cells in human subjects. |
| 4903 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is recognized as a major autoantigen for autoimmune type 1 diabetes (T1D) in the NOD mouse model. |
| 4904 | 16493034 | This study was undertaken to examine CD4+ T cell responses toward IGRP in human subjects. |
| 4905 | 16493034 | The tetramer-guided epitope mapping approach was used to identify IGRP-specific CD4+ T cell epitopes. |
| 4906 | 16493034 | More than 80% of subjects with either DRB1*0401 or DRB1*0301 haplotype have IGRP-specific CD4+ T cell responses for at least one IGRP epitope. |
| 4907 | 16493034 | IGRP-specific T cells from both healthy and T1D groups produce both gamma-IFN and IL-10. |
| 4908 | 16493034 | DRA1*0101/DRB1*0401 IGRP(247-259)-restricted T cells also show cross-reactivity to an epitope derived from liver/kidney glucose-6-phosphatase. |
| 4909 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD4+ T cells in human subjects. |
| 4910 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is recognized as a major autoantigen for autoimmune type 1 diabetes (T1D) in the NOD mouse model. |
| 4911 | 16493034 | This study was undertaken to examine CD4+ T cell responses toward IGRP in human subjects. |
| 4912 | 16493034 | The tetramer-guided epitope mapping approach was used to identify IGRP-specific CD4+ T cell epitopes. |
| 4913 | 16493034 | More than 80% of subjects with either DRB1*0401 or DRB1*0301 haplotype have IGRP-specific CD4+ T cell responses for at least one IGRP epitope. |
| 4914 | 16493034 | IGRP-specific T cells from both healthy and T1D groups produce both gamma-IFN and IL-10. |
| 4915 | 16493034 | DRA1*0101/DRB1*0401 IGRP(247-259)-restricted T cells also show cross-reactivity to an epitope derived from liver/kidney glucose-6-phosphatase. |
| 4916 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD4+ T cells in human subjects. |
| 4917 | 16493034 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is recognized as a major autoantigen for autoimmune type 1 diabetes (T1D) in the NOD mouse model. |
| 4918 | 16493034 | This study was undertaken to examine CD4+ T cell responses toward IGRP in human subjects. |
| 4919 | 16493034 | The tetramer-guided epitope mapping approach was used to identify IGRP-specific CD4+ T cell epitopes. |
| 4920 | 16493034 | More than 80% of subjects with either DRB1*0401 or DRB1*0301 haplotype have IGRP-specific CD4+ T cell responses for at least one IGRP epitope. |
| 4921 | 16493034 | IGRP-specific T cells from both healthy and T1D groups produce both gamma-IFN and IL-10. |
| 4922 | 16493034 | DRA1*0101/DRB1*0401 IGRP(247-259)-restricted T cells also show cross-reactivity to an epitope derived from liver/kidney glucose-6-phosphatase. |
| 4923 | 16493087 | In both humans and NOD mice, particular MHC genes are primary contributors to development of the autoreactive CD4+ and CD8+ T cell responses against pancreatic beta cells that cause type 1 diabetes (T1D). |
| 4924 | 16493087 | In this study, we show that transgenic expression in NOD mice of HLA-A*0201, in the absence of murine class I MHC molecules, is sufficient to mediate autoreactive CD8+ T cell responses contributing to T1D development. |
| 4925 | 16493087 | CD8+ T cells from the transgenic mice are cytotoxic to murine and human HLA-A*0201-positive islet cells. |
| 4926 | 16493087 | Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is one of several important T1D autoantigens in standard NOD mice. |
| 4927 | 16493087 | Three IGRP-derived peptides were identified as targets of diabetogenic HLA-A*0201-restricted T cells in our NOD transgenic stock. |
| 4928 | 16506667 | On the immunohistochemical examination, infiltration of CD4- and CD8-positive T lymphocytes was detected in the lacrimal gland, the submandibular gland, the gall bladder and the pancreas. |
| 4929 | 16525991 | Therapeutic potential of self-antigen-specific CD4+ CD25+ regulatory T cells selected in vitro from a polyclonal repertoire. |
| 4930 | 16525991 | CD4+ CD25+ regulatory T cells (Treg) play a major role in the prevention of autoimmune diseases. |
| 4931 | 16525991 | Therapeutic potential of self-antigen-specific CD4+ CD25+ regulatory T cells selected in vitro from a polyclonal repertoire. |
| 4932 | 16525991 | CD4+ CD25+ regulatory T cells (Treg) play a major role in the prevention of autoimmune diseases. |
| 4933 | 16542367 | In contrast, the CD4+CD25(high)CCR4+ T cell population increased during the same period (mean change 11.5%, P = 0.0036). |
| 4934 | 16542367 | A negative correlation was found between the decline in IgA-tTG and CD4+CD25high T cells expressing CD45RO (r = -0.49, P = 0.03) and CCR4 (r = -0.54, P = 0.01). |
| 4935 | 16542367 | In contrast, the CD4+CD25(high)CCR4+ T cell population increased during the same period (mean change 11.5%, P = 0.0036). |
| 4936 | 16542367 | A negative correlation was found between the decline in IgA-tTG and CD4+CD25high T cells expressing CD45RO (r = -0.49, P = 0.03) and CCR4 (r = -0.54, P = 0.01). |
| 4937 | 16567523 | CD4+ CD25+ regulatory T-cells inhibit the islet innate immune response and promote islet engraftment. |
| 4938 | 16567523 | CD4+ CD25+ regulatory T-cells inhibit islet chemokine expression through a cell contact-dependent, soluble factor-independent mechanism and inhibit effector T-cell migration to the islet. |
| 4939 | 16567523 | CD4+ CD25+ regulatory T-cells inhibit the islet innate immune response and promote islet engraftment. |
| 4940 | 16567523 | CD4+ CD25+ regulatory T-cells inhibit islet chemokine expression through a cell contact-dependent, soluble factor-independent mechanism and inhibit effector T-cell migration to the islet. |
| 4941 | 16572390 | CD4+ CD25+ Foxp3+ regulatory T cells (Treg) are natural suppressors of autoimmunity but they can also dampen the effective clearance of infectious organisms. |
| 4942 | 16580840 | It has long been established that type 1 diabetes (T1D) is a T cell-mediated autoimmune disease, with CD4+ and CD8+ T cells being largely responsible for the destruction of beta cells within the pancreatic islets of Langerhans. |
| 4943 | 16585551 | Intranasal vaccination with proinsulin DNA induces regulatory CD4+ T cells that prevent experimental autoimmune diabetes. |
| 4944 | 16585551 | We found that intranasal vaccination of NOD mice with plasmid DNA encoding mouse proinsulin II-induced CD4+ T(reg) that suppressed diabetes development, both after adoptive cotransfer with "diabetogenic" spleen cells and after transfer into NOD mice given cyclophosphamide to accelerate diabetes onset. |
| 4945 | 16585551 | In contrast to prototypic CD4+ CD25+ T(reg), CD4+ T(reg) induced by proinsulin DNA were both CD25+ and CD25- and not defined by markers such as glucocorticoid-induced TNFR-related protein (GITR), CD103, or Foxp3. |
| 4946 | 16585551 | However, diabetes was prevented when DNA vaccination was performed under the cover of CD40 ligand blockade, known to prevent priming of CTL by mucosal Ag. |
| 4947 | 16585551 | Intranasal vaccination with proinsulin DNA induces regulatory CD4+ T cells that prevent experimental autoimmune diabetes. |
| 4948 | 16585551 | We found that intranasal vaccination of NOD mice with plasmid DNA encoding mouse proinsulin II-induced CD4+ T(reg) that suppressed diabetes development, both after adoptive cotransfer with "diabetogenic" spleen cells and after transfer into NOD mice given cyclophosphamide to accelerate diabetes onset. |
| 4949 | 16585551 | In contrast to prototypic CD4+ CD25+ T(reg), CD4+ T(reg) induced by proinsulin DNA were both CD25+ and CD25- and not defined by markers such as glucocorticoid-induced TNFR-related protein (GITR), CD103, or Foxp3. |
| 4950 | 16585551 | However, diabetes was prevented when DNA vaccination was performed under the cover of CD40 ligand blockade, known to prevent priming of CTL by mucosal Ag. |
| 4951 | 16585551 | Intranasal vaccination with proinsulin DNA induces regulatory CD4+ T cells that prevent experimental autoimmune diabetes. |
| 4952 | 16585551 | We found that intranasal vaccination of NOD mice with plasmid DNA encoding mouse proinsulin II-induced CD4+ T(reg) that suppressed diabetes development, both after adoptive cotransfer with "diabetogenic" spleen cells and after transfer into NOD mice given cyclophosphamide to accelerate diabetes onset. |
| 4953 | 16585551 | In contrast to prototypic CD4+ CD25+ T(reg), CD4+ T(reg) induced by proinsulin DNA were both CD25+ and CD25- and not defined by markers such as glucocorticoid-induced TNFR-related protein (GITR), CD103, or Foxp3. |
| 4954 | 16585551 | However, diabetes was prevented when DNA vaccination was performed under the cover of CD40 ligand blockade, known to prevent priming of CTL by mucosal Ag. |
| 4955 | 16585549 | Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion. |
| 4956 | 16585549 | Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate. |
| 4957 | 16585549 | ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells. |
| 4958 | 16585549 | Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect. |
| 4959 | 16585549 | However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies. |
| 4960 | 16585549 | Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice. |
| 4961 | 16585549 | These changes were corrected when CD38 deficiency was combined with ART2 deficiency. |
| 4962 | 16585549 | Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset. |
| 4963 | 16585549 | Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7. |
| 4964 | 16585549 | Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion. |
| 4965 | 16585549 | Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate. |
| 4966 | 16585549 | ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells. |
| 4967 | 16585549 | Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect. |
| 4968 | 16585549 | However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies. |
| 4969 | 16585549 | Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice. |
| 4970 | 16585549 | These changes were corrected when CD38 deficiency was combined with ART2 deficiency. |
| 4971 | 16585549 | Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset. |
| 4972 | 16585549 | Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7. |
| 4973 | 16585568 | Control of autoimmune myocarditis and multiorgan inflammation by glucocorticoid-induced TNF receptor family-related protein(high), Foxp3-expressing CD25+ and CD25- regulatory T cells. |
| 4974 | 16585568 | The transcription factor Foxp3 is currently the most specific marker for natural CD4+ Treg, but it would be useful if other Treg markers, particularly cell surface molecules, could be elucidated. |
| 4975 | 16585568 | We demonstrate in this study that the vast majority of Foxp3-expressing CD4+ T cells (whether CD25+ or CD25-) show constitutive high-level expression of glucocorticoid-induced TNFR family-related gene/protein (GITR). |
| 4976 | 16585568 | Transfer of T cell or thymocyte suspensions depleted of GITR(high) cells produces in BALB/c nude mice a wider spectrum and more severe forms of autoimmune diseases than does transfer of similar cell suspensions depleted of CD25+ CD4+ T cells only. |
| 4977 | 16585568 | Control of autoimmune myocarditis and multiorgan inflammation by glucocorticoid-induced TNF receptor family-related protein(high), Foxp3-expressing CD25+ and CD25- regulatory T cells. |
| 4978 | 16585568 | The transcription factor Foxp3 is currently the most specific marker for natural CD4+ Treg, but it would be useful if other Treg markers, particularly cell surface molecules, could be elucidated. |
| 4979 | 16585568 | We demonstrate in this study that the vast majority of Foxp3-expressing CD4+ T cells (whether CD25+ or CD25-) show constitutive high-level expression of glucocorticoid-induced TNFR family-related gene/protein (GITR). |
| 4980 | 16585568 | Transfer of T cell or thymocyte suspensions depleted of GITR(high) cells produces in BALB/c nude mice a wider spectrum and more severe forms of autoimmune diseases than does transfer of similar cell suspensions depleted of CD25+ CD4+ T cells only. |
| 4981 | 16585568 | Control of autoimmune myocarditis and multiorgan inflammation by glucocorticoid-induced TNF receptor family-related protein(high), Foxp3-expressing CD25+ and CD25- regulatory T cells. |
| 4982 | 16585568 | The transcription factor Foxp3 is currently the most specific marker for natural CD4+ Treg, but it would be useful if other Treg markers, particularly cell surface molecules, could be elucidated. |
| 4983 | 16585568 | We demonstrate in this study that the vast majority of Foxp3-expressing CD4+ T cells (whether CD25+ or CD25-) show constitutive high-level expression of glucocorticoid-induced TNFR family-related gene/protein (GITR). |
| 4984 | 16585568 | Transfer of T cell or thymocyte suspensions depleted of GITR(high) cells produces in BALB/c nude mice a wider spectrum and more severe forms of autoimmune diseases than does transfer of similar cell suspensions depleted of CD25+ CD4+ T cells only. |
| 4985 | 16606670 | PD-1 has two ligands: PD-1 ligand 1 (PD-L1), which is expressed broadly on hematopoietic and parenchymal cells, including pancreatic islet cells; and PD-L2, which is restricted to macrophages and dendritic cells. |
| 4986 | 16606670 | To investigate whether PD-L1 and PD-L2 have synergistic or unique roles in regulating T cell activation and tolerance, we generated mice lacking PD-L1 and PD-L2 (PD-L1/PD-L2(-/-) mice) and compared them to mice lacking either PD-L. |
| 4987 | 16606670 | PD-L1 and PD-L2 have overlapping functions in inhibiting interleukin-2 and interferon-gamma production during T cell activation. |
| 4988 | 16606670 | Our studies with bone marrow chimeras demonstrate that PD-L1/PD-L2 expression only on antigen-presenting cells is insufficient to prevent the early onset diabetes that develops in PD-L1/PD-L2(-/-) non-obese diabetic mice. |
| 4989 | 16606670 | PD-L1 inhibits pathogenic self-reactive CD4+ T cell-mediated tissue destruction and effector cytokine production. |
| 4990 | 16613348 | IELs expressed CD3, CD4 (42%), CD8 (36%), and granzyme B (0.2%), whereas T-cell intracytoplasmic antigen (TIA) 1 was not expressed. |
| 4991 | 16619338 | MG administration effectively regulated the immune imbalance in diabetic mice, principally by upregulating the CD4(+) T lymphocyte subsets, and remodeling the intracellular cytokine profiles (reducing the expression of pro-inflammatory Th1 cytokines towards a beneficial Th2 pattern), ascribed to its induction and upregulation of HO-1. |
| 4992 | 16621191 | We have shown previously that incorporation of a cDNA coding for the pro-apoptotic protein BAX into plasmid DNA coding for a secreted form of the pancreatic beta-cell antigen glutamic acid decarboxylase (GAD) promotes prevention of type 1 diabetes in non-obese diabetic (NOD) mice. |
| 4993 | 16621191 | In addition, immunological analysis revealed that the DNA vaccine induced CD4(+)CD25(+) T cells cultured from draining lymph nodes that had immunosuppressive function in vitro. |
| 4994 | 16621191 | Data also revealed that CD4(+)CD25(-) T cells from mice immunized with the DNA vaccine yielded a cell population that was foxp3(+), showed increased expression of CD25 compared to control, and had immunosuppressive function in vitro, indicating that Tregs could have developed from antigen-induced, peripheral T lymphocytes. |
| 4995 | 16621191 | We have shown previously that incorporation of a cDNA coding for the pro-apoptotic protein BAX into plasmid DNA coding for a secreted form of the pancreatic beta-cell antigen glutamic acid decarboxylase (GAD) promotes prevention of type 1 diabetes in non-obese diabetic (NOD) mice. |
| 4996 | 16621191 | In addition, immunological analysis revealed that the DNA vaccine induced CD4(+)CD25(+) T cells cultured from draining lymph nodes that had immunosuppressive function in vitro. |
| 4997 | 16621191 | Data also revealed that CD4(+)CD25(-) T cells from mice immunized with the DNA vaccine yielded a cell population that was foxp3(+), showed increased expression of CD25 compared to control, and had immunosuppressive function in vitro, indicating that Tregs could have developed from antigen-induced, peripheral T lymphocytes. |
| 4998 | 16675487 | We have established a novel CD4 and CD8 double-positive CD25+ T regulatory (Treg) clone, MT-5B, from lymph nodes of type 1 diabetes prone non-obese diabetic (NOD) mice immunized with CFA. |
| 4999 | 16700888 | CD4+CD25+ regulatory T cells in health and disease. |
| 5000 | 16700888 | Various populations of Treg cells have been described, including thymically derived CD4(+)CD25(+) Treg cells. |
| 5001 | 16700888 | In addition, a second subset of Treg cells, type 1 T regulatoary (Tr1) and Th3 cells, exert their suppressive capacity via cytokines such as interleukin-10 and transforming growth factor-beta and are contact independent. 4. |
| 5002 | 16700888 | The present review summarizes the characteristics and molecular basis of CD4(+)CD25(+) Treg cells, as well as their therapeutic potential in modulating inflammatory diseases, such as inflammatory bowel disease and rheumatoid arthritis. |
| 5003 | 16700888 | CD4+CD25+ regulatory T cells in health and disease. |
| 5004 | 16700888 | Various populations of Treg cells have been described, including thymically derived CD4(+)CD25(+) Treg cells. |
| 5005 | 16700888 | In addition, a second subset of Treg cells, type 1 T regulatoary (Tr1) and Th3 cells, exert their suppressive capacity via cytokines such as interleukin-10 and transforming growth factor-beta and are contact independent. 4. |
| 5006 | 16700888 | The present review summarizes the characteristics and molecular basis of CD4(+)CD25(+) Treg cells, as well as their therapeutic potential in modulating inflammatory diseases, such as inflammatory bowel disease and rheumatoid arthritis. |
| 5007 | 16700888 | CD4+CD25+ regulatory T cells in health and disease. |
| 5008 | 16700888 | Various populations of Treg cells have been described, including thymically derived CD4(+)CD25(+) Treg cells. |
| 5009 | 16700888 | In addition, a second subset of Treg cells, type 1 T regulatoary (Tr1) and Th3 cells, exert their suppressive capacity via cytokines such as interleukin-10 and transforming growth factor-beta and are contact independent. 4. |
| 5010 | 16700888 | The present review summarizes the characteristics and molecular basis of CD4(+)CD25(+) Treg cells, as well as their therapeutic potential in modulating inflammatory diseases, such as inflammatory bowel disease and rheumatoid arthritis. |
| 5011 | 16709812 | NTX had only a minor effect in NOD mice protected from diabetes by transgenic expression of the beta cell autoantigen proinsulin in APCs, inferring that accelerated diabetes after NTX is largely due to failure to regulate proinsulin-specific T cells. |
| 5012 | 16709812 | Transfer of prototypic CD4+CD25+ regulatory T cells also prevented diabetes in NTX-NOD mice; however, the induction of these cells by oral insulin in euthymic mice depended on the integrity of TCRgammadelta IEL. |
| 5013 | 16713179 | Autoimmune regulatory cells were CD4(+)CD25(+), but not CD4(+)CD25(-), T cells. |
| 5014 | 16718939 | Good's syndrome is the association of thymoma with immunodeficiency, characterized by hypogammaglobulinaemia, depleted B-cells, diminished T-cells and inversion of the CD4/CD8 ratio. |
| 5015 | 16731818 | Glucagon-like peptide 1 (GLP-1) exhibits considerable potential for the treatment of type 2 diabetes because of its effects on stimulation of insulin secretion and the inhibition of gastric emptying, appetite, and glucagon secretion. |
| 5016 | 16731818 | We now report that MT-Exendin mice develop extensive tissue lymphocytic infiltration with increased numbers of CD4(+) and CD8a(+) cells in the liver and/or kidney and increased numbers of B220(+) cells present in the pancreas and liver. |
| 5017 | 16731819 | Induction of tolerance in type 1 diabetes via both CD4+CD25+ T regulatory cells and T regulatory type 1 cells. |
| 5018 | 16731819 | Rapamycin mediates accumulation in the pancreas of suppressive CD4(+)CD25(+)FoxP3(+) Tr cells, which prevent diabetes. |
| 5019 | 16731819 | Induction of tolerance in type 1 diabetes via both CD4+CD25+ T regulatory cells and T regulatory type 1 cells. |
| 5020 | 16731819 | Rapamycin mediates accumulation in the pancreas of suppressive CD4(+)CD25(+)FoxP3(+) Tr cells, which prevent diabetes. |
| 5021 | 16751371 | IL-1 is a key proinflammatory driver of several autoimmune diseases including juvenile inflammatory arthritis, diseases with mutations in the NALP/cryopyrin complex and Crohn's disease, and is genetically or clinically associated with many others. |
| 5022 | 16751371 | Here we show that autoimmune-prone NOD and IL-1 receptor antagonist-deficient C57BL/6 mice both produce high levels of IL-1, which drives autoreactive effector cell expansion. |
| 5023 | 16751371 | IL-1beta drives proliferation and cytokine production by CD4(+)CD25(+)FoxP3(-) effector/memory T cells, attenuates CD4(+)CD25(+)FoxP3(+) regulatory T cell function, and allows escape of CD4(+)CD25(-) autoreactive effectors from suppression. |
| 5024 | 16751422 | We report in this study that leptin receptor (ObR) is expressed on resting normal mouse CD4(+), CD8(+), B cells, and monocyte/macrophages. |
| 5025 | 16751422 | Leptin binding to ObR results in increased STAT-3 activation in T cells, with a different activation pattern in resting vs anti-CD3 Ab stimulated T cells. |
| 5026 | 16751422 | B lymphocytes appear to be more susceptible to the antiapoptotic effects of leptin, and they show higher surface expression of ObR, compared with T cells. |
| 5027 | 16751422 | Moreover, CD4(+) T cells isolated from ObR-deficient mice displayed a reduced proliferative response, compared with normal controls. |
| 5028 | 16751422 | Furthermore, ObR/STAT-3-mediated signaling in T lymphocytes is decreased in the diet-induced obese mouse model of obesity and leptin resistance. |
| 5029 | 16751422 | In summary, our findings show that the ObR is expressed on normal mouse lymphocyte subsets, that leptin plays a role in lymphocyte survival, and that leptin alters the ObR/STAT-3-mediated signaling in T cells. |
| 5030 | 16751422 | We report in this study that leptin receptor (ObR) is expressed on resting normal mouse CD4(+), CD8(+), B cells, and monocyte/macrophages. |
| 5031 | 16751422 | Leptin binding to ObR results in increased STAT-3 activation in T cells, with a different activation pattern in resting vs anti-CD3 Ab stimulated T cells. |
| 5032 | 16751422 | B lymphocytes appear to be more susceptible to the antiapoptotic effects of leptin, and they show higher surface expression of ObR, compared with T cells. |
| 5033 | 16751422 | Moreover, CD4(+) T cells isolated from ObR-deficient mice displayed a reduced proliferative response, compared with normal controls. |
| 5034 | 16751422 | Furthermore, ObR/STAT-3-mediated signaling in T lymphocytes is decreased in the diet-induced obese mouse model of obesity and leptin resistance. |
| 5035 | 16751422 | In summary, our findings show that the ObR is expressed on normal mouse lymphocyte subsets, that leptin plays a role in lymphocyte survival, and that leptin alters the ObR/STAT-3-mediated signaling in T cells. |
| 5036 | 16781893 | Genetic studies demonstrated a 34.4 kb deletion at Xq28 which included AVPR2, the gene responsible for NDI; ARHGAP4, a hematopoietic specific gene encoding a GTPase-activating protein; and a highly conserved segment of DNA between ARHGAP4 and ARD1A, a gene involved in the response to hypoxia. |
| 5037 | 16781893 | Other patients with NDI, but without immunodeficiency, have had deletions that remove all ARHGAP4 except exon 1; however, no other patients have had deletions of the highly conserved intragenic region between ARHGAP4 and ARD1A. |
| 5038 | 16781893 | X chromosome inactivation studies, done on sorted cells from the mother and grandmother of the patient, carriers of the deletion, demonstrated exclusive use of the non-mutant X chromosome as the active X in CD4 and CD8 T cells. |
| 5039 | 16784487 | Characteristics of rat CD4(+)CD25(+) T cells and their ability to prevent not only diabetes but also insulitis in an adoptive transfer model in BB rats. |
| 5040 | 16784487 | Human and mouse CD4(+)CD25(+) T cells have been intensively studied through the last decade. |
| 5041 | 16784487 | This study describes the phenotype of rat CD4(+)CD25(+) Foxp3(+) T cells and the site in which they exert regulation in a transfer-induced autoimmune diabetes model. |
| 5042 | 16784487 | Several proteins and mRNAs are up-regulated in unstimulated rat CD4(+)CD25(+) T cells compared with CD4(+)CD25(-) T cells, including Foxp3, Lag-3, CD80, interleukin 10 (IL-10) and CTLA-4. |
| 5043 | 16784487 | To investigate CD4(+)CD25(+) T cells in vivo, we transferred three million diabetogenic T cells either alone or in combination with two million CD4(+)CD25(+) T cells to 30-day-old BB rats. |
| 5044 | 16784487 | By contrast, rats receiving both diabetogenic T cells and CD4(+)CD25(+) T cells had no insulitis at any time. |
| 5045 | 16784487 | Characteristics of rat CD4(+)CD25(+) T cells and their ability to prevent not only diabetes but also insulitis in an adoptive transfer model in BB rats. |
| 5046 | 16784487 | Human and mouse CD4(+)CD25(+) T cells have been intensively studied through the last decade. |
| 5047 | 16784487 | This study describes the phenotype of rat CD4(+)CD25(+) Foxp3(+) T cells and the site in which they exert regulation in a transfer-induced autoimmune diabetes model. |
| 5048 | 16784487 | Several proteins and mRNAs are up-regulated in unstimulated rat CD4(+)CD25(+) T cells compared with CD4(+)CD25(-) T cells, including Foxp3, Lag-3, CD80, interleukin 10 (IL-10) and CTLA-4. |
| 5049 | 16784487 | To investigate CD4(+)CD25(+) T cells in vivo, we transferred three million diabetogenic T cells either alone or in combination with two million CD4(+)CD25(+) T cells to 30-day-old BB rats. |
| 5050 | 16784487 | By contrast, rats receiving both diabetogenic T cells and CD4(+)CD25(+) T cells had no insulitis at any time. |
| 5051 | 16784487 | Characteristics of rat CD4(+)CD25(+) T cells and their ability to prevent not only diabetes but also insulitis in an adoptive transfer model in BB rats. |
| 5052 | 16784487 | Human and mouse CD4(+)CD25(+) T cells have been intensively studied through the last decade. |
| 5053 | 16784487 | This study describes the phenotype of rat CD4(+)CD25(+) Foxp3(+) T cells and the site in which they exert regulation in a transfer-induced autoimmune diabetes model. |
| 5054 | 16784487 | Several proteins and mRNAs are up-regulated in unstimulated rat CD4(+)CD25(+) T cells compared with CD4(+)CD25(-) T cells, including Foxp3, Lag-3, CD80, interleukin 10 (IL-10) and CTLA-4. |
| 5055 | 16784487 | To investigate CD4(+)CD25(+) T cells in vivo, we transferred three million diabetogenic T cells either alone or in combination with two million CD4(+)CD25(+) T cells to 30-day-old BB rats. |
| 5056 | 16784487 | By contrast, rats receiving both diabetogenic T cells and CD4(+)CD25(+) T cells had no insulitis at any time. |
| 5057 | 16784487 | Characteristics of rat CD4(+)CD25(+) T cells and their ability to prevent not only diabetes but also insulitis in an adoptive transfer model in BB rats. |
| 5058 | 16784487 | Human and mouse CD4(+)CD25(+) T cells have been intensively studied through the last decade. |
| 5059 | 16784487 | This study describes the phenotype of rat CD4(+)CD25(+) Foxp3(+) T cells and the site in which they exert regulation in a transfer-induced autoimmune diabetes model. |
| 5060 | 16784487 | Several proteins and mRNAs are up-regulated in unstimulated rat CD4(+)CD25(+) T cells compared with CD4(+)CD25(-) T cells, including Foxp3, Lag-3, CD80, interleukin 10 (IL-10) and CTLA-4. |
| 5061 | 16784487 | To investigate CD4(+)CD25(+) T cells in vivo, we transferred three million diabetogenic T cells either alone or in combination with two million CD4(+)CD25(+) T cells to 30-day-old BB rats. |
| 5062 | 16784487 | By contrast, rats receiving both diabetogenic T cells and CD4(+)CD25(+) T cells had no insulitis at any time. |
| 5063 | 16784487 | Characteristics of rat CD4(+)CD25(+) T cells and their ability to prevent not only diabetes but also insulitis in an adoptive transfer model in BB rats. |
| 5064 | 16784487 | Human and mouse CD4(+)CD25(+) T cells have been intensively studied through the last decade. |
| 5065 | 16784487 | This study describes the phenotype of rat CD4(+)CD25(+) Foxp3(+) T cells and the site in which they exert regulation in a transfer-induced autoimmune diabetes model. |
| 5066 | 16784487 | Several proteins and mRNAs are up-regulated in unstimulated rat CD4(+)CD25(+) T cells compared with CD4(+)CD25(-) T cells, including Foxp3, Lag-3, CD80, interleukin 10 (IL-10) and CTLA-4. |
| 5067 | 16784487 | To investigate CD4(+)CD25(+) T cells in vivo, we transferred three million diabetogenic T cells either alone or in combination with two million CD4(+)CD25(+) T cells to 30-day-old BB rats. |
| 5068 | 16784487 | By contrast, rats receiving both diabetogenic T cells and CD4(+)CD25(+) T cells had no insulitis at any time. |
| 5069 | 16784487 | Characteristics of rat CD4(+)CD25(+) T cells and their ability to prevent not only diabetes but also insulitis in an adoptive transfer model in BB rats. |
| 5070 | 16784487 | Human and mouse CD4(+)CD25(+) T cells have been intensively studied through the last decade. |
| 5071 | 16784487 | This study describes the phenotype of rat CD4(+)CD25(+) Foxp3(+) T cells and the site in which they exert regulation in a transfer-induced autoimmune diabetes model. |
| 5072 | 16784487 | Several proteins and mRNAs are up-regulated in unstimulated rat CD4(+)CD25(+) T cells compared with CD4(+)CD25(-) T cells, including Foxp3, Lag-3, CD80, interleukin 10 (IL-10) and CTLA-4. |
| 5073 | 16784487 | To investigate CD4(+)CD25(+) T cells in vivo, we transferred three million diabetogenic T cells either alone or in combination with two million CD4(+)CD25(+) T cells to 30-day-old BB rats. |
| 5074 | 16784487 | By contrast, rats receiving both diabetogenic T cells and CD4(+)CD25(+) T cells had no insulitis at any time. |
| 5075 | 16785498 | CD4+ T cell reactivity to proinsulin-2 was independent of proinsulin-2 expression in radiation-sensitive bone marrow-derived cells. |
| 5076 | 16785498 | Although chimeric animals had proinsulin-2-reactive CD4+ T cells in their peripheral repertoire, they displayed no insulitis or insulin Abs, suggesting additional protective mechanisms. |
| 5077 | 16785498 | In a model involving transfer to immunodeficient (CD3epsilon(-/-)) mice, naive and proinsulin-2-primed CD4+ T cells were not activated, but could be activated by immunization regardless of whether the recipient mice expressed proinsulin-2. |
| 5078 | 16785498 | Furthermore, we could not identify a role for putative specific T cells regulating proinsulin-2-reactive CD4+ T in transfer experiments. |
| 5079 | 16785498 | CD4+ T cell reactivity to proinsulin-2 was independent of proinsulin-2 expression in radiation-sensitive bone marrow-derived cells. |
| 5080 | 16785498 | Although chimeric animals had proinsulin-2-reactive CD4+ T cells in their peripheral repertoire, they displayed no insulitis or insulin Abs, suggesting additional protective mechanisms. |
| 5081 | 16785498 | In a model involving transfer to immunodeficient (CD3epsilon(-/-)) mice, naive and proinsulin-2-primed CD4+ T cells were not activated, but could be activated by immunization regardless of whether the recipient mice expressed proinsulin-2. |
| 5082 | 16785498 | Furthermore, we could not identify a role for putative specific T cells regulating proinsulin-2-reactive CD4+ T in transfer experiments. |
| 5083 | 16785498 | CD4+ T cell reactivity to proinsulin-2 was independent of proinsulin-2 expression in radiation-sensitive bone marrow-derived cells. |
| 5084 | 16785498 | Although chimeric animals had proinsulin-2-reactive CD4+ T cells in their peripheral repertoire, they displayed no insulitis or insulin Abs, suggesting additional protective mechanisms. |
| 5085 | 16785498 | In a model involving transfer to immunodeficient (CD3epsilon(-/-)) mice, naive and proinsulin-2-primed CD4+ T cells were not activated, but could be activated by immunization regardless of whether the recipient mice expressed proinsulin-2. |
| 5086 | 16785498 | Furthermore, we could not identify a role for putative specific T cells regulating proinsulin-2-reactive CD4+ T in transfer experiments. |
| 5087 | 16785498 | CD4+ T cell reactivity to proinsulin-2 was independent of proinsulin-2 expression in radiation-sensitive bone marrow-derived cells. |
| 5088 | 16785498 | Although chimeric animals had proinsulin-2-reactive CD4+ T cells in their peripheral repertoire, they displayed no insulitis or insulin Abs, suggesting additional protective mechanisms. |
| 5089 | 16785498 | In a model involving transfer to immunodeficient (CD3epsilon(-/-)) mice, naive and proinsulin-2-primed CD4+ T cells were not activated, but could be activated by immunization regardless of whether the recipient mice expressed proinsulin-2. |
| 5090 | 16785498 | Furthermore, we could not identify a role for putative specific T cells regulating proinsulin-2-reactive CD4+ T in transfer experiments. |
| 5091 | 16792673 | Lower percentages of CD4+ T cells (P = 0.03) and CD4+ CD25high cells (P = 0.06) expressing intracellular CTLA-4 were detected in samples from children with CTLA-4 +49GG compared to children with the +49AA genotype. |
| 5092 | 16792673 | Similarly, lower percentages of CD4+ (P = 0.002) and CD4+ CD25high (P = 0.002) cells expressing CTLA-4 were observed in children positive for HLA DQA1*0501-DQB1*0201 and DQA1*0301-DQB1*0302 (P = 0.04 for CD4+ and P = 0.02 for CD4+ CD25high) risk haplotypes when compared to children without these alleles. |
| 5093 | 16792673 | The percentage of CD25high cells among CD4+ cells was correlated inversely with CTLA-4 mRNA expression in PBMC (r = -0.56, P = 0.03). |
| 5094 | 16792673 | Decreased levels of CTLA-4 in CD4+ and CD4+ CD25high cells in individuals with CTLA-4 and HLA class II alleles associated with T1D may contribute to the initiation and/or progression of autoimmune response. |
| 5095 | 16792673 | Lower percentages of CD4+ T cells (P = 0.03) and CD4+ CD25high cells (P = 0.06) expressing intracellular CTLA-4 were detected in samples from children with CTLA-4 +49GG compared to children with the +49AA genotype. |
| 5096 | 16792673 | Similarly, lower percentages of CD4+ (P = 0.002) and CD4+ CD25high (P = 0.002) cells expressing CTLA-4 were observed in children positive for HLA DQA1*0501-DQB1*0201 and DQA1*0301-DQB1*0302 (P = 0.04 for CD4+ and P = 0.02 for CD4+ CD25high) risk haplotypes when compared to children without these alleles. |
| 5097 | 16792673 | The percentage of CD25high cells among CD4+ cells was correlated inversely with CTLA-4 mRNA expression in PBMC (r = -0.56, P = 0.03). |
| 5098 | 16792673 | Decreased levels of CTLA-4 in CD4+ and CD4+ CD25high cells in individuals with CTLA-4 and HLA class II alleles associated with T1D may contribute to the initiation and/or progression of autoimmune response. |
| 5099 | 16792673 | Lower percentages of CD4+ T cells (P = 0.03) and CD4+ CD25high cells (P = 0.06) expressing intracellular CTLA-4 were detected in samples from children with CTLA-4 +49GG compared to children with the +49AA genotype. |
| 5100 | 16792673 | Similarly, lower percentages of CD4+ (P = 0.002) and CD4+ CD25high (P = 0.002) cells expressing CTLA-4 were observed in children positive for HLA DQA1*0501-DQB1*0201 and DQA1*0301-DQB1*0302 (P = 0.04 for CD4+ and P = 0.02 for CD4+ CD25high) risk haplotypes when compared to children without these alleles. |
| 5101 | 16792673 | The percentage of CD25high cells among CD4+ cells was correlated inversely with CTLA-4 mRNA expression in PBMC (r = -0.56, P = 0.03). |
| 5102 | 16792673 | Decreased levels of CTLA-4 in CD4+ and CD4+ CD25high cells in individuals with CTLA-4 and HLA class II alleles associated with T1D may contribute to the initiation and/or progression of autoimmune response. |
| 5103 | 16792673 | Lower percentages of CD4+ T cells (P = 0.03) and CD4+ CD25high cells (P = 0.06) expressing intracellular CTLA-4 were detected in samples from children with CTLA-4 +49GG compared to children with the +49AA genotype. |
| 5104 | 16792673 | Similarly, lower percentages of CD4+ (P = 0.002) and CD4+ CD25high (P = 0.002) cells expressing CTLA-4 were observed in children positive for HLA DQA1*0501-DQB1*0201 and DQA1*0301-DQB1*0302 (P = 0.04 for CD4+ and P = 0.02 for CD4+ CD25high) risk haplotypes when compared to children without these alleles. |
| 5105 | 16792673 | The percentage of CD25high cells among CD4+ cells was correlated inversely with CTLA-4 mRNA expression in PBMC (r = -0.56, P = 0.03). |
| 5106 | 16792673 | Decreased levels of CTLA-4 in CD4+ and CD4+ CD25high cells in individuals with CTLA-4 and HLA class II alleles associated with T1D may contribute to the initiation and/or progression of autoimmune response. |
| 5107 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5108 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5109 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5110 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5111 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5112 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5113 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5114 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5115 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5116 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5117 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5118 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5119 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5120 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5121 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5122 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5123 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5124 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5125 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5126 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5127 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5128 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5129 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5130 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5131 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5132 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5133 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5134 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5135 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5136 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5137 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5138 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5139 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5140 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5141 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5142 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5143 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5144 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5145 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5146 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5147 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5148 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5149 | 16804081 | Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice. |
| 5150 | 16804081 | CD4(+)CD25(+) regulatory cells play a crucial role in controlling various autoimmune diseases, and a deficiency in their number or function could be involved in disease development. |
| 5151 | 16804081 | The current study shows that NOD mice had fewer CD4(+)CD25(+) regulatory cells, which expressed normal levels of glucocorticoid-induced tumor necrosis factor receptor and cytotoxic T-lymphocyte-associated antigen-4. |
| 5152 | 16804081 | We have also found that NOD CD4(+)CD25(+) cells regulate poorly in vitro after stimulation with anti-CD3 and NOD APCs in comparison with B6 CD4(+)CD25(+) cells stimulated with B6 APCs. |
| 5153 | 16804081 | Surprisingly, stimulation of NOD CD4(+)CD25(+) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4(+)CD25(+) cells properly. |
| 5154 | 16804081 | Interestingly, APCs from disease-free (>30 weeks of age), but not diabetic, NOD mice were able to activate CD4(+)CD25(+) regulatory function in vitro and apparently in vivo because only spleens of disease-free NOD mice contained potent CD4(+)CD25(+) regulatory cells that prevented disease development when transferred into young NOD recipients. |
| 5155 | 16804081 | These data suggest that the failure of NOD APCs to activate CD4(+)CD25(+) regulatory cells may play an important role in controlling type 1 diabetes development in NOD mice. |
| 5156 | 16809320 | Interaction of antigen-presenting cell CD1d with distinct natural killer T-cell ("NKT") populations can induce rapid gamma interferon (IFN-gamma) production and NK-cell activation. |
| 5157 | 16809320 | However, this was not reflected in the relative levels of NK-cell activation but rather by the responses of both CD4(+) and CD8(+) T-cell populations. |
| 5158 | 16809320 | Repeated EMCV infection in vitro induced less IFN-gamma and alpha interferon (IFN-alpha) from CD1d-deficient splenocytes than with the wild type. |
| 5159 | 16818678 | Most T reg cells are defined based on expression of CD4, CD25, and the transcription factor, FoxP3. |
| 5160 | 16818678 | We found that the IL-7 receptor (CD127) is down-regulated on a subset of CD4(+) T cells in peripheral blood. |
| 5161 | 16818678 | A combination of CD4, CD25, and CD127 resulted in a highly purified population of T reg cells accounting for significantly more cells that previously identified based on other cell surface markers. |
| 5162 | 16818678 | In fact, cells separated based solely on CD4 and CD127 expression were anergic and, although representing at least three times the number of cells (including both CD25(+)CD4(+) and CD25(-)CD4(+) T cell subsets), were as suppressive as the "classic" CD4(+)CD25(hi) T reg cell subset. |
| 5163 | 16818678 | Most T reg cells are defined based on expression of CD4, CD25, and the transcription factor, FoxP3. |
| 5164 | 16818678 | We found that the IL-7 receptor (CD127) is down-regulated on a subset of CD4(+) T cells in peripheral blood. |
| 5165 | 16818678 | A combination of CD4, CD25, and CD127 resulted in a highly purified population of T reg cells accounting for significantly more cells that previously identified based on other cell surface markers. |
| 5166 | 16818678 | In fact, cells separated based solely on CD4 and CD127 expression were anergic and, although representing at least three times the number of cells (including both CD25(+)CD4(+) and CD25(-)CD4(+) T cell subsets), were as suppressive as the "classic" CD4(+)CD25(hi) T reg cell subset. |
| 5167 | 16818678 | Most T reg cells are defined based on expression of CD4, CD25, and the transcription factor, FoxP3. |
| 5168 | 16818678 | We found that the IL-7 receptor (CD127) is down-regulated on a subset of CD4(+) T cells in peripheral blood. |
| 5169 | 16818678 | A combination of CD4, CD25, and CD127 resulted in a highly purified population of T reg cells accounting for significantly more cells that previously identified based on other cell surface markers. |
| 5170 | 16818678 | In fact, cells separated based solely on CD4 and CD127 expression were anergic and, although representing at least three times the number of cells (including both CD25(+)CD4(+) and CD25(-)CD4(+) T cell subsets), were as suppressive as the "classic" CD4(+)CD25(hi) T reg cell subset. |
| 5171 | 16818678 | Most T reg cells are defined based on expression of CD4, CD25, and the transcription factor, FoxP3. |
| 5172 | 16818678 | We found that the IL-7 receptor (CD127) is down-regulated on a subset of CD4(+) T cells in peripheral blood. |
| 5173 | 16818678 | A combination of CD4, CD25, and CD127 resulted in a highly purified population of T reg cells accounting for significantly more cells that previously identified based on other cell surface markers. |
| 5174 | 16818678 | In fact, cells separated based solely on CD4 and CD127 expression were anergic and, although representing at least three times the number of cells (including both CD25(+)CD4(+) and CD25(-)CD4(+) T cell subsets), were as suppressive as the "classic" CD4(+)CD25(hi) T reg cell subset. |
| 5175 | 16835866 | The purpose of this study was to observe the islet changes of pancreas in insulin-dependent diabetes mellitus (IDDM) mice in comparison to normal mice after application of an extract from Siraitia grosvenori fruits containing mogrosides, in particular, mogroside V. |
| 5176 | 16835866 | In addition, alloxan induced a notable increase in the expression of CD8+ lymphocytes to form a dramatic decrease in CD4+/CD8+ ratio (while CD4+ was unchanged). |
| 5177 | 16835866 | Furthermore, at low dose, MG regulated the immune imbalance observed in alloxan-induced IDDM mice by up-regulating the CD4+ T-lymphocyte subsets and CD4/CD8 ratio, and altering the intracellular cytokine profiles. |
| 5178 | 16835866 | The expression of the pro-inflammatory Th1 cytokines: IFN-gamma, TNF-alpha in splenic lymphocytes was altered toward a beneficial Th2 pattern. |
| 5179 | 16835866 | The purpose of this study was to observe the islet changes of pancreas in insulin-dependent diabetes mellitus (IDDM) mice in comparison to normal mice after application of an extract from Siraitia grosvenori fruits containing mogrosides, in particular, mogroside V. |
| 5180 | 16835866 | In addition, alloxan induced a notable increase in the expression of CD8+ lymphocytes to form a dramatic decrease in CD4+/CD8+ ratio (while CD4+ was unchanged). |
| 5181 | 16835866 | Furthermore, at low dose, MG regulated the immune imbalance observed in alloxan-induced IDDM mice by up-regulating the CD4+ T-lymphocyte subsets and CD4/CD8 ratio, and altering the intracellular cytokine profiles. |
| 5182 | 16835866 | The expression of the pro-inflammatory Th1 cytokines: IFN-gamma, TNF-alpha in splenic lymphocytes was altered toward a beneficial Th2 pattern. |
| 5183 | 16838180 | During the past 10 years, CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) have been extensively studied for their function in autoimmune disease. |
| 5184 | 16838180 | However, downmodulation of dendritic cell function and secretion of inhibitory cytokines such as IL-10 and TGF-beta might underlie Treg function in vivo. |
| 5185 | 16860296 | Therefore, we conclude that CD4+, CD25+ regulatory T cells are required for the induction as well as maintenance of tolerance in this gene therapy model. |
| 5186 | 16868084 | Recently, we have identified proinsulin (P-Ins)(73-90) as an immunodominant T cell epitope of HLA-DRB1*0401 (DR4) subjects with beta-islet cell autoimmunity and of HLA-DR4/CD4 double-transgenic mice immunized with human P-Ins. |
| 5187 | 16868084 | The human T cell clone was forkhead transcription factor 3 (Foxp3)-positive, a marker for regulatory T cell lineages, and secreted predominantly IL-5, IL-10, and low levels of IFNgamma in response to P-Ins(73-90). |
| 5188 | 16879996 | Neither the introduction of activated, self-antigen-specific CD4(+) helper T cells nor a global inflammatory stimulus were sufficient to activate the low-avidity CD8(+) T cells and did not break tolerance. |
| 5189 | 16887976 | Little is known about the in vivo conditions in which CD4+CD25+ regulatory T cells (T(reg)) exert their suppressive effect in nonlymphopenic mice. |
| 5190 | 16918689 | CD4+CD25+ regulatory T cells (Treg) constitute an important mechanism of peripheral immune tolerance. |
| 5191 | 16920929 | CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic mice. |
| 5192 | 16920929 | Unlike in standard NOD mice, alpha-galactosylceramide pretreatment did not protect the CD38-deficient stock from T1D induced by an adoptively transferred pancreatic beta cell-autoreactive CD8 T cell clone (AI4). |
| 5193 | 16920929 | We found that in the absence of CD38, ADP-ribosyltransferase 2 preferentially activates apoptotic deletion of peripheral iNKT cells, especially the CD4+ subset. |
| 5194 | 16920929 | CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic mice. |
| 5195 | 16920929 | Unlike in standard NOD mice, alpha-galactosylceramide pretreatment did not protect the CD38-deficient stock from T1D induced by an adoptively transferred pancreatic beta cell-autoreactive CD8 T cell clone (AI4). |
| 5196 | 16920929 | We found that in the absence of CD38, ADP-ribosyltransferase 2 preferentially activates apoptotic deletion of peripheral iNKT cells, especially the CD4+ subset. |
| 5197 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5198 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5199 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5200 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5201 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5202 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5203 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5204 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5205 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5206 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5207 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5208 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5209 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5210 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5211 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5212 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5213 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5214 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5215 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5216 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5217 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5218 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5219 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5220 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5221 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5222 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5223 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5224 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5225 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5226 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5227 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5228 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5229 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5230 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5231 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5232 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5233 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5234 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5235 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5236 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5237 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5238 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5239 | 16951329 | Protection from type 1 diabetes by invariant NK T cells requires the activity of CD4+CD25+ regulatory T cells. |
| 5240 | 16951329 | To further investigate how iNKT cells protect from T1D, we analyzed whether iNKT cells require the presence of another subset(s) of regulatory T cells (Treg), such as CD4+ CD25+ Treg, for this protection. |
| 5241 | 16951329 | We found that CD4+ CD25+ T cells from NOD.CD1d(-/-) mice deficient in iNKT cell function similarly in vitro to CD4+ CD25+ T cells from wild-type NOD mice and suppress the proliferation of NOD T responder cells upon alpha-GalCer stimulation. |
| 5242 | 16951329 | Cotransfer of NOD diabetogenic T cells with CD4+ CD25+ Tregs from NOD mice pretreated with alpha-GalCer demonstrated that activated iNKT cells do not influence the ability of T(regs) to inhibit the transfer of T1D. |
| 5243 | 16951329 | In contrast, protection from T1D mediated by transfer of activated iNKT cells requires the activity of CD4+ CD25+ T cells, because splenocytes pretreated with alpha-GalCer and then inactivated by anti-CD25 of CD25+ cells did not protect from T1D. |
| 5244 | 16951329 | Similarly, mice inactivated of CD4+ CD25+ T cells before alpha-GalCer treatment were also not protected from T1D. |
| 5245 | 16951329 | Our data suggest that CD4+ CD25+ T cells retain their function during iNKT cell activation, and that the activity of CD4+ CD25+ Tregs is required for iNKT cells to transfer protection from T1D. |
| 5246 | 16960873 | In addition, the vitamin D(3) analog did not stimulate an enhancement in the expression of CD4 and CD25 in BB rats as it does in NOD mice, which may explain the failure of this as well as other antidiabetic treatments in the BB animal model of type 1 diabetes. |
| 5247 | 16970282 | B7-H4.Ig protein was purified from the culture supernatant of 293T cells transfected by a B7-H4.Ig plasmid (pMIgV, containing a human B7-H4 cDNA and a mouse IgG2a Fc cDNA). |
| 5248 | 16970282 | Our preliminary studies showed that immobilized fusion protein human B7-H4.Ig (coated with 5 microg/ml for 2 h at 37 degrees C), but not control Ig, clearly inhibited the proliferation of activated CD4+ and CD8+ T cells of patients induced by anti-CD3 antibody in CFSE assays. |
| 5249 | 16972262 | BB rats were therefore checked at day 21 up to day 90 of life for blood glucose, insulin levels, degree of islet infiltration, expression of proinflammatory and protective cytokines and antibodies including CD4, CD8, CD25, LFA-1, and ICAM-1. |
| 5250 | 16972262 | We found that islets of non-diabetic BB rats became positive to both IL-1beta and IL-4 very early on, confirming a local but intense production of both cytokines within the islets during the initial non-diabetic period. |
| 5251 | 16972262 | In addition, we observed that the production of these interleukins together with the expression levels of CD4 and CD25 are events predictive for type 1 diabetes onset in non-diabetic BB rats, as for non-obese diabetic (NOD) mice. |
| 5252 | 16972262 | In particular, the production of IL-1beta and IL-4 during the non-diabetic period together with the lack of enhancement of CD4 and CD25, indicating selective recruitment of activated T cells, may explain the failure of anti-diabetic treatments in this animal model of type 1 diabetes. |
| 5253 | 16972262 | BB rats were therefore checked at day 21 up to day 90 of life for blood glucose, insulin levels, degree of islet infiltration, expression of proinflammatory and protective cytokines and antibodies including CD4, CD8, CD25, LFA-1, and ICAM-1. |
| 5254 | 16972262 | We found that islets of non-diabetic BB rats became positive to both IL-1beta and IL-4 very early on, confirming a local but intense production of both cytokines within the islets during the initial non-diabetic period. |
| 5255 | 16972262 | In addition, we observed that the production of these interleukins together with the expression levels of CD4 and CD25 are events predictive for type 1 diabetes onset in non-diabetic BB rats, as for non-obese diabetic (NOD) mice. |
| 5256 | 16972262 | In particular, the production of IL-1beta and IL-4 during the non-diabetic period together with the lack of enhancement of CD4 and CD25, indicating selective recruitment of activated T cells, may explain the failure of anti-diabetic treatments in this animal model of type 1 diabetes. |
| 5257 | 16972262 | BB rats were therefore checked at day 21 up to day 90 of life for blood glucose, insulin levels, degree of islet infiltration, expression of proinflammatory and protective cytokines and antibodies including CD4, CD8, CD25, LFA-1, and ICAM-1. |
| 5258 | 16972262 | We found that islets of non-diabetic BB rats became positive to both IL-1beta and IL-4 very early on, confirming a local but intense production of both cytokines within the islets during the initial non-diabetic period. |
| 5259 | 16972262 | In addition, we observed that the production of these interleukins together with the expression levels of CD4 and CD25 are events predictive for type 1 diabetes onset in non-diabetic BB rats, as for non-obese diabetic (NOD) mice. |
| 5260 | 16972262 | In particular, the production of IL-1beta and IL-4 during the non-diabetic period together with the lack of enhancement of CD4 and CD25, indicating selective recruitment of activated T cells, may explain the failure of anti-diabetic treatments in this animal model of type 1 diabetes. |
| 5261 | 16979383 | We have identified for the first time an age-dependent spontaneous loss of tolerance to two self-antigenic epitopes derived from putative diabetes-associated antigens glutamic acid decarboxylase (GAD65) and glial fibrillary acidic protein (GFAP) in RIP-B7/DRB1*0404 HLA transgenic mice. |
| 5262 | 16979383 | Diabetic and older non-diabetic mice exhibited a proliferative response to an immunodominant epitope from GAD65 (555-567) and also from GFAP (240-252) but not from an immunogenic epitope from diabetes-associated islet-specific glucose-6-phosphatase catalytic subunit-related protein. |
| 5263 | 16979383 | Islet infiltrates in older non-diabetic mice and diabetic mice contain CD4(+)/FoxP3(+) cells and suggest the presence of a regulatory mechanism prior and during diabetic disease. |
| 5264 | 17005288 | To investigate the pathogenesis of LADA, we examined the lymphocyte subsets including the CD4(+)CD25(+) T-cells in 60 LADA patients and 30 patients of type 2 diabetes and 30 healthy individuals by FACS. |
| 5265 | 17005288 | And we compared the expression of FOXP3 mRNA in CD4(+) T-cell between 10 patients of LADA and 10 matched healthy individuals by real time PCR. |
| 5266 | 17005288 | The percent of CD4(+)CD25(+) T-cells were higher (11.89+/-4.96% versus 8.16+/-3.65%, P<0.01), and the percent CD8(+) T-cells elevated (24.58+/-6.80% versus 19.39+/-7.12, P<0.01) in LADA patients than healthy individuals. |
| 5267 | 17005288 | While the expression of FOXP3 mRNA in CD4(+) T-cell was markedly decreased in LADA patients (0.52-fold, n=10, P=0.004) compared with normal subjects. |
| 5268 | 17005288 | To investigate the pathogenesis of LADA, we examined the lymphocyte subsets including the CD4(+)CD25(+) T-cells in 60 LADA patients and 30 patients of type 2 diabetes and 30 healthy individuals by FACS. |
| 5269 | 17005288 | And we compared the expression of FOXP3 mRNA in CD4(+) T-cell between 10 patients of LADA and 10 matched healthy individuals by real time PCR. |
| 5270 | 17005288 | The percent of CD4(+)CD25(+) T-cells were higher (11.89+/-4.96% versus 8.16+/-3.65%, P<0.01), and the percent CD8(+) T-cells elevated (24.58+/-6.80% versus 19.39+/-7.12, P<0.01) in LADA patients than healthy individuals. |
| 5271 | 17005288 | While the expression of FOXP3 mRNA in CD4(+) T-cell was markedly decreased in LADA patients (0.52-fold, n=10, P=0.004) compared with normal subjects. |
| 5272 | 17005288 | To investigate the pathogenesis of LADA, we examined the lymphocyte subsets including the CD4(+)CD25(+) T-cells in 60 LADA patients and 30 patients of type 2 diabetes and 30 healthy individuals by FACS. |
| 5273 | 17005288 | And we compared the expression of FOXP3 mRNA in CD4(+) T-cell between 10 patients of LADA and 10 matched healthy individuals by real time PCR. |
| 5274 | 17005288 | The percent of CD4(+)CD25(+) T-cells were higher (11.89+/-4.96% versus 8.16+/-3.65%, P<0.01), and the percent CD8(+) T-cells elevated (24.58+/-6.80% versus 19.39+/-7.12, P<0.01) in LADA patients than healthy individuals. |
| 5275 | 17005288 | While the expression of FOXP3 mRNA in CD4(+) T-cell was markedly decreased in LADA patients (0.52-fold, n=10, P=0.004) compared with normal subjects. |
| 5276 | 17005288 | To investigate the pathogenesis of LADA, we examined the lymphocyte subsets including the CD4(+)CD25(+) T-cells in 60 LADA patients and 30 patients of type 2 diabetes and 30 healthy individuals by FACS. |
| 5277 | 17005288 | And we compared the expression of FOXP3 mRNA in CD4(+) T-cell between 10 patients of LADA and 10 matched healthy individuals by real time PCR. |
| 5278 | 17005288 | The percent of CD4(+)CD25(+) T-cells were higher (11.89+/-4.96% versus 8.16+/-3.65%, P<0.01), and the percent CD8(+) T-cells elevated (24.58+/-6.80% versus 19.39+/-7.12, P<0.01) in LADA patients than healthy individuals. |
| 5279 | 17005288 | While the expression of FOXP3 mRNA in CD4(+) T-cell was markedly decreased in LADA patients (0.52-fold, n=10, P=0.004) compared with normal subjects. |
| 5280 | 17015694 | A 20-Mb region of chromosome 4 controls TNF-alpha-mediated CD8+ T cell aggression toward beta cells in type 1 diabetes. |
| 5281 | 17015694 | To identify some of these recessive alleles, we crossed TNF-alpha-NOD mice to diabetes-resistant congenic NOD mice having protective alleles at insulin-dependent diabetes (Idd) loci that control spontaneous T1D at either the preinsulitis (Idd3.Idd5) or postinsulitis (Idd9) phases. |
| 5282 | 17015694 | Lack of protection was not at the level of T cell priming, the efficacy of islet-infiltrating APCs to present islet peptides, nor the ability of high levels of CD4+ Foxp3+ T cells to accumulate in the islets. |
| 5283 | 17015713 | The therapeutic effect of gal-1-DC was accompanied by increased percentage of apoptotic T cells and reduced number of IFN-gamma-secreting CD4+ T cells in pancreatic lymph nodes. |
| 5284 | 17032246 | In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. |
| 5285 | 17032246 | Immune regulatory function of CD4+CD25+ T cells was tested in vitro. |
| 5286 | 17032246 | Significant differences in CD4+CD25+ but not in NK T cells have been identified. |
| 5287 | 17032246 | Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). |
| 5288 | 17032246 | Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. |
| 5289 | 17032246 | In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. |
| 5290 | 17032246 | In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. |
| 5291 | 17032246 | Immune regulatory function of CD4+CD25+ T cells was tested in vitro. |
| 5292 | 17032246 | Significant differences in CD4+CD25+ but not in NK T cells have been identified. |
| 5293 | 17032246 | Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). |
| 5294 | 17032246 | Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. |
| 5295 | 17032246 | In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. |
| 5296 | 17032246 | In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. |
| 5297 | 17032246 | Immune regulatory function of CD4+CD25+ T cells was tested in vitro. |
| 5298 | 17032246 | Significant differences in CD4+CD25+ but not in NK T cells have been identified. |
| 5299 | 17032246 | Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). |
| 5300 | 17032246 | Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. |
| 5301 | 17032246 | In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. |
| 5302 | 17032246 | In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. |
| 5303 | 17032246 | Immune regulatory function of CD4+CD25+ T cells was tested in vitro. |
| 5304 | 17032246 | Significant differences in CD4+CD25+ but not in NK T cells have been identified. |
| 5305 | 17032246 | Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). |
| 5306 | 17032246 | Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. |
| 5307 | 17032246 | In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. |
| 5308 | 17032246 | In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. |
| 5309 | 17032246 | Immune regulatory function of CD4+CD25+ T cells was tested in vitro. |
| 5310 | 17032246 | Significant differences in CD4+CD25+ but not in NK T cells have been identified. |
| 5311 | 17032246 | Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). |
| 5312 | 17032246 | Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. |
| 5313 | 17032246 | In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. |
| 5314 | 17032246 | In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. |
| 5315 | 17032246 | Immune regulatory function of CD4+CD25+ T cells was tested in vitro. |
| 5316 | 17032246 | Significant differences in CD4+CD25+ but not in NK T cells have been identified. |
| 5317 | 17032246 | Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). |
| 5318 | 17032246 | Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. |
| 5319 | 17032246 | In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. |
| 5320 | 17045415 | Furthermore, it is our contention, that in response to beta cell apoptosis during normal remodeling of the pancreas and CCL19/CCL21 expression within the pancreatic lymph nodes (PLNs), gluten-loaded dendritic cells migrate from the small intestine to the PLNs. |
| 5321 | 17045415 | These dendritic cells present gluten-derived antigens on the surface of the PLNs, which leads to migration of CD4(-)CD8(-) gammadelta and CD4(-)CD8(+) alphabeta T cells to the pancreas where they mediate Fas and perforin dependent cytotoxicity. |
| 5322 | 17045460 | SOCS-1 protects from virally-induced CD8 T cell mediated type 1 diabetes. |
| 5323 | 17045460 | CTL-mediated beta-cell killing can occur via perforin-mediated lysis, Fas-Fas-L interaction, and the secretion of TNF-alpha or IFN-gamma. |
| 5324 | 17045460 | Suppressor of cytokine signaling-1 (SOCS-1) represses several crucial cytokine signaling pathways simultaneously, among them IFN-gamma and IL-1-beta. |
| 5325 | 17045460 | We therefore evaluated the protective capacity of islet cell SOCS-1 expression in the CD8(+) mediated RIP-LCMV diabetes model. |
| 5326 | 17045460 | Not only absence of MHC-I and Fas upregulation, but also resistance to cytokine-induced killing of beta-cells and a complete lack of CXCL-10 (IP10) production in islets led to a lack of islet infiltration and impaired activation of autoaggressive CD4(+) and CD8(+) T-cells in these mice. |
| 5327 | 17045841 | Two recent studies have demonstrated that downregulation of the interleukin-7 receptor (CD127) distinguishes Treg cells from activated T cells, facilitating both Treg-cell purification and their functional characterization in human diseases. |
| 5328 | 17045841 | CD127 uniquely enables the purification of FOXP3+ Treg cells and, potentially, also "adaptive" regulatory T-cell subsets from the CD4+CD25- T-cell population. |
| 5329 | 17081781 | Cellular interactions promoting the in vivo expansion of CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells for maintenance of immune tolerance remain poorly defined. |
| 5330 | 17081781 | Here we report that mobilized Lin(-)Sca-1(+)c-kit(+) (LSK) hematopoietic progenitor cells (HPCs), unlike medullary hematopoietic stem cells (HSCs), selectively drove the direct, immediate expansion of functional host-derived Treg cells, thereby preventing the progression to overt spontaneous autoimmune diabetes in nonobese diabetic mice. |
| 5331 | 17081781 | Treg cell expansion required cell-to-cell contact and Notch3 signaling, which was mediated selectively through the Notch ligand Jagged2 expressed by the multipotent HPC subset, as assessed by small interfering RNA (siRNA) silencing. |
| 5332 | 17082572 | Cyclophosphamide-induced type-1 diabetes in the NOD mouse is associated with a reduction of CD4+CD25+Foxp3+ regulatory T cells. |
| 5333 | 17082572 | We demonstrate in this study that CY targets CD4+CD25+Foxp3+ Tregs in vivo. |
| 5334 | 17082572 | CD4+CD25+ T cells isolated from CY-treated mice display reduced suppressive activity in vitro and increased expression of apoptotic markers. |
| 5335 | 17082572 | T1D progression was effectively prevented by adoptive transfer of a small number of islet Ag-specific CD4+CD25+ Tregs to CY-treated recipients. |
| 5336 | 17082572 | We conclude that acceleration of T1D by CY is associated with a reduction in CD4+CD25+Foxp3+ Tregs and can be prevented by transfer of CD4+CD25+ Tregs. |
| 5337 | 17082572 | Cyclophosphamide-induced type-1 diabetes in the NOD mouse is associated with a reduction of CD4+CD25+Foxp3+ regulatory T cells. |
| 5338 | 17082572 | We demonstrate in this study that CY targets CD4+CD25+Foxp3+ Tregs in vivo. |
| 5339 | 17082572 | CD4+CD25+ T cells isolated from CY-treated mice display reduced suppressive activity in vitro and increased expression of apoptotic markers. |
| 5340 | 17082572 | T1D progression was effectively prevented by adoptive transfer of a small number of islet Ag-specific CD4+CD25+ Tregs to CY-treated recipients. |
| 5341 | 17082572 | We conclude that acceleration of T1D by CY is associated with a reduction in CD4+CD25+Foxp3+ Tregs and can be prevented by transfer of CD4+CD25+ Tregs. |
| 5342 | 17082572 | Cyclophosphamide-induced type-1 diabetes in the NOD mouse is associated with a reduction of CD4+CD25+Foxp3+ regulatory T cells. |
| 5343 | 17082572 | We demonstrate in this study that CY targets CD4+CD25+Foxp3+ Tregs in vivo. |
| 5344 | 17082572 | CD4+CD25+ T cells isolated from CY-treated mice display reduced suppressive activity in vitro and increased expression of apoptotic markers. |
| 5345 | 17082572 | T1D progression was effectively prevented by adoptive transfer of a small number of islet Ag-specific CD4+CD25+ Tregs to CY-treated recipients. |
| 5346 | 17082572 | We conclude that acceleration of T1D by CY is associated with a reduction in CD4+CD25+Foxp3+ Tregs and can be prevented by transfer of CD4+CD25+ Tregs. |
| 5347 | 17082572 | Cyclophosphamide-induced type-1 diabetes in the NOD mouse is associated with a reduction of CD4+CD25+Foxp3+ regulatory T cells. |
| 5348 | 17082572 | We demonstrate in this study that CY targets CD4+CD25+Foxp3+ Tregs in vivo. |
| 5349 | 17082572 | CD4+CD25+ T cells isolated from CY-treated mice display reduced suppressive activity in vitro and increased expression of apoptotic markers. |
| 5350 | 17082572 | T1D progression was effectively prevented by adoptive transfer of a small number of islet Ag-specific CD4+CD25+ Tregs to CY-treated recipients. |
| 5351 | 17082572 | We conclude that acceleration of T1D by CY is associated with a reduction in CD4+CD25+Foxp3+ Tregs and can be prevented by transfer of CD4+CD25+ Tregs. |
| 5352 | 17082572 | Cyclophosphamide-induced type-1 diabetes in the NOD mouse is associated with a reduction of CD4+CD25+Foxp3+ regulatory T cells. |
| 5353 | 17082572 | We demonstrate in this study that CY targets CD4+CD25+Foxp3+ Tregs in vivo. |
| 5354 | 17082572 | CD4+CD25+ T cells isolated from CY-treated mice display reduced suppressive activity in vitro and increased expression of apoptotic markers. |
| 5355 | 17082572 | T1D progression was effectively prevented by adoptive transfer of a small number of islet Ag-specific CD4+CD25+ Tregs to CY-treated recipients. |
| 5356 | 17082572 | We conclude that acceleration of T1D by CY is associated with a reduction in CD4+CD25+Foxp3+ Tregs and can be prevented by transfer of CD4+CD25+ Tregs. |
| 5357 | 17087189 | The immune phenotype of lymphocytes (CD3+, CD4+, CDr8, CD20+, and CD56+ cells) were studied using flow cytometry (FACS-analysis); their ultrastructure was studied by means of electron microscopy. |
| 5358 | 17088564 | Here we demonstrate that disease-associated autoreactive T cells from patients with type-1 diabetes mellitus or rheumatoid arthritis (RA) are mainly CD4+ CCR7- CD45RA- effector memory T cells (T(EM) cells) with elevated Kv1.3 potassium channel expression. |
| 5359 | 17088564 | In T(EM) cells, Kv1.3 traffics to the immunological synapse during antigen presentation where it colocalizes with Kvbeta2, SAP97, ZIP, p56(lck), and CD4. |
| 5360 | 17088564 | Although Kv1.3 inhibitors [ShK(L5)-amide (SL5) and PAP1] do not prevent immunological synapse formation, they suppress Ca2+-signaling, cytokine production, and proliferation of autoantigen-specific T(EM) cells at pharmacologically relevant concentrations while sparing other classes of T cells. |
| 5361 | 17088564 | Here we demonstrate that disease-associated autoreactive T cells from patients with type-1 diabetes mellitus or rheumatoid arthritis (RA) are mainly CD4+ CCR7- CD45RA- effector memory T cells (T(EM) cells) with elevated Kv1.3 potassium channel expression. |
| 5362 | 17088564 | In T(EM) cells, Kv1.3 traffics to the immunological synapse during antigen presentation where it colocalizes with Kvbeta2, SAP97, ZIP, p56(lck), and CD4. |
| 5363 | 17088564 | Although Kv1.3 inhibitors [ShK(L5)-amide (SL5) and PAP1] do not prevent immunological synapse formation, they suppress Ca2+-signaling, cytokine production, and proliferation of autoantigen-specific T(EM) cells at pharmacologically relevant concentrations while sparing other classes of T cells. |
| 5364 | 17100770 | Evidence for immunological priming and increased frequency of CD4+ CD25+ cord blood T cells in children born to mothers with type 1 diabetes. |
| 5365 | 17100770 | Levels of interleukin (IL)-1beta (P = 0.022), tumour necrosis factor (TNF)-alpha (P = 0.002) and IL-8 (P = 0.0012), as well as the frequency of CD4(+) CD25(+) T cells (P < 0.01) were significantly increased, and the increased levels correlated positively with anti-GAD65 autoantibody (GADA) levels. |
| 5366 | 17100770 | Moreover, CD4(+) CD25(+) T cells of children born to T1D mothers exhibited a more pronounced memory phenotype with increased CCR4 expression and down-regulation of CD62L. |
| 5367 | 17100770 | Evidence for immunological priming and increased frequency of CD4+ CD25+ cord blood T cells in children born to mothers with type 1 diabetes. |
| 5368 | 17100770 | Levels of interleukin (IL)-1beta (P = 0.022), tumour necrosis factor (TNF)-alpha (P = 0.002) and IL-8 (P = 0.0012), as well as the frequency of CD4(+) CD25(+) T cells (P < 0.01) were significantly increased, and the increased levels correlated positively with anti-GAD65 autoantibody (GADA) levels. |
| 5369 | 17100770 | Moreover, CD4(+) CD25(+) T cells of children born to T1D mothers exhibited a more pronounced memory phenotype with increased CCR4 expression and down-regulation of CD62L. |
| 5370 | 17100770 | Evidence for immunological priming and increased frequency of CD4+ CD25+ cord blood T cells in children born to mothers with type 1 diabetes. |
| 5371 | 17100770 | Levels of interleukin (IL)-1beta (P = 0.022), tumour necrosis factor (TNF)-alpha (P = 0.002) and IL-8 (P = 0.0012), as well as the frequency of CD4(+) CD25(+) T cells (P < 0.01) were significantly increased, and the increased levels correlated positively with anti-GAD65 autoantibody (GADA) levels. |
| 5372 | 17100770 | Moreover, CD4(+) CD25(+) T cells of children born to T1D mothers exhibited a more pronounced memory phenotype with increased CCR4 expression and down-regulation of CD62L. |
| 5373 | 17111929 | Regulatory T-cells CD4+CD25+Foxp3, possessing suppressory activity, play the key role in the development of autoimmune diseases, maintenance of peripheral tolerance in transplantation immunity, and the prevention of a pathological immune response to intestinal microflora or microbial infection. |
| 5374 | 17111929 | A decrease in the total number of circulating CD4+CD25+ regulatory T-cells and their suppressive activity have been found in patients suffering from various autoimmune diseases, such as type 1 diabetes, multiple sclerosis, autoimmune hepatitis, psoriatic arthritis, juvenile idiopathic arthritis, and systemic lupus erythematosus (SLE). |
| 5375 | 17111929 | The authors of this study investigated the phenotypic characteristics of peripheral blood lymphocytes in 31 SLE patients and the effect of treatment on the content of CD4+CD25+ T-cells before and after pulse therapy with methylprednisolone and cyclophosphan. |
| 5376 | 17111929 | The data from this research confirm the development of a defect of CD4+CD25+ T-cells at the active phase of SLE, and a possibility to partially correct this defect with an effective therapy. |
| 5377 | 17111929 | Regulatory T-cells CD4+CD25+Foxp3, possessing suppressory activity, play the key role in the development of autoimmune diseases, maintenance of peripheral tolerance in transplantation immunity, and the prevention of a pathological immune response to intestinal microflora or microbial infection. |
| 5378 | 17111929 | A decrease in the total number of circulating CD4+CD25+ regulatory T-cells and their suppressive activity have been found in patients suffering from various autoimmune diseases, such as type 1 diabetes, multiple sclerosis, autoimmune hepatitis, psoriatic arthritis, juvenile idiopathic arthritis, and systemic lupus erythematosus (SLE). |
| 5379 | 17111929 | The authors of this study investigated the phenotypic characteristics of peripheral blood lymphocytes in 31 SLE patients and the effect of treatment on the content of CD4+CD25+ T-cells before and after pulse therapy with methylprednisolone and cyclophosphan. |
| 5380 | 17111929 | The data from this research confirm the development of a defect of CD4+CD25+ T-cells at the active phase of SLE, and a possibility to partially correct this defect with an effective therapy. |
| 5381 | 17111929 | Regulatory T-cells CD4+CD25+Foxp3, possessing suppressory activity, play the key role in the development of autoimmune diseases, maintenance of peripheral tolerance in transplantation immunity, and the prevention of a pathological immune response to intestinal microflora or microbial infection. |
| 5382 | 17111929 | A decrease in the total number of circulating CD4+CD25+ regulatory T-cells and their suppressive activity have been found in patients suffering from various autoimmune diseases, such as type 1 diabetes, multiple sclerosis, autoimmune hepatitis, psoriatic arthritis, juvenile idiopathic arthritis, and systemic lupus erythematosus (SLE). |
| 5383 | 17111929 | The authors of this study investigated the phenotypic characteristics of peripheral blood lymphocytes in 31 SLE patients and the effect of treatment on the content of CD4+CD25+ T-cells before and after pulse therapy with methylprednisolone and cyclophosphan. |
| 5384 | 17111929 | The data from this research confirm the development of a defect of CD4+CD25+ T-cells at the active phase of SLE, and a possibility to partially correct this defect with an effective therapy. |
| 5385 | 17111929 | Regulatory T-cells CD4+CD25+Foxp3, possessing suppressory activity, play the key role in the development of autoimmune diseases, maintenance of peripheral tolerance in transplantation immunity, and the prevention of a pathological immune response to intestinal microflora or microbial infection. |
| 5386 | 17111929 | A decrease in the total number of circulating CD4+CD25+ regulatory T-cells and their suppressive activity have been found in patients suffering from various autoimmune diseases, such as type 1 diabetes, multiple sclerosis, autoimmune hepatitis, psoriatic arthritis, juvenile idiopathic arthritis, and systemic lupus erythematosus (SLE). |
| 5387 | 17111929 | The authors of this study investigated the phenotypic characteristics of peripheral blood lymphocytes in 31 SLE patients and the effect of treatment on the content of CD4+CD25+ T-cells before and after pulse therapy with methylprednisolone and cyclophosphan. |
| 5388 | 17111929 | The data from this research confirm the development of a defect of CD4+CD25+ T-cells at the active phase of SLE, and a possibility to partially correct this defect with an effective therapy. |
| 5389 | 17114428 | The numbers of CD4(+)CD25(+)Foxp3(+) T cells in thymus and periphery of Ii chain-deficient NOD mice were similar to those found in normal NOD mice, in contrast to conventional CD4(+) T cells whose numbers were reduced. |
| 5390 | 17114453 | Using both models, we analyzed CD4+CD25+ and CD4+CD45RC- candidate rat Treg populations. |
| 5391 | 17114453 | In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-beta and IL-10, suggesting that they are natural Tregs. |
| 5392 | 17114453 | Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. |
| 5393 | 17114453 | The disease-suppressing CD4+CD45RC-CD25- population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. |
| 5394 | 17114453 | We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. |
| 5395 | 17114453 | Using both models, we analyzed CD4+CD25+ and CD4+CD45RC- candidate rat Treg populations. |
| 5396 | 17114453 | In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-beta and IL-10, suggesting that they are natural Tregs. |
| 5397 | 17114453 | Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. |
| 5398 | 17114453 | The disease-suppressing CD4+CD45RC-CD25- population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. |
| 5399 | 17114453 | We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. |
| 5400 | 17114453 | Using both models, we analyzed CD4+CD25+ and CD4+CD45RC- candidate rat Treg populations. |
| 5401 | 17114453 | In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-beta and IL-10, suggesting that they are natural Tregs. |
| 5402 | 17114453 | Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. |
| 5403 | 17114453 | The disease-suppressing CD4+CD45RC-CD25- population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. |
| 5404 | 17114453 | We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. |
| 5405 | 17114453 | Using both models, we analyzed CD4+CD25+ and CD4+CD45RC- candidate rat Treg populations. |
| 5406 | 17114453 | In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-beta and IL-10, suggesting that they are natural Tregs. |
| 5407 | 17114453 | Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. |
| 5408 | 17114453 | The disease-suppressing CD4+CD45RC-CD25- population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. |
| 5409 | 17114453 | We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. |
| 5410 | 17114453 | Using both models, we analyzed CD4+CD25+ and CD4+CD45RC- candidate rat Treg populations. |
| 5411 | 17114453 | In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-beta and IL-10, suggesting that they are natural Tregs. |
| 5412 | 17114453 | Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. |
| 5413 | 17114453 | The disease-suppressing CD4+CD45RC-CD25- population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. |
| 5414 | 17114453 | We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. |
| 5415 | 17116220 | The expression of inflammatory chemokine receptors CCR1, CCR2, CCR4, CCR5, CCR6 and CXCR3 was investigated on circulating T-cell subsets, and CCR1, CCR2 and CCR5 on circulating monocytes before and after IVIg treatment in patients with immune-mediated neuropathies (MMN, n = 7; GBS, n = 1; CIDP, n = 2). |
| 5416 | 17116220 | Furthermore, the proportion of CD45RO-positive CD4+ or CD8+ T-cell subsets was not changed by IVIg treatment. |
| 5417 | 17127455 | Type 1 Diabetes (T1D) is an autoimmune disease requiring contributions from effectors in both CD4+ and CD8+ T cell compartments in order to destroy insulin producing pancreatic beta cells. |
| 5418 | 17130491 | Natural CD4(+)CD25(high) regulatory T-cells are derived from thymus, and accordingly human insulin-specific regulatory T-cells should exist. |
| 5419 | 17130491 | The mRNA expression of regulatory T-cell markers (transforming growth factor-beta, Foxp3, cytotoxic T-lymphocyte antigen-4 [CTLA-4], and inducible co-stimulator [ICOS]) or cytokines (gamma-interferon [IFN-gamma], interleukin [IL]-5, IL-4) was measured by quantitative RT-PCR. |
| 5420 | 17130491 | The secretion of IFN-gamma, IL-2, IL-4, IL-5, and IL-10 was also studied. |
| 5421 | 17130491 | The expression of Foxp3, CTLA-4, and ICOS mRNAs in PBMCs stimulated with bovine or human insulin was higher in patients on insulin treatment than in patients studied before starting insulin treatment. |
| 5422 | 17130491 | The insulin-induced Foxp3 protein expression in CD4(+)CD25(high) cells was detectable in flow cytometry. |
| 5423 | 17130491 | Insulin stimulation in vitro induced increased expression of regulatory T-cell markers, Foxp3, CTLA-4, and ICOS only in patients treated with insulin, suggesting that treatment with human insulin activates insulin-specific regulatory T-cells in children with newly diagnosed type 1 diabetes. |
| 5424 | 17130491 | Natural CD4(+)CD25(high) regulatory T-cells are derived from thymus, and accordingly human insulin-specific regulatory T-cells should exist. |
| 5425 | 17130491 | The mRNA expression of regulatory T-cell markers (transforming growth factor-beta, Foxp3, cytotoxic T-lymphocyte antigen-4 [CTLA-4], and inducible co-stimulator [ICOS]) or cytokines (gamma-interferon [IFN-gamma], interleukin [IL]-5, IL-4) was measured by quantitative RT-PCR. |
| 5426 | 17130491 | The secretion of IFN-gamma, IL-2, IL-4, IL-5, and IL-10 was also studied. |
| 5427 | 17130491 | The expression of Foxp3, CTLA-4, and ICOS mRNAs in PBMCs stimulated with bovine or human insulin was higher in patients on insulin treatment than in patients studied before starting insulin treatment. |
| 5428 | 17130491 | The insulin-induced Foxp3 protein expression in CD4(+)CD25(high) cells was detectable in flow cytometry. |
| 5429 | 17130491 | Insulin stimulation in vitro induced increased expression of regulatory T-cell markers, Foxp3, CTLA-4, and ICOS only in patients treated with insulin, suggesting that treatment with human insulin activates insulin-specific regulatory T-cells in children with newly diagnosed type 1 diabetes. |
| 5430 | 17130492 | A panel of human GAD (hGAD65)-specific CD4 T-cell lines and hybridomas was generated to serve as detection reagents for evaluating the peptide occupancy of DQ8 and DR4. |
| 5431 | 17130526 | A mini meta-analysis of studies on CD4+CD25+ T cells in human type 1 diabetes: report of the Immunology of Diabetes Society T Cell Workshop. |
| 5432 | 17130526 | In health, immunological tolerance is maintained by multiple central and peripheral mechanisms including the action of a specialized set of regulatory T cells characterized by expression of CD4 and CD25 (CD4+CD25+ Treg). |
| 5433 | 17130526 | A mini meta-analysis of studies on CD4+CD25+ T cells in human type 1 diabetes: report of the Immunology of Diabetes Society T Cell Workshop. |
| 5434 | 17130526 | In health, immunological tolerance is maintained by multiple central and peripheral mechanisms including the action of a specialized set of regulatory T cells characterized by expression of CD4 and CD25 (CD4+CD25+ Treg). |
| 5435 | 17130545 | As well, KRV infection preferentially activates effector T cells, such as Th1-like CD45RC(+)CD4(+) T cells and CD8(+) T cells, and downregulates regulatory T cells, such as Th2-like CD45RC(-)CD4(+) T cells. |
| 5436 | 17130553 | The purpose of this article was to investigate the expression levels of CXC chemokine receptor 3 (CXCR3) and CC chemokine receptor 5 (CCR5) on CD4 T cells as Th1 markers in Japanese patients with type 1 diabetes and control subjects. |
| 5437 | 17130553 | CXCR3 expression on CD4 T cells in patients with a fulminant pattern of onset was significantly lower than that in the other groups, and that in patients with a typical pattern of onset was significantly higher than that in the other groups. |
| 5438 | 17130553 | CCR5 expression on CD4 T cells was not different among the three clinical phenotypes. |
| 5439 | 17130553 | The purpose of this article was to investigate the expression levels of CXC chemokine receptor 3 (CXCR3) and CC chemokine receptor 5 (CCR5) on CD4 T cells as Th1 markers in Japanese patients with type 1 diabetes and control subjects. |
| 5440 | 17130553 | CXCR3 expression on CD4 T cells in patients with a fulminant pattern of onset was significantly lower than that in the other groups, and that in patients with a typical pattern of onset was significantly higher than that in the other groups. |
| 5441 | 17130553 | CCR5 expression on CD4 T cells was not different among the three clinical phenotypes. |
| 5442 | 17130553 | The purpose of this article was to investigate the expression levels of CXC chemokine receptor 3 (CXCR3) and CC chemokine receptor 5 (CCR5) on CD4 T cells as Th1 markers in Japanese patients with type 1 diabetes and control subjects. |
| 5443 | 17130553 | CXCR3 expression on CD4 T cells in patients with a fulminant pattern of onset was significantly lower than that in the other groups, and that in patients with a typical pattern of onset was significantly higher than that in the other groups. |
| 5444 | 17130553 | CCR5 expression on CD4 T cells was not different among the three clinical phenotypes. |
| 5445 | 17130555 | Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis. |
| 5446 | 17130555 | Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance. |
| 5447 | 17130555 | Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg. |
| 5448 | 17130555 | Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg. |
| 5449 | 17130555 | In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions. |
| 5450 | 17130555 | Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling. |
| 5451 | 17130555 | Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis. |
| 5452 | 17130555 | Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance. |
| 5453 | 17130555 | Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg. |
| 5454 | 17130555 | Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg. |
| 5455 | 17130555 | In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions. |
| 5456 | 17130555 | Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling. |
| 5457 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5458 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5459 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5460 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5461 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5462 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5463 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5464 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5465 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5466 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5467 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5468 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5469 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5470 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5471 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5472 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5473 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5474 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5475 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5476 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5477 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5478 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5479 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5480 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5481 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5482 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5483 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5484 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5485 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5486 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5487 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5488 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5489 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5490 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5491 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5492 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5493 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5494 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5495 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5496 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5497 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5498 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5499 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5500 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5501 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5502 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5503 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5504 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5505 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5506 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5507 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5508 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5509 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5510 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5511 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5512 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5513 | 17142730 | Rapamycin promotes expansion of functional CD4+CD25+FOXP3+ regulatory T cells of both healthy subjects and type 1 diabetic patients. |
| 5514 | 17142730 | CD4+CD25+FOXP3+ T regulatory cells (Tregs) are pivotal for the induction and maintenance of peripheral tolerance in both mice and humans. |
| 5515 | 17142730 | Rapamycin has been shown to promote tolerance in experimental models and to favor CD4+CD25+ Treg-dependent suppression. |
| 5516 | 17142730 | We recently reported that rapamycin allows in vitro expansion of murine CD4+CD25+FoxP3+ Tregs, which preserve their suppressive function. |
| 5517 | 17142730 | In the current study, we show that activation of human CD4+ T cells from healthy subjects in the presence of rapamycin leads to growth of CD4+CD25+FOXP3+ Tregs and to selective depletion of CD4+CD25- T effector cells, which are highly sensitive to the antiproliferative effect of the compound. |
| 5518 | 17142730 | The rapamycin-expanded Tregs suppress proliferation of both syngeneic and allogeneic CD4+ and CD8+ T cells. |
| 5519 | 17142730 | Interestingly, rapamycin promotes expansion of functional CD4+CD25+FOXP3+ Tregs also in type 1 diabetic patients, in whom a defect in freshly isolated CD4+CD25+ Tregs has been reported. |
| 5520 | 17142730 | The capacity of rapamycin to allow growth of functional CD4+CD25+FOXP3+ Tregs, but also to deplete T effector cells, can be exploited for the design of novel and safe in vitro protocols for cellular immunotherapy in T cell-mediated diseases. |
| 5521 | 17151140 | We tested CD4, CD8, and CD161 expression and IL-4 and IFN-gamma production on TCR stimulation. |
| 5522 | 17161871 | Results showed that CB-SC could significantly inhibit lymphocyte proliferation and reduce tyrosine phosphorylation of STAT5 in both PHA- and IL-2-stimulated lymphocytes, along with the regulation on the phenotypes of CD4+ and CD8+ T cells. |
| 5523 | 17161871 | Additionally, CB-SC also suppressed the proliferation of IL-2-stimulated CD4+CD25+ regulatory T cells. |
| 5524 | 17161871 | Mechanism studies revealed that programmed death receptor-1 ligand 1 (PD-L1) expressed on CB-SC membrane, together with a soluble factor nitric oxide (NO) released by PHA-stimulated CB-SC, not prostaglandin E2 (PGE2) and transforming growth factor-beta1 (TGF-beta1), mainly contributed to the T cell suppression induced by CB-SC, as demonstrated by blocking experiments with a nitric oxide synthase inhibitor (Nomega-nitro-l-arginine, l-NNA) and a neutralizing antibody to PD-L1. |
| 5525 | 17161871 | Results showed that CB-SC could significantly inhibit lymphocyte proliferation and reduce tyrosine phosphorylation of STAT5 in both PHA- and IL-2-stimulated lymphocytes, along with the regulation on the phenotypes of CD4+ and CD8+ T cells. |
| 5526 | 17161871 | Additionally, CB-SC also suppressed the proliferation of IL-2-stimulated CD4+CD25+ regulatory T cells. |
| 5527 | 17161871 | Mechanism studies revealed that programmed death receptor-1 ligand 1 (PD-L1) expressed on CB-SC membrane, together with a soluble factor nitric oxide (NO) released by PHA-stimulated CB-SC, not prostaglandin E2 (PGE2) and transforming growth factor-beta1 (TGF-beta1), mainly contributed to the T cell suppression induced by CB-SC, as demonstrated by blocking experiments with a nitric oxide synthase inhibitor (Nomega-nitro-l-arginine, l-NNA) and a neutralizing antibody to PD-L1. |
| 5528 | 17162357 | Oral Ag induces Th2 (IL-4/IL-10) and Th3 (TGF-beta) regulatory T cells (Tregs) plus CD4+CD25+ regulatory cells and LAP+T cells. |
| 5529 | 17162357 | Induction of oral tolerance is enhanced by IL-4, IL-10, anti-IL-12, TGF-beta, cholera toxin B subunit (CTB), Flt-3 ligand, anti-CD40 ligand and continuous feeding of Ag. |
| 5530 | 17163450 | CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65. |
| 5531 | 17163450 | It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery. |
| 5532 | 17163450 | However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells. |
| 5533 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 5534 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 5535 | 17163450 | Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population. |
| 5536 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 5537 | 17163450 | CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65. |
| 5538 | 17163450 | It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery. |
| 5539 | 17163450 | However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells. |
| 5540 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 5541 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 5542 | 17163450 | Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population. |
| 5543 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 5544 | 17163450 | CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65. |
| 5545 | 17163450 | It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery. |
| 5546 | 17163450 | However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells. |
| 5547 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 5548 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 5549 | 17163450 | Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population. |
| 5550 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 5551 | 17163450 | CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65. |
| 5552 | 17163450 | It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery. |
| 5553 | 17163450 | However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells. |
| 5554 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 5555 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 5556 | 17163450 | Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population. |
| 5557 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 5558 | 17163450 | CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65. |
| 5559 | 17163450 | It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery. |
| 5560 | 17163450 | However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells. |
| 5561 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 5562 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 5563 | 17163450 | Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population. |
| 5564 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 5565 | 17163450 | CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65. |
| 5566 | 17163450 | It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery. |
| 5567 | 17163450 | However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells. |
| 5568 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 5569 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 5570 | 17163450 | Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population. |
| 5571 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 5572 | 17164429 | Distinct regulation of autoreactive CD4 T cell expansion by interleukin-4 under conditions of lymphopenia. |
| 5573 | 17164429 | Here, we show that IL-4 only enhances the expansion of autoreactive CD4 T cells during lymphopenia and that neither the presence of islet IL-4 nor IL-4 deficiency affects T cell expansion significantly under conditions of immunosufficiency. |
| 5574 | 17164429 | The ability of IL-4 to promote autoreactive CD4 T cell expansion is therefore sensitive to the degree of host immunodeficiency. |
| 5575 | 17164429 | Paradoxically, IL-4 receptor-deficient, autoreactive CD4 T cells proliferate more extensively than wild-type T cells in immunodeficient hosts, suggesting that the growth-promoting effect of islet IL-4 acts indirectly. |
| 5576 | 17164429 | Distinct regulation of autoreactive CD4 T cell expansion by interleukin-4 under conditions of lymphopenia. |
| 5577 | 17164429 | Here, we show that IL-4 only enhances the expansion of autoreactive CD4 T cells during lymphopenia and that neither the presence of islet IL-4 nor IL-4 deficiency affects T cell expansion significantly under conditions of immunosufficiency. |
| 5578 | 17164429 | The ability of IL-4 to promote autoreactive CD4 T cell expansion is therefore sensitive to the degree of host immunodeficiency. |
| 5579 | 17164429 | Paradoxically, IL-4 receptor-deficient, autoreactive CD4 T cells proliferate more extensively than wild-type T cells in immunodeficient hosts, suggesting that the growth-promoting effect of islet IL-4 acts indirectly. |
| 5580 | 17164429 | Distinct regulation of autoreactive CD4 T cell expansion by interleukin-4 under conditions of lymphopenia. |
| 5581 | 17164429 | Here, we show that IL-4 only enhances the expansion of autoreactive CD4 T cells during lymphopenia and that neither the presence of islet IL-4 nor IL-4 deficiency affects T cell expansion significantly under conditions of immunosufficiency. |
| 5582 | 17164429 | The ability of IL-4 to promote autoreactive CD4 T cell expansion is therefore sensitive to the degree of host immunodeficiency. |
| 5583 | 17164429 | Paradoxically, IL-4 receptor-deficient, autoreactive CD4 T cells proliferate more extensively than wild-type T cells in immunodeficient hosts, suggesting that the growth-promoting effect of islet IL-4 acts indirectly. |
| 5584 | 17164429 | Distinct regulation of autoreactive CD4 T cell expansion by interleukin-4 under conditions of lymphopenia. |
| 5585 | 17164429 | Here, we show that IL-4 only enhances the expansion of autoreactive CD4 T cells during lymphopenia and that neither the presence of islet IL-4 nor IL-4 deficiency affects T cell expansion significantly under conditions of immunosufficiency. |
| 5586 | 17164429 | The ability of IL-4 to promote autoreactive CD4 T cell expansion is therefore sensitive to the degree of host immunodeficiency. |
| 5587 | 17164429 | Paradoxically, IL-4 receptor-deficient, autoreactive CD4 T cells proliferate more extensively than wild-type T cells in immunodeficient hosts, suggesting that the growth-promoting effect of islet IL-4 acts indirectly. |
| 5588 | 17176958 | Thymic lymphatic endothelial cells showed suggestive expression patterns of the functional molecules lymphatic vascular endothelial hyaluronan receptor (LYVE)-1, CCL21, CD31 and podoplanin. |
| 5589 | 17176958 | The CD4- and CD8-positive T cells frequently penetrated through the slender lymphatic walls. |
| 5590 | 17192481 | Modulating protective and pathogenic CD4+ subsets via CD137 in type 1 diabetes. |
| 5591 | 17192481 | CD137 (TNFRSF9) is an activation-inducible T-cell costimulatory molecule and a member of the tumor necrosis factor (TNF) receptor superfamily. |
| 5592 | 17192481 | Transfer of CD4(+), but not CD8(+), cells from anti-CD137-treated pre-diabetic NOD mice into NOD-scid mice delayed diabetes onset. |
| 5593 | 17192481 | Anti-CD137 treatment significantly increased the number of CD4(+)CD25(+) cells, which demonstrated intracellular Foxp3 expression and in vitro suppressive activity. |
| 5594 | 17192481 | The CD4(+)CD25(+) cell subset from anti-CD137-treated mice transferred complete protection from diabetes, whereas the CD4(+)CD25(-) cell subset offered no significant protection. |
| 5595 | 17192481 | Modulating protective and pathogenic CD4+ subsets via CD137 in type 1 diabetes. |
| 5596 | 17192481 | CD137 (TNFRSF9) is an activation-inducible T-cell costimulatory molecule and a member of the tumor necrosis factor (TNF) receptor superfamily. |
| 5597 | 17192481 | Transfer of CD4(+), but not CD8(+), cells from anti-CD137-treated pre-diabetic NOD mice into NOD-scid mice delayed diabetes onset. |
| 5598 | 17192481 | Anti-CD137 treatment significantly increased the number of CD4(+)CD25(+) cells, which demonstrated intracellular Foxp3 expression and in vitro suppressive activity. |
| 5599 | 17192481 | The CD4(+)CD25(+) cell subset from anti-CD137-treated mice transferred complete protection from diabetes, whereas the CD4(+)CD25(-) cell subset offered no significant protection. |
| 5600 | 17192481 | Modulating protective and pathogenic CD4+ subsets via CD137 in type 1 diabetes. |
| 5601 | 17192481 | CD137 (TNFRSF9) is an activation-inducible T-cell costimulatory molecule and a member of the tumor necrosis factor (TNF) receptor superfamily. |
| 5602 | 17192481 | Transfer of CD4(+), but not CD8(+), cells from anti-CD137-treated pre-diabetic NOD mice into NOD-scid mice delayed diabetes onset. |
| 5603 | 17192481 | Anti-CD137 treatment significantly increased the number of CD4(+)CD25(+) cells, which demonstrated intracellular Foxp3 expression and in vitro suppressive activity. |
| 5604 | 17192481 | The CD4(+)CD25(+) cell subset from anti-CD137-treated mice transferred complete protection from diabetes, whereas the CD4(+)CD25(-) cell subset offered no significant protection. |
| 5605 | 17192481 | Modulating protective and pathogenic CD4+ subsets via CD137 in type 1 diabetes. |
| 5606 | 17192481 | CD137 (TNFRSF9) is an activation-inducible T-cell costimulatory molecule and a member of the tumor necrosis factor (TNF) receptor superfamily. |
| 5607 | 17192481 | Transfer of CD4(+), but not CD8(+), cells from anti-CD137-treated pre-diabetic NOD mice into NOD-scid mice delayed diabetes onset. |
| 5608 | 17192481 | Anti-CD137 treatment significantly increased the number of CD4(+)CD25(+) cells, which demonstrated intracellular Foxp3 expression and in vitro suppressive activity. |
| 5609 | 17192481 | The CD4(+)CD25(+) cell subset from anti-CD137-treated mice transferred complete protection from diabetes, whereas the CD4(+)CD25(-) cell subset offered no significant protection. |
| 5610 | 17198560 | [Decrease of FOXP3 mRNA in CD4+ T cells in latent autoimmune diabetes in adult]. |
| 5611 | 17200197 | To this end, we have used transgenic mice expressing the model autoantigen ovalbumin in pancreatic islets and transgenic ovalbumin-specific CD4 and CD8 T cells. |
| 5612 | 17202352 | Successful Ag activation of naive T helper cells requires at least two signals consisting of TCR and CD28 on the T cell interacting with MHC II and CD80/CD86, respectively, on APCs. |
| 5613 | 17202352 | We have reported that modulation of redox balance with a catalytic antioxidant effectively inhibited the generation of third signal components from the innate immune response (TNF-alpha, IL-1beta, ROS). |
| 5614 | 17202352 | Modulating redox balance led to decreased Ag-specific T cell proliferation and IFN-gamma synthesis by diminishing ROS production in the APC, which affected TNF-alpha levels produced by CD4(+) T cells and impairing effector function. |
| 5615 | 17206281 | At-risk and recent-onset type 1 diabetic subjects have increased apoptosis in the CD4+CD25+ T-cell fraction. |
| 5616 | 17210729 | Dendritic cell-expanded, islet-specific CD4+ CD25+ CD62L+ regulatory T cells restore normoglycemia in diabetic NOD mice. |
| 5617 | 17210729 | We tested whether dendritic cell (DC)-expanded, islet antigen-specific CD4+ CD25+ suppressor T cells could treat diabetes at later stages of disease, when most of the insulin-producing islet beta cells had been destroyed by infiltrating lymphocytes. |
| 5618 | 17210729 | CD4+ CD25+ CD62L+ regulatory T cells (T reg cells) from BDC2.5 T cell receptor transgenic mice were expanded with antigen-pulsed DCs and IL-2, and were then injected into NOD mice. |
| 5619 | 17210729 | Dendritic cell-expanded, islet-specific CD4+ CD25+ CD62L+ regulatory T cells restore normoglycemia in diabetic NOD mice. |
| 5620 | 17210729 | We tested whether dendritic cell (DC)-expanded, islet antigen-specific CD4+ CD25+ suppressor T cells could treat diabetes at later stages of disease, when most of the insulin-producing islet beta cells had been destroyed by infiltrating lymphocytes. |
| 5621 | 17210729 | CD4+ CD25+ CD62L+ regulatory T cells (T reg cells) from BDC2.5 T cell receptor transgenic mice were expanded with antigen-pulsed DCs and IL-2, and were then injected into NOD mice. |
| 5622 | 17210729 | Dendritic cell-expanded, islet-specific CD4+ CD25+ CD62L+ regulatory T cells restore normoglycemia in diabetic NOD mice. |
| 5623 | 17210729 | We tested whether dendritic cell (DC)-expanded, islet antigen-specific CD4+ CD25+ suppressor T cells could treat diabetes at later stages of disease, when most of the insulin-producing islet beta cells had been destroyed by infiltrating lymphocytes. |
| 5624 | 17210729 | CD4+ CD25+ CD62L+ regulatory T cells (T reg cells) from BDC2.5 T cell receptor transgenic mice were expanded with antigen-pulsed DCs and IL-2, and were then injected into NOD mice. |
| 5625 | 17237411 | In this study, we report the production and characterization of a NOD.Nkrp1(b).Nkt1(b) congenic mouse strain, apply microarray expression analyses to limit candidate genes within the 95% confidence region, identify Slamf1 (encoding signaling lymphocyte activation molecule) and Slamf6 (encoding Ly108) as potential candidates, and demonstrate retarded signaling lymphocyte activation molecule expression during T cell development of NOD mice, resulting in reduced expression at the CD4(+)CD8(+) stage, which is consistent with decreased NKT cell production and deranged tolerance induction in NOD mice. |
| 5626 | 17244154 | Reduced CCR4, interleukin-13 and GATA-3 up-regulation in response to type 2 cytokines of cord blood T lymphocytes in infants at genetic risk of type 1 diabetes. |
| 5627 | 17244154 | After culture of CB lymphocytes in type 2 cytokine environment newborn infants carrying DR4-DQ8 haplotype (n=18) showed reduced percentage of CD4 T cells expressing CCR4 (P=0 x 009) and the level of CCR4 mRNA was decreased (P=0 x 008). |
| 5628 | 17244154 | In addition, lower secretion of IL-13 and expression of GATA-3 in CB lymphocytes cultured in type 2 cytokine environment were found in the infants with DR4-DQ8 haplotype (P=0 x 020 and P=0 x 004, respectively) in comparison to newborn infants without DR4-DQ8 and DR3-DQ2 haplotypes (n=37). |
| 5629 | 17267595 | Here we report that injection of donor bone marrow and CD4+ T cell-depleted spleen cells induced chimerism without causing GVHD in overtly diabetic NOD mice conditioned with anti-CD3/CD8 and that induction of chimerism in new-onset diabetic NOD mice led to elimination of insulitis, regeneration of host beta cells, and reversal of hyperglycemia. |
| 5630 | 17277113 | Cognate CD4+ help elicited by resting dendritic cells does not impair the induction of peripheral tolerance in CD8+ T cells. |
| 5631 | 17277113 | In contrast, DC can be "licensed" by CD4(+) T cells to induce cytotoxic function in CD8(+) T cells. |
| 5632 | 17277113 | The question that then arises, whether CD4(+) T cell help could impair peripheral tolerance induction in self-reactive CD8(+) T cells, has not been addressed. |
| 5633 | 17277113 | In this study we show that CD4(+) T cell activation by resting DC results in helper function that transiently promotes the expansion and differentiation of cognate CD8(+) T cells. |
| 5634 | 17277113 | However, both the CD4(+) and CD8(+) T cell populations ultimately undergo partial deletion and acquire Ag unresponsiveness, disabling their ability to destroy OVA-expressing pancreatic beta cells and cause diabetes. |
| 5635 | 17277113 | Thus, effective peripheral tolerance can be induced by resting DC in the presence of CD4(+) and CD8(+) T cells with specificity for the same Ag. |
| 5636 | 17277113 | Cognate CD4+ help elicited by resting dendritic cells does not impair the induction of peripheral tolerance in CD8+ T cells. |
| 5637 | 17277113 | In contrast, DC can be "licensed" by CD4(+) T cells to induce cytotoxic function in CD8(+) T cells. |
| 5638 | 17277113 | The question that then arises, whether CD4(+) T cell help could impair peripheral tolerance induction in self-reactive CD8(+) T cells, has not been addressed. |
| 5639 | 17277113 | In this study we show that CD4(+) T cell activation by resting DC results in helper function that transiently promotes the expansion and differentiation of cognate CD8(+) T cells. |
| 5640 | 17277113 | However, both the CD4(+) and CD8(+) T cell populations ultimately undergo partial deletion and acquire Ag unresponsiveness, disabling their ability to destroy OVA-expressing pancreatic beta cells and cause diabetes. |
| 5641 | 17277113 | Thus, effective peripheral tolerance can be induced by resting DC in the presence of CD4(+) and CD8(+) T cells with specificity for the same Ag. |
| 5642 | 17277113 | Cognate CD4+ help elicited by resting dendritic cells does not impair the induction of peripheral tolerance in CD8+ T cells. |
| 5643 | 17277113 | In contrast, DC can be "licensed" by CD4(+) T cells to induce cytotoxic function in CD8(+) T cells. |
| 5644 | 17277113 | The question that then arises, whether CD4(+) T cell help could impair peripheral tolerance induction in self-reactive CD8(+) T cells, has not been addressed. |
| 5645 | 17277113 | In this study we show that CD4(+) T cell activation by resting DC results in helper function that transiently promotes the expansion and differentiation of cognate CD8(+) T cells. |
| 5646 | 17277113 | However, both the CD4(+) and CD8(+) T cell populations ultimately undergo partial deletion and acquire Ag unresponsiveness, disabling their ability to destroy OVA-expressing pancreatic beta cells and cause diabetes. |
| 5647 | 17277113 | Thus, effective peripheral tolerance can be induced by resting DC in the presence of CD4(+) and CD8(+) T cells with specificity for the same Ag. |
| 5648 | 17277113 | Cognate CD4+ help elicited by resting dendritic cells does not impair the induction of peripheral tolerance in CD8+ T cells. |
| 5649 | 17277113 | In contrast, DC can be "licensed" by CD4(+) T cells to induce cytotoxic function in CD8(+) T cells. |
| 5650 | 17277113 | The question that then arises, whether CD4(+) T cell help could impair peripheral tolerance induction in self-reactive CD8(+) T cells, has not been addressed. |
| 5651 | 17277113 | In this study we show that CD4(+) T cell activation by resting DC results in helper function that transiently promotes the expansion and differentiation of cognate CD8(+) T cells. |
| 5652 | 17277113 | However, both the CD4(+) and CD8(+) T cell populations ultimately undergo partial deletion and acquire Ag unresponsiveness, disabling their ability to destroy OVA-expressing pancreatic beta cells and cause diabetes. |
| 5653 | 17277113 | Thus, effective peripheral tolerance can be induced by resting DC in the presence of CD4(+) and CD8(+) T cells with specificity for the same Ag. |
| 5654 | 17277113 | Cognate CD4+ help elicited by resting dendritic cells does not impair the induction of peripheral tolerance in CD8+ T cells. |
| 5655 | 17277113 | In contrast, DC can be "licensed" by CD4(+) T cells to induce cytotoxic function in CD8(+) T cells. |
| 5656 | 17277113 | The question that then arises, whether CD4(+) T cell help could impair peripheral tolerance induction in self-reactive CD8(+) T cells, has not been addressed. |
| 5657 | 17277113 | In this study we show that CD4(+) T cell activation by resting DC results in helper function that transiently promotes the expansion and differentiation of cognate CD8(+) T cells. |
| 5658 | 17277113 | However, both the CD4(+) and CD8(+) T cell populations ultimately undergo partial deletion and acquire Ag unresponsiveness, disabling their ability to destroy OVA-expressing pancreatic beta cells and cause diabetes. |
| 5659 | 17277113 | Thus, effective peripheral tolerance can be induced by resting DC in the presence of CD4(+) and CD8(+) T cells with specificity for the same Ag. |
| 5660 | 17277113 | Cognate CD4+ help elicited by resting dendritic cells does not impair the induction of peripheral tolerance in CD8+ T cells. |
| 5661 | 17277113 | In contrast, DC can be "licensed" by CD4(+) T cells to induce cytotoxic function in CD8(+) T cells. |
| 5662 | 17277113 | The question that then arises, whether CD4(+) T cell help could impair peripheral tolerance induction in self-reactive CD8(+) T cells, has not been addressed. |
| 5663 | 17277113 | In this study we show that CD4(+) T cell activation by resting DC results in helper function that transiently promotes the expansion and differentiation of cognate CD8(+) T cells. |
| 5664 | 17277113 | However, both the CD4(+) and CD8(+) T cell populations ultimately undergo partial deletion and acquire Ag unresponsiveness, disabling their ability to destroy OVA-expressing pancreatic beta cells and cause diabetes. |
| 5665 | 17277113 | Thus, effective peripheral tolerance can be induced by resting DC in the presence of CD4(+) and CD8(+) T cells with specificity for the same Ag. |
| 5666 | 17277778 | Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4(+) CD25(+) regulatory T cells, which are critical for maintaining immune homeostasis. |
| 5667 | 17289146 | Blocking studies in B7-1KO mice suggest that B7-H1 provides negative signals for anti islet CD4 and CD8 T-cell expansion but is differentially required for their priming. |
| 5668 | 17298964 | CD4+ CD25+ regulatory T-cells in acute coronary syndromes. |
| 5669 | 17302896 | We therefore examined the recently activated circulating T cell population [CD3+, human leucocyte antigen D-related (HLA-DR+)] using cytokine production and 10 additional subset markers [CD69, CD25, CD122, CD30, CD44v6, CD57, CD71, CCR3 (CD193), CCR5 (CD195) or CXCR3 (CD183)], comparing newly diagnosed adult (ND) (age 18-40 years) patients (n=19) to patients with diabetes for >10 years [long-standing (LS), n=19] and HLA-matched controls (C, n=16). |
| 5670 | 17302896 | No differences in basal or stimulated production of interleukin (IL)-4, IL-10, IL-13 or interferon (IFN)-gamma by CD3+ DR+ enriched cells were observed between the different groups of subjects. |
| 5671 | 17302896 | However, among the CD3+ DR+ population, significant expansions appeared to be present in the very small CD30+, CD69+ and CD122+ subpopulations. |
| 5672 | 17302896 | A confirmatory study was then performed using new subjects (ND=26, LS=15), three-colour flow cytometry, unseparated cells and three additional subset markers (CD38, CD134, CD4/CD25). |
| 5673 | 17303808 | Flow cytometry analysis revealed no significant difference in the percentages of CD4(+)CD25(+) regulatory T-cells between saline-treated and AAV-HO-1-treated groups. |
| 5674 | 17307871 | CD4(+)CD25(+)Foxp3(+) regulatory T cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natural) or differentiated in the periphery outside the thymus (induced). |
| 5675 | 17307871 | Here we show that beta-cell peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4(+)CD25(+)Foxp3(+) T cells from naïve islet-specific CD4(+)CD25(-) T cells in the presence of TGF-beta1. |
| 5676 | 17307871 | These results indicate a role for DCs in the induction of antigen-specific CD4(+)CD25(+)Foxp3(+) T cells that can inhibit fully developed autoimmunity in a nonlymphopoenic host, providing an important potential strategy for immunotherapy in patients with autoimmune diabetes. |
| 5677 | 17307871 | CD4(+)CD25(+)Foxp3(+) regulatory T cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natural) or differentiated in the periphery outside the thymus (induced). |
| 5678 | 17307871 | Here we show that beta-cell peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4(+)CD25(+)Foxp3(+) T cells from naïve islet-specific CD4(+)CD25(-) T cells in the presence of TGF-beta1. |
| 5679 | 17307871 | These results indicate a role for DCs in the induction of antigen-specific CD4(+)CD25(+)Foxp3(+) T cells that can inhibit fully developed autoimmunity in a nonlymphopoenic host, providing an important potential strategy for immunotherapy in patients with autoimmune diabetes. |
| 5680 | 17307871 | CD4(+)CD25(+)Foxp3(+) regulatory T cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natural) or differentiated in the periphery outside the thymus (induced). |
| 5681 | 17307871 | Here we show that beta-cell peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4(+)CD25(+)Foxp3(+) T cells from naïve islet-specific CD4(+)CD25(-) T cells in the presence of TGF-beta1. |
| 5682 | 17307871 | These results indicate a role for DCs in the induction of antigen-specific CD4(+)CD25(+)Foxp3(+) T cells that can inhibit fully developed autoimmunity in a nonlymphopoenic host, providing an important potential strategy for immunotherapy in patients with autoimmune diabetes. |
| 5683 | 17317763 | To define the parameters influencing the efficacy of antigen-specific immunotherapy once diabetes is established, plasmid DNA (pDNA) vaccination was used to suppress autoimmune-mediated destruction of syngeneic islet grafts in diabetic NOD recipients. pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD65), interleukin (IL)-4 (pIL4), and IL-10 (pIL10) significantly delayed the onset of recurrent diabetes compared with pGAD65+pIL10-vaccinated recipients. |
| 5684 | 17317763 | Despite differences in efficacy, a similar frequency of GAD65-specific CD4(+) T-cells secreting IL-4, IL-10, or interferon-gamma were detected in mice treated with pGAD65+pIL4+pIL10 and pGAD65+pIL10. |
| 5685 | 17317763 | However, the frequency of FoxP3-expressing CD4(+)CD25(+)CD62L(hi) T-cells was increased in the renal and pancreatic lymph nodes of diabetic recipients vaccinated with pGAD65+pIL4+pIL10. |
| 5686 | 17317763 | These immunoregulatory CD4(+)CD25(+) T-cells (CD4(+)CD25(+) Treg) exhibited enhanced in vivo and in vitro suppressor activity that partially was transforming growth factor-beta dependent. |
| 5687 | 17317763 | Furthermore, duration of islet graft protection in pGAD65+pIL4+pIL10-vaccinated diabetic recipients correlated with the persistence of CD4(+)CD25(+) Treg. |
| 5688 | 17317763 | These data demonstrate that the frequency and maintenance of FoxP3-expressing CD4(+)CD25(+) Treg influence antigen-induced suppression of ongoing beta-cell autoimmunity in diabetic recipients. |
| 5689 | 17317763 | To define the parameters influencing the efficacy of antigen-specific immunotherapy once diabetes is established, plasmid DNA (pDNA) vaccination was used to suppress autoimmune-mediated destruction of syngeneic islet grafts in diabetic NOD recipients. pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD65), interleukin (IL)-4 (pIL4), and IL-10 (pIL10) significantly delayed the onset of recurrent diabetes compared with pGAD65+pIL10-vaccinated recipients. |
| 5690 | 17317763 | Despite differences in efficacy, a similar frequency of GAD65-specific CD4(+) T-cells secreting IL-4, IL-10, or interferon-gamma were detected in mice treated with pGAD65+pIL4+pIL10 and pGAD65+pIL10. |
| 5691 | 17317763 | However, the frequency of FoxP3-expressing CD4(+)CD25(+)CD62L(hi) T-cells was increased in the renal and pancreatic lymph nodes of diabetic recipients vaccinated with pGAD65+pIL4+pIL10. |
| 5692 | 17317763 | These immunoregulatory CD4(+)CD25(+) T-cells (CD4(+)CD25(+) Treg) exhibited enhanced in vivo and in vitro suppressor activity that partially was transforming growth factor-beta dependent. |
| 5693 | 17317763 | Furthermore, duration of islet graft protection in pGAD65+pIL4+pIL10-vaccinated diabetic recipients correlated with the persistence of CD4(+)CD25(+) Treg. |
| 5694 | 17317763 | These data demonstrate that the frequency and maintenance of FoxP3-expressing CD4(+)CD25(+) Treg influence antigen-induced suppression of ongoing beta-cell autoimmunity in diabetic recipients. |
| 5695 | 17317763 | To define the parameters influencing the efficacy of antigen-specific immunotherapy once diabetes is established, plasmid DNA (pDNA) vaccination was used to suppress autoimmune-mediated destruction of syngeneic islet grafts in diabetic NOD recipients. pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD65), interleukin (IL)-4 (pIL4), and IL-10 (pIL10) significantly delayed the onset of recurrent diabetes compared with pGAD65+pIL10-vaccinated recipients. |
| 5696 | 17317763 | Despite differences in efficacy, a similar frequency of GAD65-specific CD4(+) T-cells secreting IL-4, IL-10, or interferon-gamma were detected in mice treated with pGAD65+pIL4+pIL10 and pGAD65+pIL10. |
| 5697 | 17317763 | However, the frequency of FoxP3-expressing CD4(+)CD25(+)CD62L(hi) T-cells was increased in the renal and pancreatic lymph nodes of diabetic recipients vaccinated with pGAD65+pIL4+pIL10. |
| 5698 | 17317763 | These immunoregulatory CD4(+)CD25(+) T-cells (CD4(+)CD25(+) Treg) exhibited enhanced in vivo and in vitro suppressor activity that partially was transforming growth factor-beta dependent. |
| 5699 | 17317763 | Furthermore, duration of islet graft protection in pGAD65+pIL4+pIL10-vaccinated diabetic recipients correlated with the persistence of CD4(+)CD25(+) Treg. |
| 5700 | 17317763 | These data demonstrate that the frequency and maintenance of FoxP3-expressing CD4(+)CD25(+) Treg influence antigen-induced suppression of ongoing beta-cell autoimmunity in diabetic recipients. |
| 5701 | 17317763 | To define the parameters influencing the efficacy of antigen-specific immunotherapy once diabetes is established, plasmid DNA (pDNA) vaccination was used to suppress autoimmune-mediated destruction of syngeneic islet grafts in diabetic NOD recipients. pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD65), interleukin (IL)-4 (pIL4), and IL-10 (pIL10) significantly delayed the onset of recurrent diabetes compared with pGAD65+pIL10-vaccinated recipients. |
| 5702 | 17317763 | Despite differences in efficacy, a similar frequency of GAD65-specific CD4(+) T-cells secreting IL-4, IL-10, or interferon-gamma were detected in mice treated with pGAD65+pIL4+pIL10 and pGAD65+pIL10. |
| 5703 | 17317763 | However, the frequency of FoxP3-expressing CD4(+)CD25(+)CD62L(hi) T-cells was increased in the renal and pancreatic lymph nodes of diabetic recipients vaccinated with pGAD65+pIL4+pIL10. |
| 5704 | 17317763 | These immunoregulatory CD4(+)CD25(+) T-cells (CD4(+)CD25(+) Treg) exhibited enhanced in vivo and in vitro suppressor activity that partially was transforming growth factor-beta dependent. |
| 5705 | 17317763 | Furthermore, duration of islet graft protection in pGAD65+pIL4+pIL10-vaccinated diabetic recipients correlated with the persistence of CD4(+)CD25(+) Treg. |
| 5706 | 17317763 | These data demonstrate that the frequency and maintenance of FoxP3-expressing CD4(+)CD25(+) Treg influence antigen-induced suppression of ongoing beta-cell autoimmunity in diabetic recipients. |
| 5707 | 17317763 | To define the parameters influencing the efficacy of antigen-specific immunotherapy once diabetes is established, plasmid DNA (pDNA) vaccination was used to suppress autoimmune-mediated destruction of syngeneic islet grafts in diabetic NOD recipients. pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD65), interleukin (IL)-4 (pIL4), and IL-10 (pIL10) significantly delayed the onset of recurrent diabetes compared with pGAD65+pIL10-vaccinated recipients. |
| 5708 | 17317763 | Despite differences in efficacy, a similar frequency of GAD65-specific CD4(+) T-cells secreting IL-4, IL-10, or interferon-gamma were detected in mice treated with pGAD65+pIL4+pIL10 and pGAD65+pIL10. |
| 5709 | 17317763 | However, the frequency of FoxP3-expressing CD4(+)CD25(+)CD62L(hi) T-cells was increased in the renal and pancreatic lymph nodes of diabetic recipients vaccinated with pGAD65+pIL4+pIL10. |
| 5710 | 17317763 | These immunoregulatory CD4(+)CD25(+) T-cells (CD4(+)CD25(+) Treg) exhibited enhanced in vivo and in vitro suppressor activity that partially was transforming growth factor-beta dependent. |
| 5711 | 17317763 | Furthermore, duration of islet graft protection in pGAD65+pIL4+pIL10-vaccinated diabetic recipients correlated with the persistence of CD4(+)CD25(+) Treg. |
| 5712 | 17317763 | These data demonstrate that the frequency and maintenance of FoxP3-expressing CD4(+)CD25(+) Treg influence antigen-induced suppression of ongoing beta-cell autoimmunity in diabetic recipients. |
| 5713 | 17324464 | Activation induced cell death (AICD) via Fas/FasL is the primary homeostatic molecular mechanism employed by the immune system to control activated T-cell responses and promote tolerance to self-antigens. |
| 5714 | 17324464 | We herein investigated the ability of a novel multimeric form of FasL chimeric with streptavidin (SA-FasL) having potent apoptotic activity to induce apoptosis in diabetogenic T cells and modulate insulin-dependent type 1 diabetes (IDDM) in an adoptive transfer model. |
| 5715 | 17324464 | This effect was associated with an increase in CD4(+)CD25(+) T cells and correlated with FoxP3 expression in pancreatic lymph nodes. |
| 5716 | 17327427 | Previous characterizations of Tregs in type 1 diabetes have used antibodies against CD4 and alpha-chain of the interleukin-2 receptor complex (CD25). |
| 5717 | 17327427 | With inclusion of this marker, two predominant populations of CD4(+)CD25(+) T-cells were identified: CD4(+)CD25(+)FOXP3(+) as well as CD4(+)FOXP3(-) T-cells expressing low levels of CD25 (CD4(+)CD25(LOW)FOXP3(-)). |
| 5718 | 17327427 | In all study groups, the frequency of CD4(+)CD25(+)FOXP3(+) cells was age independent, whereas CD4(+)CD25(LOW)FOXP3(-) cell frequencies strongly associated with age. |
| 5719 | 17327427 | In terms of additional markers for delineating cells of Treg lineage, FOXP3(+) cells were CD127(-) to CD127(LOW) whereas CD25(+) cells were less restricted in their expression of this marker, with CD127 expressed across a continuum of levels. |
| 5720 | 17327427 | Importantly, no differences were observed in the frequency of CD4(+)CD25(+)FOXP3(+) T-cells in individuals with or at varying degrees of risk for type 1 diabetes. |
| 5721 | 17327427 | Previous characterizations of Tregs in type 1 diabetes have used antibodies against CD4 and alpha-chain of the interleukin-2 receptor complex (CD25). |
| 5722 | 17327427 | With inclusion of this marker, two predominant populations of CD4(+)CD25(+) T-cells were identified: CD4(+)CD25(+)FOXP3(+) as well as CD4(+)FOXP3(-) T-cells expressing low levels of CD25 (CD4(+)CD25(LOW)FOXP3(-)). |
| 5723 | 17327427 | In all study groups, the frequency of CD4(+)CD25(+)FOXP3(+) cells was age independent, whereas CD4(+)CD25(LOW)FOXP3(-) cell frequencies strongly associated with age. |
| 5724 | 17327427 | In terms of additional markers for delineating cells of Treg lineage, FOXP3(+) cells were CD127(-) to CD127(LOW) whereas CD25(+) cells were less restricted in their expression of this marker, with CD127 expressed across a continuum of levels. |
| 5725 | 17327427 | Importantly, no differences were observed in the frequency of CD4(+)CD25(+)FOXP3(+) T-cells in individuals with or at varying degrees of risk for type 1 diabetes. |
| 5726 | 17327427 | Previous characterizations of Tregs in type 1 diabetes have used antibodies against CD4 and alpha-chain of the interleukin-2 receptor complex (CD25). |
| 5727 | 17327427 | With inclusion of this marker, two predominant populations of CD4(+)CD25(+) T-cells were identified: CD4(+)CD25(+)FOXP3(+) as well as CD4(+)FOXP3(-) T-cells expressing low levels of CD25 (CD4(+)CD25(LOW)FOXP3(-)). |
| 5728 | 17327427 | In all study groups, the frequency of CD4(+)CD25(+)FOXP3(+) cells was age independent, whereas CD4(+)CD25(LOW)FOXP3(-) cell frequencies strongly associated with age. |
| 5729 | 17327427 | In terms of additional markers for delineating cells of Treg lineage, FOXP3(+) cells were CD127(-) to CD127(LOW) whereas CD25(+) cells were less restricted in their expression of this marker, with CD127 expressed across a continuum of levels. |
| 5730 | 17327427 | Importantly, no differences were observed in the frequency of CD4(+)CD25(+)FOXP3(+) T-cells in individuals with or at varying degrees of risk for type 1 diabetes. |
| 5731 | 17327427 | Previous characterizations of Tregs in type 1 diabetes have used antibodies against CD4 and alpha-chain of the interleukin-2 receptor complex (CD25). |
| 5732 | 17327427 | With inclusion of this marker, two predominant populations of CD4(+)CD25(+) T-cells were identified: CD4(+)CD25(+)FOXP3(+) as well as CD4(+)FOXP3(-) T-cells expressing low levels of CD25 (CD4(+)CD25(LOW)FOXP3(-)). |
| 5733 | 17327427 | In all study groups, the frequency of CD4(+)CD25(+)FOXP3(+) cells was age independent, whereas CD4(+)CD25(LOW)FOXP3(-) cell frequencies strongly associated with age. |
| 5734 | 17327427 | In terms of additional markers for delineating cells of Treg lineage, FOXP3(+) cells were CD127(-) to CD127(LOW) whereas CD25(+) cells were less restricted in their expression of this marker, with CD127 expressed across a continuum of levels. |
| 5735 | 17327427 | Importantly, no differences were observed in the frequency of CD4(+)CD25(+)FOXP3(+) T-cells in individuals with or at varying degrees of risk for type 1 diabetes. |
| 5736 | 17327428 | Although CD4+ T-cell assays have met with limited success, CD8+ T-cells are increasingly recognized as key actors in the diabetes of the NOD mouse. |
| 5737 | 17327428 | Taking advantage of a panel of HLA-A2-restricted beta-cell epitopes derived from preproinsulin, GAD, and islet glucose-6-phosphatase catalytic subunit-related protein (IGRP), we have implemented an islet-specific CD8+ T-cell interferon-gamma enzyme-linked immunospot (ISL8Spot) assay. |
| 5738 | 17336387 | In the NOD mouse, some previous studies argued in favor of a regulatory role for GAD-specific CD4+ T cells, and no diabetogenic CD8+ T cells specific for GAD have been identified so far, discrediting the importance of GAD in beta-cell injury. |
| 5739 | 17336387 | Here, we identified, in the NOD model, a relevant GAD CD8+ T cell epitope (GAD(90-98)) using immunization with a plasmid encoding GAD, a protocol relying on in vivo processing of peptides from the autoantigenic protein. |
| 5740 | 17336387 | In pancreatic lymph nodes of naïve female NOD mice, CD8+ T lymphocytes recognizing GAD(90-98) peptide were detected during the initial phase of invasive insulitis (between 4 and 8 weeks of age), suggesting an important role for these cells in the first stage of the disease. |
| 5741 | 17336387 | GAD(90-98) specific CD8+ lymphocytes lysed efficiently islet cells in vitro and transferred diabetes into NOD(SCID) mice (100%). |
| 5742 | 17346153 | The Janus face of CD4+CD25+ regulatory T cells in cancer and autoimmunity. |
| 5743 | 17346189 | Multiple apoptotic pathways play a role in destructive insulitis, including perforin/granzyme, Fas/Fas-ligand (FasL), and other members of the necrosis factor superfamily. |
| 5744 | 17346189 | There may be a preferential use of perforin/granzyme in CD8(+) T cell-mediated lysis, which participates in onset of autoimmunity, and a predominance of FasL in CD4(+) T cell-mediated insulitis. |
| 5745 | 17346189 | Several cytokines released in the inflammatory infiltrate induce Fas expression in beta cells, priming them to FasL-mediated apoptosis. |
| 5746 | 17349009 | In the context of a T cell-mediated autoimmune disease such as type 1 diabetes, CD4 and CD8 T cell recognition of islet autoantigenic epitopes is a key step in the autoimmune cascade. |
| 5747 | 17349009 | Targets of both CD4 and CD8 T cells are listed for human type 1 diabetes, for humanized [human leucocyte antigen (HLA)-transgenic] mouse models, and for the major spontaneous disease model, the non-obese diabetic (NOD) mouse. |
| 5748 | 17349009 | In the context of a T cell-mediated autoimmune disease such as type 1 diabetes, CD4 and CD8 T cell recognition of islet autoantigenic epitopes is a key step in the autoimmune cascade. |
| 5749 | 17349009 | Targets of both CD4 and CD8 T cells are listed for human type 1 diabetes, for humanized [human leucocyte antigen (HLA)-transgenic] mouse models, and for the major spontaneous disease model, the non-obese diabetic (NOD) mouse. |
| 5750 | 17371968 | Peroxisome proliferator-activated receptor (PPAR)gamma is a nuclear hormone receptor primarily characterized for its effect on insulin metabolism. |
| 5751 | 17371968 | However, the relationship between PPARgamma ligands and CD4+CD25+ regulatory T cells (Tregs) has not been examined. |
| 5752 | 17372610 | Here, we develop a model where IL-2 deficiency precipitates a breakdown of self-tolerance and progression to diabetes, and its action upon diabetogenic islet-specific CD4 T cells can be tracked. |
| 5753 | 17372610 | We find that IL-2 is not required for Aire-dependent thymic clonal deletion of high-avidity diabetogenic clones, but is essential for thymic formation of islet-specific Foxp3-expressing CD4 T cells. |
| 5754 | 17372610 | The absence of IL-2 results in the expansion of low-avidity Foxp3(-) islet-reactive CD4 T cells. |
| 5755 | 17372610 | Here, we develop a model where IL-2 deficiency precipitates a breakdown of self-tolerance and progression to diabetes, and its action upon diabetogenic islet-specific CD4 T cells can be tracked. |
| 5756 | 17372610 | We find that IL-2 is not required for Aire-dependent thymic clonal deletion of high-avidity diabetogenic clones, but is essential for thymic formation of islet-specific Foxp3-expressing CD4 T cells. |
| 5757 | 17372610 | The absence of IL-2 results in the expansion of low-avidity Foxp3(-) islet-reactive CD4 T cells. |
| 5758 | 17372610 | Here, we develop a model where IL-2 deficiency precipitates a breakdown of self-tolerance and progression to diabetes, and its action upon diabetogenic islet-specific CD4 T cells can be tracked. |
| 5759 | 17372610 | We find that IL-2 is not required for Aire-dependent thymic clonal deletion of high-avidity diabetogenic clones, but is essential for thymic formation of islet-specific Foxp3-expressing CD4 T cells. |
| 5760 | 17372610 | The absence of IL-2 results in the expansion of low-avidity Foxp3(-) islet-reactive CD4 T cells. |
| 5761 | 17374136 | The CXCR4/CXCL12 (SDF-1) signalling pathway protects non-obese diabetic mouse from autoimmune diabetes. |
| 5762 | 17374136 | The chemokine stromal cell-derived factor-1 CXCL-12 (SDF-1) and its ligand the CXCR4 chemokine receptor are important regulatory elements. |
| 5763 | 17374136 | CXCR4 is expressed on the surface of CD4(+) T cells, dendritic cells and B lymphocytes. |
| 5764 | 17374136 | This effect was associated with an increase of interferon (IFN)-gamma mRNA and a reduction of interleukin (IL)-4 mRNA levels both in PLNs and isolated islets. |
| 5765 | 17374136 | AMD3100 also reduced IL-4 and IL-10 production of plate-bound anti-CD3 and anti-CD28-stimulated splenocytes. |
| 5766 | 17374136 | Immunofluorescence studies indicated that AMD3100 reduced the number of CXCR4(+) and SDF-1 positive cells in the inflamed islets. |
| 5767 | 17374136 | We can conclude that the CXCL-12/CXCR4 pathway has protective effects against autoimmune diabetes. |
| 5768 | 17389382 | Previous results have shown that CD4(+)CD25(+) regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. |
| 5769 | 17389382 | This finding contrasts with a large body of work suggesting that CD4(+)CD25(high) Tregs act in a cytokine-independent manner, thus suggesting that another type of Treg is operational in this setting. |
| 5770 | 17389382 | Our present results show that a subset of foxP3(+) cells present within a CD4(+)CD25(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-beta-dependent manner, a functional property typical of "adaptive" regulatory T cells. |
| 5771 | 17389382 | Importantly, in two distinct in vivo models, these TGF-beta-dependent adaptive CD4(+)CD25(low) T cells can be induced from peripheral CD4(+)CD25(-) T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance. |
| 5772 | 17389382 | Previous results have shown that CD4(+)CD25(+) regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. |
| 5773 | 17389382 | This finding contrasts with a large body of work suggesting that CD4(+)CD25(high) Tregs act in a cytokine-independent manner, thus suggesting that another type of Treg is operational in this setting. |
| 5774 | 17389382 | Our present results show that a subset of foxP3(+) cells present within a CD4(+)CD25(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-beta-dependent manner, a functional property typical of "adaptive" regulatory T cells. |
| 5775 | 17389382 | Importantly, in two distinct in vivo models, these TGF-beta-dependent adaptive CD4(+)CD25(low) T cells can be induced from peripheral CD4(+)CD25(-) T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance. |
| 5776 | 17389382 | Previous results have shown that CD4(+)CD25(+) regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. |
| 5777 | 17389382 | This finding contrasts with a large body of work suggesting that CD4(+)CD25(high) Tregs act in a cytokine-independent manner, thus suggesting that another type of Treg is operational in this setting. |
| 5778 | 17389382 | Our present results show that a subset of foxP3(+) cells present within a CD4(+)CD25(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-beta-dependent manner, a functional property typical of "adaptive" regulatory T cells. |
| 5779 | 17389382 | Importantly, in two distinct in vivo models, these TGF-beta-dependent adaptive CD4(+)CD25(low) T cells can be induced from peripheral CD4(+)CD25(-) T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance. |
| 5780 | 17389382 | Previous results have shown that CD4(+)CD25(+) regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. |
| 5781 | 17389382 | This finding contrasts with a large body of work suggesting that CD4(+)CD25(high) Tregs act in a cytokine-independent manner, thus suggesting that another type of Treg is operational in this setting. |
| 5782 | 17389382 | Our present results show that a subset of foxP3(+) cells present within a CD4(+)CD25(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-beta-dependent manner, a functional property typical of "adaptive" regulatory T cells. |
| 5783 | 17389382 | Importantly, in two distinct in vivo models, these TGF-beta-dependent adaptive CD4(+)CD25(low) T cells can be induced from peripheral CD4(+)CD25(-) T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance. |
| 5784 | 17390713 | Increase of specific TCR Vbeta repertoires was often observed in patients with positive anti-glutamic acid decarboxylase antibody, and this tendency was more evident among CD8+ T cells than in CD4+ T cells. |
| 5785 | 17407193 | A role for the activating NK-receptor NKG2D has been indicated in several autoimmune diseases in humans and in animal models of type 1 diabetes and multiple sclerosis, and treatment with monoclonal antibodies to NKG2D attenuated disease severity in these models. |
| 5786 | 17407193 | In an adoptive transfer-induced model of colitis, we found a significantly higher frequency of CD4(+)NKG2D(+) cells in blood, mesenteric lymph nodes, colon, and spleen from colitic mice compared to BALB/c donor-mice. |
| 5787 | 17407193 | We conclude that the frequency of CD4(+)NKG2D(+) cells increase during development of experimental colitis. |
| 5788 | 17407193 | A role for the activating NK-receptor NKG2D has been indicated in several autoimmune diseases in humans and in animal models of type 1 diabetes and multiple sclerosis, and treatment with monoclonal antibodies to NKG2D attenuated disease severity in these models. |
| 5789 | 17407193 | In an adoptive transfer-induced model of colitis, we found a significantly higher frequency of CD4(+)NKG2D(+) cells in blood, mesenteric lymph nodes, colon, and spleen from colitic mice compared to BALB/c donor-mice. |
| 5790 | 17407193 | We conclude that the frequency of CD4(+)NKG2D(+) cells increase during development of experimental colitis. |
| 5791 | 17412560 | Converting antigen-specific diabetogenic CD4 and CD8 T cells to TGF-beta producing non-pathogenic regulatory cells following FoxP3 transduction. |
| 5792 | 17412560 | Regulatory activity was not limited to CD4 T cells as potent diabetogenic CD8 T cells specific for insulin, were also reduced in pathogenicity by FoxP3 induction. |
| 5793 | 17412560 | The disease suppressive effect, in both CD4 and CD8 cells, was more evident in spontaneously diabetes-prone NOD hosts (non-lymphopenic) than in lymphopenic NOD.scid hosts. |
| 5794 | 17412560 | Converting antigen-specific diabetogenic CD4 and CD8 T cells to TGF-beta producing non-pathogenic regulatory cells following FoxP3 transduction. |
| 5795 | 17412560 | Regulatory activity was not limited to CD4 T cells as potent diabetogenic CD8 T cells specific for insulin, were also reduced in pathogenicity by FoxP3 induction. |
| 5796 | 17412560 | The disease suppressive effect, in both CD4 and CD8 cells, was more evident in spontaneously diabetes-prone NOD hosts (non-lymphopenic) than in lymphopenic NOD.scid hosts. |
| 5797 | 17412560 | Converting antigen-specific diabetogenic CD4 and CD8 T cells to TGF-beta producing non-pathogenic regulatory cells following FoxP3 transduction. |
| 5798 | 17412560 | Regulatory activity was not limited to CD4 T cells as potent diabetogenic CD8 T cells specific for insulin, were also reduced in pathogenicity by FoxP3 induction. |
| 5799 | 17412560 | The disease suppressive effect, in both CD4 and CD8 cells, was more evident in spontaneously diabetes-prone NOD hosts (non-lymphopenic) than in lymphopenic NOD.scid hosts. |
| 5800 | 17428252 | Diabetes in non-obese diabetic mice is not associated with quantitative changes in CD4+ CD25+ Foxp3+ regulatory T cells. |
| 5801 | 17428252 | Although we show here that CD25+ cells delay diabetes onset in non-obese diabetic (NOD) mice, we found, in contrast to previous reports, neither an age-related decline nor a decline following onset of diabetes in the frequency of CD4+ CD25+ Foxp3+ regulatory T cells. |
| 5802 | 17428252 | Diabetes in non-obese diabetic mice is not associated with quantitative changes in CD4+ CD25+ Foxp3+ regulatory T cells. |
| 5803 | 17428252 | Although we show here that CD25+ cells delay diabetes onset in non-obese diabetic (NOD) mice, we found, in contrast to previous reports, neither an age-related decline nor a decline following onset of diabetes in the frequency of CD4+ CD25+ Foxp3+ regulatory T cells. |
| 5804 | 17430175 | The vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are two neuropeptides belonging to the VIP/secretin/glucagon family of peptides. |
| 5805 | 17430175 | In addition, VIP/PACAP reduce the expression of costimulatory molecules (particularly CD80 and CD86) on the antigen-presenting cells, and therefore reduce stimulation of antigen-specific CD4(+) T cells. |
| 5806 | 17437531 | An early age-related increase in the frequency of CD4+ Foxp3+ cells in BDC2.5NOD mice. |
| 5807 | 17438291 | A replicate linkage confirmed these positions and showed that the same region also controls clonal deviation toward the CD4(+)FoxP3(+) regulatory T cell lineage. |
| 5808 | 17446653 | An elderly patient with sarcoidosis manifesting panhypopituitarism with central diabetes insipidus. |
| 5809 | 17446653 | The presence of bilateral hilar lymphadenopathy and increased CD4/CD8 ratio in bronchoalveolar lavage fluid was diagnostic for lung sarcoidosis. |
| 5810 | 17456848 | Oral anti-CD3 mAb increased the expression of LAP on CD4(+) T-cells, and these cells could adoptively transfer protection. |
| 5811 | 17475829 | Several naturally occurring anti-insulin CD4 T cells were isolated from islet infiltrates of NOD mice. |
| 5812 | 17475849 | We examine the consequence of Ab-mediated uptake of self Ag by dendritic cells in the rat insulin promoter-membrane OVA model and identify a role for the inhibitory FcgammaRIIB in the maintenance of peripheral CD8 T cell tolerance. |
| 5813 | 17475849 | Effector differentiation of diabetogenic OT-I CD8+ T cells is enhanced in rat insulin promoter-membrane OVA mice lacking FcgammaRIIB, resulting in a high incidence of diabetes. |
| 5814 | 17475849 | In these MHC II-restricted responses, the presence of FcgammaRIIB only modestly affected initial CD4 T cell proliferative responses, suggesting that FcgammaRIIB limited effector cell differentiation primarily by inhibiting DC activation. |
| 5815 | 17483582 | Can we talk about CD4+CD28- lymphocytes as a risk factor for ischemic stroke? |
| 5816 | 17485666 | After immunizations, all animals developed an HCV-specific immune response including IFN-gamma(+), IL-2(+), CD4(+), and CD8(+) T cell and proliferative lymphocyte responses against core, E1, and E2. |
| 5817 | 17487333 | Over the past years, evidence has been gathered to suggest that the dysfunction of CD4(+)CD25(+) regulatory T (Treg) cells, and the interleukin-10 (IL10) -secreting type 1 regulatory T (Tr1) cells are associated with disease onset in diabetic patients. |
| 5818 | 17487333 | Although CD4(+)CD25(+) Treg cells develop as a distinct lineage of T cells in the thymus, results from recent studies have shown that they can also arise independently from the peripheral pool of conventional CD4(+) lymphocytes. |
| 5819 | 17487333 | These observations have led to the development of various methods to convert peripheral CD4(+) T cells into CD4(+)CD25(+) Treg and Tr1 cells in vitro or to induce the development and expansion of Treg cell subsets in vivo. |
| 5820 | 17487333 | Over the past years, evidence has been gathered to suggest that the dysfunction of CD4(+)CD25(+) regulatory T (Treg) cells, and the interleukin-10 (IL10) -secreting type 1 regulatory T (Tr1) cells are associated with disease onset in diabetic patients. |
| 5821 | 17487333 | Although CD4(+)CD25(+) Treg cells develop as a distinct lineage of T cells in the thymus, results from recent studies have shown that they can also arise independently from the peripheral pool of conventional CD4(+) lymphocytes. |
| 5822 | 17487333 | These observations have led to the development of various methods to convert peripheral CD4(+) T cells into CD4(+)CD25(+) Treg and Tr1 cells in vitro or to induce the development and expansion of Treg cell subsets in vivo. |
| 5823 | 17487333 | Over the past years, evidence has been gathered to suggest that the dysfunction of CD4(+)CD25(+) regulatory T (Treg) cells, and the interleukin-10 (IL10) -secreting type 1 regulatory T (Tr1) cells are associated with disease onset in diabetic patients. |
| 5824 | 17487333 | Although CD4(+)CD25(+) Treg cells develop as a distinct lineage of T cells in the thymus, results from recent studies have shown that they can also arise independently from the peripheral pool of conventional CD4(+) lymphocytes. |
| 5825 | 17487333 | These observations have led to the development of various methods to convert peripheral CD4(+) T cells into CD4(+)CD25(+) Treg and Tr1 cells in vitro or to induce the development and expansion of Treg cell subsets in vivo. |
| 5826 | 17491665 | CD4+ CD25+ regulatory T cells were also a focus of interest. |
| 5827 | 17491665 | Talks that I will discuss focused on the role of molecules such as GITR, Foxp3 and B7 for the development and function of regulatory T cells and the importance of these molecules in the prevention of autoimmunity. |
| 5828 | 17491665 | As well, a novel form of CTLA-4 and the use of 4-1BB co-stimulation blockade for the control of autoimmunity will be discussed. |
| 5829 | 17491676 | CD4(+)CD25(+) T cells or type 1 regulatory T cells) is currently becoming more widespread. |
| 5830 | 17491689 | Rosiglitazone is an insulin-sensitizing drug that is a ligand for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). |
| 5831 | 17491689 | Blood glucose level (BGL), serum insulin level and pancreatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and NO were measured. |
| 5832 | 17491689 | Histopathological examination and immunohistochemical determination of CD4 and CD8 T lymphocytes in the pancreatic islets were performed. |
| 5833 | 17491689 | The results showed that rosiglitazone treatment resulted in a significant decrease in the BGL and the pancreatic levels of TNF-alpha, IFN-gamma and NO compared to diabetic mice. |
| 5834 | 17491689 | The destroyed pancreatic islets were regenerated and became free from both CD4 and CD8 T cells after treatment. |
| 5835 | 17491689 | Rosiglitazone is an insulin-sensitizing drug that is a ligand for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). |
| 5836 | 17491689 | Blood glucose level (BGL), serum insulin level and pancreatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and NO were measured. |
| 5837 | 17491689 | Histopathological examination and immunohistochemical determination of CD4 and CD8 T lymphocytes in the pancreatic islets were performed. |
| 5838 | 17491689 | The results showed that rosiglitazone treatment resulted in a significant decrease in the BGL and the pancreatic levels of TNF-alpha, IFN-gamma and NO compared to diabetic mice. |
| 5839 | 17491689 | The destroyed pancreatic islets were regenerated and became free from both CD4 and CD8 T cells after treatment. |
| 5840 | 17507865 | [The significance of regulatory CD4+CD25+ T cells in the pathogenesis and treatment of kidney disease]. |
| 5841 | 17507865 | This paper presents the latest knowledge concerning the occurrence of natural regulatory T cells of CD4+CD25+ phenotype and their role in the pathogeneses of immune system diseases. |
| 5842 | 17507865 | [The significance of regulatory CD4+CD25+ T cells in the pathogenesis and treatment of kidney disease]. |
| 5843 | 17507865 | This paper presents the latest knowledge concerning the occurrence of natural regulatory T cells of CD4+CD25+ phenotype and their role in the pathogeneses of immune system diseases. |
| 5844 | 17513748 | In this study, we report that the cytopiloyne from B. pilosa, which is structurally different from the above-mentioned polyacetylenes and inhibits CD4(+) T cell proliferation, effectively prevents the development of diabetes in nonobese diabetic mice as evidenced by a normal level of blood glucose and insulin and normal pancreatic islet architecture. |
| 5845 | 17513748 | Coculture assays imply that this decrease in CD4(+) T cells involves the Fas ligand/Fas pathway. |
| 5846 | 17513748 | In this study, we report that the cytopiloyne from B. pilosa, which is structurally different from the above-mentioned polyacetylenes and inhibits CD4(+) T cell proliferation, effectively prevents the development of diabetes in nonobese diabetic mice as evidenced by a normal level of blood glucose and insulin and normal pancreatic islet architecture. |
| 5847 | 17513748 | Coculture assays imply that this decrease in CD4(+) T cells involves the Fas ligand/Fas pathway. |
| 5848 | 17513752 | The TCR repertoires of Tconv and Treg cells were equally broad, were distinct, yet overlapped significantly, representing a less strict partition than previously seen between CD4 and CD8 T cells. |
| 5849 | 17517665 | This effect was associated with a recruitment of Foxp3(+) CD4 T cells around islets. |
| 5850 | 17534268 | Foxp3-transduced CD4(+)T-cells have been used for treating autoimmune diseases such as type I diabetes. |
| 5851 | 17534268 | We designed and tested a new strategy that involves converting pathogenic CD4(+)Th1 cells into regulatory T-cells by lentiviral transduction with Foxp3 under the control of interferon-gamma (IFN-gamma) promoter (IgammaP-Foxp3). |
| 5852 | 17534268 | Foxp3-transduced CD4(+)T-cells have been used for treating autoimmune diseases such as type I diabetes. |
| 5853 | 17534268 | We designed and tested a new strategy that involves converting pathogenic CD4(+)Th1 cells into regulatory T-cells by lentiviral transduction with Foxp3 under the control of interferon-gamma (IFN-gamma) promoter (IgammaP-Foxp3). |
| 5854 | 17546295 | Effects on CD4+ and CD8+ lymphocytes. |
| 5855 | 17565417 | Islet antigens are presented by human leukocyte antigen (HLA) class I and II molecules and are recognized by CD8(+) and CD4(+) autoreactive T cells in type 1 diabetic individuals. |
| 5856 | 17568845 | No significant changes were observed in the serum levels of creatine phosphokinase, hepatic enzymes, CD4+, CD8+ and viral load. |
| 5857 | 17590177 | The non-obese diabetic (NOD) mouse develops insulin-dependent diabetes mellitus (IDDM) spontaneously as a consequence of an autoimmune process that leads to destruction of the insulin-producing beta cells of the pancreas. |
| 5858 | 17590177 | IDDM is characterized by increased T helper 1 (Th1) cell responses toward several autoantigens, including Hsp60, glutamic acid decarboxylase and insulin. |
| 5859 | 17590177 | This change included reduction of CD4(+) and CD8(+) T cells infiltration, appearance of CD25(+) cells influx and an increased staining for interleukin (IL)-10 in the islets. |
| 5860 | 17607359 | Additionally, CD4(+) T cells from B16:A-dKO mice immunized with native insulin B:9-23 peptide promoted IAAs in NOD/SCID mice. |
| 5861 | 17615584 | The diabetogenic, insulin-specific CD8 T cell response primed in the experimental autoimmune diabetes model in RIP-B7.1 mice. |
| 5862 | 17615584 | EAD induction critically depends on CD8 T cells and is independent of CD4 T cells. |
| 5863 | 17615584 | To be diabetogenic, ppins-specific CD8 T cells had to express IFN-gamma. |
| 5864 | 17615584 | Neither expression of perforin nor signaling through the type I IFN receptor is an essential component of this pathogenic CD8 T cell phenotype. |
| 5865 | 17615584 | Diabetogenic CD8 T cells specifically recognize the Kb-restricted A12-21 epitope of the insulin A-chain. |
| 5866 | 17627890 | The PD-1-PDL1 pathway plays a critical role in regulating autoimmune diabetes as blockade or deficiency of PD-1 or PDL1 results in accelerated disease in NOD mice. |
| 5867 | 17627890 | Administration of blocking anti-PDL1 antibody to CD4+ T cell-deficient, CD8+ T cell-deficient and B cell-deficient mice demonstrated that PDL1-mediated regulation of autoreactive CD4+ and CD8+ T cells is critical for diabetes development. |
| 5868 | 17627890 | This concept was confirmed by adoptive transfer studies utilizing lymphocytes from BDC2.5 and 4.1 (CD4+) TCR transgenic mice and 8.3 (CD8+) TCR transgenic mice; efforts showing increased proliferation of both CD4+ and CD8+ T cells following PDL1 blockade in vivo. |
| 5869 | 17627890 | These data provide strong evidence that PDL1 regulates autoimmune diabetes by limiting the expansion of CD4+ and CD8+ autoreactive T cells, and define the timing and locale of PDL1-mediated regulation of type 1 diabetes. |
| 5870 | 17627890 | The PD-1-PDL1 pathway plays a critical role in regulating autoimmune diabetes as blockade or deficiency of PD-1 or PDL1 results in accelerated disease in NOD mice. |
| 5871 | 17627890 | Administration of blocking anti-PDL1 antibody to CD4+ T cell-deficient, CD8+ T cell-deficient and B cell-deficient mice demonstrated that PDL1-mediated regulation of autoreactive CD4+ and CD8+ T cells is critical for diabetes development. |
| 5872 | 17627890 | This concept was confirmed by adoptive transfer studies utilizing lymphocytes from BDC2.5 and 4.1 (CD4+) TCR transgenic mice and 8.3 (CD8+) TCR transgenic mice; efforts showing increased proliferation of both CD4+ and CD8+ T cells following PDL1 blockade in vivo. |
| 5873 | 17627890 | These data provide strong evidence that PDL1 regulates autoimmune diabetes by limiting the expansion of CD4+ and CD8+ autoreactive T cells, and define the timing and locale of PDL1-mediated regulation of type 1 diabetes. |
| 5874 | 17627890 | The PD-1-PDL1 pathway plays a critical role in regulating autoimmune diabetes as blockade or deficiency of PD-1 or PDL1 results in accelerated disease in NOD mice. |
| 5875 | 17627890 | Administration of blocking anti-PDL1 antibody to CD4+ T cell-deficient, CD8+ T cell-deficient and B cell-deficient mice demonstrated that PDL1-mediated regulation of autoreactive CD4+ and CD8+ T cells is critical for diabetes development. |
| 5876 | 17627890 | This concept was confirmed by adoptive transfer studies utilizing lymphocytes from BDC2.5 and 4.1 (CD4+) TCR transgenic mice and 8.3 (CD8+) TCR transgenic mice; efforts showing increased proliferation of both CD4+ and CD8+ T cells following PDL1 blockade in vivo. |
| 5877 | 17627890 | These data provide strong evidence that PDL1 regulates autoimmune diabetes by limiting the expansion of CD4+ and CD8+ autoreactive T cells, and define the timing and locale of PDL1-mediated regulation of type 1 diabetes. |
| 5878 | 17675466 | Insulin peptide B:9-23 is a major autoantigen in type 1 diabetes that contains two distinct CD4 epitopes (B:9-16 and B:13-23). |
| 5879 | 17675466 | In this study, we report that the elimination of the CTL epitope from the B:9-23 peptide by amino acid substitution (with alanine) at positions B:16 and 19 (A16,19 altered peptide ligand) or truncation of the C-terminal amino acids from the peptide (B:9-21), neither of which stimulated the proliferation of insulin B:15-23 reactive CD8 T cells, provided significant intranasally induced suppression of diabetes when coadministered with a potent mucosal adjuvant cholera toxin (CT). |
| 5880 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 5881 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 5882 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 5883 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 5884 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 5885 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 5886 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 5887 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 5888 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 5889 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 5890 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 5891 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 5892 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 5893 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 5894 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 5895 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 5896 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 5897 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 5898 | 17709886 | While some progress has been made towards these goals, additional investigations are needed to address the aforementioned knowledge voids including the role for regulatory T cells (Treg), defined by their co-expression of CD4 and CD25 as well as the transcription factor FOXP3, in the pathogenesis and natural history of type 1 diabetes. |
| 5899 | 17716860 | Our data indicate that NOD derived FTOC produce a smaller percentage of double negative (CD4(-)/CD8(-)) thymocytes expressing TNF receptors compared to non-diabetic C57BL/6 (B6) derived FTOC. |
| 5900 | 17716860 | Neutralization of this endogenous TNF-alpha production in NOD derived FTOC with soluble TNF receptor (sTNF R1) rescued insulin production in our in vitro T1DM model. |
| 5901 | 17724131 | Yet conversion of mature conventional CD4(+) T (T conv) cell lymphocytes can be achieved in several conditions, such as transforming growth factor beta treatment, homeostatic expansion, or chronic exposure to low-dose antigen. |
| 5902 | 17785799 | Granulocyte-macrophage colony-stimulating factor prevents diabetes development in NOD mice by inducing tolerogenic dendritic cells that sustain the suppressive function of CD4+CD25+ regulatory T cells. |
| 5903 | 17785799 | The protection was associated with a marked increase in the number of tolerogenic immature splenic DCs and in the number of Foxp3+CD4+CD25+ regulatory T cells (Tregs). |
| 5904 | 17785799 | Activated DCs from GM-CSF-protected mice expressed lower levels of MHC class II and CD80/CD86 molecules, produced more IL-10 and were less effective in stimulating diabetogenic CD8+ T cells than DCs of PBS-treated NOD mice. |
| 5905 | 17785799 | Depletion of CD11c+ DCs before transfer released diabetogenic T cells from the suppressive effect of CD4+CD25+ Tregs, thereby promoting the development of diabetes. |
| 5906 | 17785799 | These results indicated that semimature DCs were required for the sustained suppressive function of CD4+CD25+ Tregs that were responsible for maintaining tolerance of diabetogenic T cells in NOD mice. |
| 5907 | 17785799 | Granulocyte-macrophage colony-stimulating factor prevents diabetes development in NOD mice by inducing tolerogenic dendritic cells that sustain the suppressive function of CD4+CD25+ regulatory T cells. |
| 5908 | 17785799 | The protection was associated with a marked increase in the number of tolerogenic immature splenic DCs and in the number of Foxp3+CD4+CD25+ regulatory T cells (Tregs). |
| 5909 | 17785799 | Activated DCs from GM-CSF-protected mice expressed lower levels of MHC class II and CD80/CD86 molecules, produced more IL-10 and were less effective in stimulating diabetogenic CD8+ T cells than DCs of PBS-treated NOD mice. |
| 5910 | 17785799 | Depletion of CD11c+ DCs before transfer released diabetogenic T cells from the suppressive effect of CD4+CD25+ Tregs, thereby promoting the development of diabetes. |
| 5911 | 17785799 | These results indicated that semimature DCs were required for the sustained suppressive function of CD4+CD25+ Tregs that were responsible for maintaining tolerance of diabetogenic T cells in NOD mice. |
| 5912 | 17785799 | Granulocyte-macrophage colony-stimulating factor prevents diabetes development in NOD mice by inducing tolerogenic dendritic cells that sustain the suppressive function of CD4+CD25+ regulatory T cells. |
| 5913 | 17785799 | The protection was associated with a marked increase in the number of tolerogenic immature splenic DCs and in the number of Foxp3+CD4+CD25+ regulatory T cells (Tregs). |
| 5914 | 17785799 | Activated DCs from GM-CSF-protected mice expressed lower levels of MHC class II and CD80/CD86 molecules, produced more IL-10 and were less effective in stimulating diabetogenic CD8+ T cells than DCs of PBS-treated NOD mice. |
| 5915 | 17785799 | Depletion of CD11c+ DCs before transfer released diabetogenic T cells from the suppressive effect of CD4+CD25+ Tregs, thereby promoting the development of diabetes. |
| 5916 | 17785799 | These results indicated that semimature DCs were required for the sustained suppressive function of CD4+CD25+ Tregs that were responsible for maintaining tolerance of diabetogenic T cells in NOD mice. |
| 5917 | 17785799 | Granulocyte-macrophage colony-stimulating factor prevents diabetes development in NOD mice by inducing tolerogenic dendritic cells that sustain the suppressive function of CD4+CD25+ regulatory T cells. |
| 5918 | 17785799 | The protection was associated with a marked increase in the number of tolerogenic immature splenic DCs and in the number of Foxp3+CD4+CD25+ regulatory T cells (Tregs). |
| 5919 | 17785799 | Activated DCs from GM-CSF-protected mice expressed lower levels of MHC class II and CD80/CD86 molecules, produced more IL-10 and were less effective in stimulating diabetogenic CD8+ T cells than DCs of PBS-treated NOD mice. |
| 5920 | 17785799 | Depletion of CD11c+ DCs before transfer released diabetogenic T cells from the suppressive effect of CD4+CD25+ Tregs, thereby promoting the development of diabetes. |
| 5921 | 17785799 | These results indicated that semimature DCs were required for the sustained suppressive function of CD4+CD25+ Tregs that were responsible for maintaining tolerance of diabetogenic T cells in NOD mice. |
| 5922 | 17785827 | The Idd6 locus on mouse chromosome 6, which controls the development of type 1 diabetes in the NOD mouse, affects proliferation rates of T cells and the activity of regulatory CD4+CD25+ T cells. |
| 5923 | 17785827 | This phenotype correlates with a diminished proliferation capacity of both CD4+CD25- effector and CD4+CD25+ regulatory T cells upon in vitro stimulation of the TLR1/TLR2 pathway by the ligand palmitoyl-3-cysteine-serine-lysine 4, and with the constitutive down-regulation of Tnf-alpha and IL-6 in macrophages of Idd6- congenic mice. |
| 5924 | 17785827 | The Idd6 locus on mouse chromosome 6, which controls the development of type 1 diabetes in the NOD mouse, affects proliferation rates of T cells and the activity of regulatory CD4+CD25+ T cells. |
| 5925 | 17785827 | This phenotype correlates with a diminished proliferation capacity of both CD4+CD25- effector and CD4+CD25+ regulatory T cells upon in vitro stimulation of the TLR1/TLR2 pathway by the ligand palmitoyl-3-cysteine-serine-lysine 4, and with the constitutive down-regulation of Tnf-alpha and IL-6 in macrophages of Idd6- congenic mice. |
| 5926 | 17804564 | Circulating CD4+CD25 high regulatory T cells and natural killer T cells in children with newly diagnosed type 1 diabetes or with diabetes-associated autoantibodies. |
| 5927 | 17804564 | We used flow cytometry to analyze the proportion of CD4(+)CD25(high) regulatory T cells and natural killer T (NKT) cells in peripheral blood obtained from 25 children with newly diagnosed type 1 diabetes, 21 nondiabetic subjects positive for two or more diabetes-associated autoantibodies, and from 39 autoantibody-negative age- and HLA-matched control subjects. |
| 5928 | 17804564 | CD4(+)CD25(high) T cells were also stained for additional markers HLA-DR, CD69, and CD62L. |
| 5929 | 17804564 | The frequency of CD4(+)CD25(high)HLA-DR(-) T cells was significantly higher in multiple autoantibody-positive children than in controls (P = 0.021). |
| 5930 | 17804564 | We also detected a significantly higher level of CD4(+)CD25(high)HLA-DR(-) and CD4(+)CD25(high)CD69(-) T cells among children expressing three to four autoantibodies when compared to the controls (P = 0.004 and P = 0.048, respectively). |
| 5931 | 17804564 | Circulating CD4+CD25 high regulatory T cells and natural killer T cells in children with newly diagnosed type 1 diabetes or with diabetes-associated autoantibodies. |
| 5932 | 17804564 | We used flow cytometry to analyze the proportion of CD4(+)CD25(high) regulatory T cells and natural killer T (NKT) cells in peripheral blood obtained from 25 children with newly diagnosed type 1 diabetes, 21 nondiabetic subjects positive for two or more diabetes-associated autoantibodies, and from 39 autoantibody-negative age- and HLA-matched control subjects. |
| 5933 | 17804564 | CD4(+)CD25(high) T cells were also stained for additional markers HLA-DR, CD69, and CD62L. |
| 5934 | 17804564 | The frequency of CD4(+)CD25(high)HLA-DR(-) T cells was significantly higher in multiple autoantibody-positive children than in controls (P = 0.021). |
| 5935 | 17804564 | We also detected a significantly higher level of CD4(+)CD25(high)HLA-DR(-) and CD4(+)CD25(high)CD69(-) T cells among children expressing three to four autoantibodies when compared to the controls (P = 0.004 and P = 0.048, respectively). |
| 5936 | 17804564 | Circulating CD4+CD25 high regulatory T cells and natural killer T cells in children with newly diagnosed type 1 diabetes or with diabetes-associated autoantibodies. |
| 5937 | 17804564 | We used flow cytometry to analyze the proportion of CD4(+)CD25(high) regulatory T cells and natural killer T (NKT) cells in peripheral blood obtained from 25 children with newly diagnosed type 1 diabetes, 21 nondiabetic subjects positive for two or more diabetes-associated autoantibodies, and from 39 autoantibody-negative age- and HLA-matched control subjects. |
| 5938 | 17804564 | CD4(+)CD25(high) T cells were also stained for additional markers HLA-DR, CD69, and CD62L. |
| 5939 | 17804564 | The frequency of CD4(+)CD25(high)HLA-DR(-) T cells was significantly higher in multiple autoantibody-positive children than in controls (P = 0.021). |
| 5940 | 17804564 | We also detected a significantly higher level of CD4(+)CD25(high)HLA-DR(-) and CD4(+)CD25(high)CD69(-) T cells among children expressing three to four autoantibodies when compared to the controls (P = 0.004 and P = 0.048, respectively). |
| 5941 | 17804564 | Circulating CD4+CD25 high regulatory T cells and natural killer T cells in children with newly diagnosed type 1 diabetes or with diabetes-associated autoantibodies. |
| 5942 | 17804564 | We used flow cytometry to analyze the proportion of CD4(+)CD25(high) regulatory T cells and natural killer T (NKT) cells in peripheral blood obtained from 25 children with newly diagnosed type 1 diabetes, 21 nondiabetic subjects positive for two or more diabetes-associated autoantibodies, and from 39 autoantibody-negative age- and HLA-matched control subjects. |
| 5943 | 17804564 | CD4(+)CD25(high) T cells were also stained for additional markers HLA-DR, CD69, and CD62L. |
| 5944 | 17804564 | The frequency of CD4(+)CD25(high)HLA-DR(-) T cells was significantly higher in multiple autoantibody-positive children than in controls (P = 0.021). |
| 5945 | 17804564 | We also detected a significantly higher level of CD4(+)CD25(high)HLA-DR(-) and CD4(+)CD25(high)CD69(-) T cells among children expressing three to four autoantibodies when compared to the controls (P = 0.004 and P = 0.048, respectively). |
| 5946 | 17804564 | Circulating CD4+CD25 high regulatory T cells and natural killer T cells in children with newly diagnosed type 1 diabetes or with diabetes-associated autoantibodies. |
| 5947 | 17804564 | We used flow cytometry to analyze the proportion of CD4(+)CD25(high) regulatory T cells and natural killer T (NKT) cells in peripheral blood obtained from 25 children with newly diagnosed type 1 diabetes, 21 nondiabetic subjects positive for two or more diabetes-associated autoantibodies, and from 39 autoantibody-negative age- and HLA-matched control subjects. |
| 5948 | 17804564 | CD4(+)CD25(high) T cells were also stained for additional markers HLA-DR, CD69, and CD62L. |
| 5949 | 17804564 | The frequency of CD4(+)CD25(high)HLA-DR(-) T cells was significantly higher in multiple autoantibody-positive children than in controls (P = 0.021). |
| 5950 | 17804564 | We also detected a significantly higher level of CD4(+)CD25(high)HLA-DR(-) and CD4(+)CD25(high)CD69(-) T cells among children expressing three to four autoantibodies when compared to the controls (P = 0.004 and P = 0.048, respectively). |
| 5951 | 17823690 | Various experimental studies have shown that human DC subsets are involved in the induction of anergy in T cells and in the differentiation of conventional CD4(+) and CD8(+) lymphocytes into the respective subtypes of Treg cells. |
| 5952 | 17876100 | In both cases, macrophages, dendritic cells, CD4+, CD8+, and B cells are present in the diseased islets. |
| 5953 | 17881563 | In this system, DC activation by CD40 engagement indeed extended their ability to present antigen to CD4(+) T cells in vivo, although different results were obtained with antigen delivered to DCs by means of endocytosis from the cell surface. |
| 5954 | 17891462 | Pancreata from female NOD mice at diagnosis and at 1, 2, 3 and 4 weeks thereafter were analysed immunohistochemically for insulin, glucagon and somatostatin cells and glucose transporter-2 (glut2) and correlated with the degree of insulitis and islet immune cell phenotypes. |
| 5955 | 17891462 | During this period, beta cells also declined sharply whereas glucagon and somatostatin cells increased, with occasional islet cells co-expressing insulin and glucagon. |
| 5956 | 17891462 | Glut2 was absent in insulin-containing cells from 1 week onwards. |
| 5957 | 17891462 | CD4 and CD8 T cells and macrophages persisted until 4 weeks, in islets with residual beta cells or extensive insulitis. |
| 5958 | 17947648 | Recruitment and activation of macrophages by pathogenic CD4 T cells in type 1 diabetes: evidence for involvement of CCR8 and CCL1. |
| 5959 | 17947648 | Adoptive transfer of diabetogenic CD4 Th1 T cell clones into young NOD or NOD.scid recipients rapidly induces onset of diabetes and also provides a system for analysis of the pancreatic infiltrate. |
| 5960 | 17947648 | Analysis of infiltrating cells after adoptive transfer by the diabetogenic T cell clone BDC-2.5 indicates that large numbers of cells staining for both F4/80 and CD11b are recruited into the pancreas where they are activated to make IL-1beta, TNF-alpha, and NO, and express the chemokine receptors CCR5, CXCR3, and CCR8. |
| 5961 | 17947648 | Diabetogenic CD4 T cell clones produce several inflammatory chemokines in vitro, but after adoptive transfer we found that the only chemokine that could be detected ex vivo was CCL1. |
| 5962 | 17947648 | These results provide the first evidence that CCR8/CCL1 interaction may play a role in type 1 diabetes through macrophage recruitment and activation. |
| 5963 | 17947648 | Recruitment and activation of macrophages by pathogenic CD4 T cells in type 1 diabetes: evidence for involvement of CCR8 and CCL1. |
| 5964 | 17947648 | Adoptive transfer of diabetogenic CD4 Th1 T cell clones into young NOD or NOD.scid recipients rapidly induces onset of diabetes and also provides a system for analysis of the pancreatic infiltrate. |
| 5965 | 17947648 | Analysis of infiltrating cells after adoptive transfer by the diabetogenic T cell clone BDC-2.5 indicates that large numbers of cells staining for both F4/80 and CD11b are recruited into the pancreas where they are activated to make IL-1beta, TNF-alpha, and NO, and express the chemokine receptors CCR5, CXCR3, and CCR8. |
| 5966 | 17947648 | Diabetogenic CD4 T cell clones produce several inflammatory chemokines in vitro, but after adoptive transfer we found that the only chemokine that could be detected ex vivo was CCL1. |
| 5967 | 17947648 | These results provide the first evidence that CCR8/CCL1 interaction may play a role in type 1 diabetes through macrophage recruitment and activation. |
| 5968 | 17947648 | Recruitment and activation of macrophages by pathogenic CD4 T cells in type 1 diabetes: evidence for involvement of CCR8 and CCL1. |
| 5969 | 17947648 | Adoptive transfer of diabetogenic CD4 Th1 T cell clones into young NOD or NOD.scid recipients rapidly induces onset of diabetes and also provides a system for analysis of the pancreatic infiltrate. |
| 5970 | 17947648 | Analysis of infiltrating cells after adoptive transfer by the diabetogenic T cell clone BDC-2.5 indicates that large numbers of cells staining for both F4/80 and CD11b are recruited into the pancreas where they are activated to make IL-1beta, TNF-alpha, and NO, and express the chemokine receptors CCR5, CXCR3, and CCR8. |
| 5971 | 17947648 | Diabetogenic CD4 T cell clones produce several inflammatory chemokines in vitro, but after adoptive transfer we found that the only chemokine that could be detected ex vivo was CCL1. |
| 5972 | 17947648 | These results provide the first evidence that CCR8/CCL1 interaction may play a role in type 1 diabetes through macrophage recruitment and activation. |
| 5973 | 17947651 | In this study, a CSFE dilution assay was used to detect glutamic acid decarboxylase 65 (GAD65)- and insulin-responsive T cells and HLA-0201*-GAD65(114-122) pentamers were used to detect CD8(+) GAD-responsive T cells in memory CD45RO(+) and naive CD45RO(-) cell populations from patients with type 1 diabetes and healthy control subjects. |
| 5974 | 17947651 | CD4(+) and CD8(+) T cells specific for GAD65 and insulin were present in patients with type 1 diabetes and control subjects. |
| 5975 | 17947651 | Within the naive CD45RO(-) cells, CD4(+) and CD8(+) T cell responses were similar between patients and controls. |
| 5976 | 17947651 | Within the memory CD45RO(+) cells, CD4(+) T cell responses against whole GAD65 and insulin and HLA-0201*-GAD65(114-122) pentamer-positive CD8(+) T cells were found in patients with type 1 diabetes, but not in control subjects (p < 0.05 for all). |
| 5977 | 17947651 | In this study, a CSFE dilution assay was used to detect glutamic acid decarboxylase 65 (GAD65)- and insulin-responsive T cells and HLA-0201*-GAD65(114-122) pentamers were used to detect CD8(+) GAD-responsive T cells in memory CD45RO(+) and naive CD45RO(-) cell populations from patients with type 1 diabetes and healthy control subjects. |
| 5978 | 17947651 | CD4(+) and CD8(+) T cells specific for GAD65 and insulin were present in patients with type 1 diabetes and control subjects. |
| 5979 | 17947651 | Within the naive CD45RO(-) cells, CD4(+) and CD8(+) T cell responses were similar between patients and controls. |
| 5980 | 17947651 | Within the memory CD45RO(+) cells, CD4(+) T cell responses against whole GAD65 and insulin and HLA-0201*-GAD65(114-122) pentamer-positive CD8(+) T cells were found in patients with type 1 diabetes, but not in control subjects (p < 0.05 for all). |
| 5981 | 17947651 | In this study, a CSFE dilution assay was used to detect glutamic acid decarboxylase 65 (GAD65)- and insulin-responsive T cells and HLA-0201*-GAD65(114-122) pentamers were used to detect CD8(+) GAD-responsive T cells in memory CD45RO(+) and naive CD45RO(-) cell populations from patients with type 1 diabetes and healthy control subjects. |
| 5982 | 17947651 | CD4(+) and CD8(+) T cells specific for GAD65 and insulin were present in patients with type 1 diabetes and control subjects. |
| 5983 | 17947651 | Within the naive CD45RO(-) cells, CD4(+) and CD8(+) T cell responses were similar between patients and controls. |
| 5984 | 17947651 | Within the memory CD45RO(+) cells, CD4(+) T cell responses against whole GAD65 and insulin and HLA-0201*-GAD65(114-122) pentamer-positive CD8(+) T cells were found in patients with type 1 diabetes, but not in control subjects (p < 0.05 for all). |
| 5985 | 17947667 | CD86 has sustained costimulatory effects on CD8 T cells. |
| 5986 | 17947667 | CD80 and CD86 both costimulate T cell activation. |
| 5987 | 17947667 | We have studied mice expressing rat insulin promoter (RIP)-CD80 and RIP-CD86 on the NOD and NOD.scid genetic background to generate in vivo models, using diabetes as a readout for cytotoxic T cell activation. |
| 5988 | 17947667 | However, the secondary in vivo response was maintained if T cells were activated through CD86 costimulation compared with CD80. |
| 5989 | 17947667 | In vitro, CD80 costimulation enhanced cytotoxicity, proliferation, and cytokine secretion in activated CD8 T cells compared with CD86 costimulation. |
| 5990 | 17947667 | We demonstrated increased CTLA-4 and programmed death-1 inhibitory molecule expression following costimulation by both CD80 and CD86 (CD80 > CD86). |
| 5991 | 17947667 | Furthermore, T cells stimulated by CD80 were more susceptible to inhibition by CD4(+)CD25(+) T cells. |
| 5992 | 17947667 | Overall, while CD86 does not stimulate an initial response as strongly as CD80, there is greater sustained activity that is seen even in the absence of continued costimulation. |
| 5993 | 17949947 | The source of TcR was a CD4(+) T(H)1(+) T-cell clone which responded to an immunodominant epitope of the human islet protein GAD65, an epitope shared with both GAD65 and GAD67 in the mouse. |
| 5994 | 17949947 | The resulting HLA-DR4/GAD-TcR transgenic mice on a Rag2(o/o)/I-Ab(o/o)/B6 background exhibited a CD4(+) infiltrate into pancreatic islets that correlated with a loss of insulin in infiltrated islets. |
| 5995 | 17949947 | T cells containing the GAD65/67 (555-567) responsive TcR undergo strong negative selection as evidenced by a 10-fold lower thymocyte cellularity compared to non-TcR transgenic mice, and clonotype peripheral T cells represented approximately 1% of CD4(+) T cells in Rag2 sufficient mice. |
| 5996 | 17949947 | Upon in vitro stimulation, GAD65/67 555-567 responsive T cells secrete interferon-gamma, minimal interleukin (IL)-2 and tumor necrosis factor-alpha, and no IL-4, IL-5, IL-10, or IL-17, consistent with a T(H)1 profile. |
| 5997 | 17949947 | These data demonstrate that CD4(+) T cells specific for a naturally processed epitope within GAD can specifically home to pancreatic islets and lead to impaired islet beta-cell function in diabetes-associated HLA-DR4 transgenic mice on the relatively non-autoimmune C57BL/6 background. |
| 5998 | 17949947 | The source of TcR was a CD4(+) T(H)1(+) T-cell clone which responded to an immunodominant epitope of the human islet protein GAD65, an epitope shared with both GAD65 and GAD67 in the mouse. |
| 5999 | 17949947 | The resulting HLA-DR4/GAD-TcR transgenic mice on a Rag2(o/o)/I-Ab(o/o)/B6 background exhibited a CD4(+) infiltrate into pancreatic islets that correlated with a loss of insulin in infiltrated islets. |
| 6000 | 17949947 | T cells containing the GAD65/67 (555-567) responsive TcR undergo strong negative selection as evidenced by a 10-fold lower thymocyte cellularity compared to non-TcR transgenic mice, and clonotype peripheral T cells represented approximately 1% of CD4(+) T cells in Rag2 sufficient mice. |
| 6001 | 17949947 | Upon in vitro stimulation, GAD65/67 555-567 responsive T cells secrete interferon-gamma, minimal interleukin (IL)-2 and tumor necrosis factor-alpha, and no IL-4, IL-5, IL-10, or IL-17, consistent with a T(H)1 profile. |
| 6002 | 17949947 | These data demonstrate that CD4(+) T cells specific for a naturally processed epitope within GAD can specifically home to pancreatic islets and lead to impaired islet beta-cell function in diabetes-associated HLA-DR4 transgenic mice on the relatively non-autoimmune C57BL/6 background. |
| 6003 | 17949947 | The source of TcR was a CD4(+) T(H)1(+) T-cell clone which responded to an immunodominant epitope of the human islet protein GAD65, an epitope shared with both GAD65 and GAD67 in the mouse. |
| 6004 | 17949947 | The resulting HLA-DR4/GAD-TcR transgenic mice on a Rag2(o/o)/I-Ab(o/o)/B6 background exhibited a CD4(+) infiltrate into pancreatic islets that correlated with a loss of insulin in infiltrated islets. |
| 6005 | 17949947 | T cells containing the GAD65/67 (555-567) responsive TcR undergo strong negative selection as evidenced by a 10-fold lower thymocyte cellularity compared to non-TcR transgenic mice, and clonotype peripheral T cells represented approximately 1% of CD4(+) T cells in Rag2 sufficient mice. |
| 6006 | 17949947 | Upon in vitro stimulation, GAD65/67 555-567 responsive T cells secrete interferon-gamma, minimal interleukin (IL)-2 and tumor necrosis factor-alpha, and no IL-4, IL-5, IL-10, or IL-17, consistent with a T(H)1 profile. |
| 6007 | 17949947 | These data demonstrate that CD4(+) T cells specific for a naturally processed epitope within GAD can specifically home to pancreatic islets and lead to impaired islet beta-cell function in diabetes-associated HLA-DR4 transgenic mice on the relatively non-autoimmune C57BL/6 background. |
| 6008 | 17949947 | The source of TcR was a CD4(+) T(H)1(+) T-cell clone which responded to an immunodominant epitope of the human islet protein GAD65, an epitope shared with both GAD65 and GAD67 in the mouse. |
| 6009 | 17949947 | The resulting HLA-DR4/GAD-TcR transgenic mice on a Rag2(o/o)/I-Ab(o/o)/B6 background exhibited a CD4(+) infiltrate into pancreatic islets that correlated with a loss of insulin in infiltrated islets. |
| 6010 | 17949947 | T cells containing the GAD65/67 (555-567) responsive TcR undergo strong negative selection as evidenced by a 10-fold lower thymocyte cellularity compared to non-TcR transgenic mice, and clonotype peripheral T cells represented approximately 1% of CD4(+) T cells in Rag2 sufficient mice. |
| 6011 | 17949947 | Upon in vitro stimulation, GAD65/67 555-567 responsive T cells secrete interferon-gamma, minimal interleukin (IL)-2 and tumor necrosis factor-alpha, and no IL-4, IL-5, IL-10, or IL-17, consistent with a T(H)1 profile. |
| 6012 | 17949947 | These data demonstrate that CD4(+) T cells specific for a naturally processed epitope within GAD can specifically home to pancreatic islets and lead to impaired islet beta-cell function in diabetes-associated HLA-DR4 transgenic mice on the relatively non-autoimmune C57BL/6 background. |
| 6013 | 17959356 | Because the vitamin D receptor is expressed on CD4+T cells and is known to affect cytokine responses, several groups have investigated the association between the vitamin D receptor gene BsmI polymorphism and type 1 diabetes. |
| 6014 | 17966038 | Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. |
| 6015 | 17966038 | We describe how CD4+ or CD8+T cells can contribute differentially to the pathogenesis of T1D using the HLA-DQ8 transgenic mouse models. |
| 6016 | 17966038 | HLA-DQ8 transgenic mice expressing the costimulatory molecule, B7.1 (RIP.B7.1), or the proinflammatory cytokine, TNF-alpha (RIP.TNF) or both (RIP.B7.RIP.TNF) under the control of rat insulin promoter (RIP) were used. |
| 6017 | 17966038 | In the RIP-B7.RIP-TNF double transgenic mouse model, either CD4+ or CD8+T cells were sufficient to precipitate diabetes in 100% of the animals. |
| 6018 | 17966038 | Thus, the relative roles of CD4+ or CD8+T cells in the pathogenesis of T1D are possibly determined by the local inflammatory stimuli. |
| 6019 | 17966038 | Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. |
| 6020 | 17966038 | We describe how CD4+ or CD8+T cells can contribute differentially to the pathogenesis of T1D using the HLA-DQ8 transgenic mouse models. |
| 6021 | 17966038 | HLA-DQ8 transgenic mice expressing the costimulatory molecule, B7.1 (RIP.B7.1), or the proinflammatory cytokine, TNF-alpha (RIP.TNF) or both (RIP.B7.RIP.TNF) under the control of rat insulin promoter (RIP) were used. |
| 6022 | 17966038 | In the RIP-B7.RIP-TNF double transgenic mouse model, either CD4+ or CD8+T cells were sufficient to precipitate diabetes in 100% of the animals. |
| 6023 | 17966038 | Thus, the relative roles of CD4+ or CD8+T cells in the pathogenesis of T1D are possibly determined by the local inflammatory stimuli. |
| 6024 | 17966038 | Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. |
| 6025 | 17966038 | We describe how CD4+ or CD8+T cells can contribute differentially to the pathogenesis of T1D using the HLA-DQ8 transgenic mouse models. |
| 6026 | 17966038 | HLA-DQ8 transgenic mice expressing the costimulatory molecule, B7.1 (RIP.B7.1), or the proinflammatory cytokine, TNF-alpha (RIP.TNF) or both (RIP.B7.RIP.TNF) under the control of rat insulin promoter (RIP) were used. |
| 6027 | 17966038 | In the RIP-B7.RIP-TNF double transgenic mouse model, either CD4+ or CD8+T cells were sufficient to precipitate diabetes in 100% of the animals. |
| 6028 | 17966038 | Thus, the relative roles of CD4+ or CD8+T cells in the pathogenesis of T1D are possibly determined by the local inflammatory stimuli. |
| 6029 | 17966038 | Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. |
| 6030 | 17966038 | We describe how CD4+ or CD8+T cells can contribute differentially to the pathogenesis of T1D using the HLA-DQ8 transgenic mouse models. |
| 6031 | 17966038 | HLA-DQ8 transgenic mice expressing the costimulatory molecule, B7.1 (RIP.B7.1), or the proinflammatory cytokine, TNF-alpha (RIP.TNF) or both (RIP.B7.RIP.TNF) under the control of rat insulin promoter (RIP) were used. |
| 6032 | 17966038 | In the RIP-B7.RIP-TNF double transgenic mouse model, either CD4+ or CD8+T cells were sufficient to precipitate diabetes in 100% of the animals. |
| 6033 | 17966038 | Thus, the relative roles of CD4+ or CD8+T cells in the pathogenesis of T1D are possibly determined by the local inflammatory stimuli. |
| 6034 | 17983444 | Protection is associated with an increased proportion of T cells with CD4+ forkhead box P3+ regulatory phenotype within the islet infiltrate of treated animals. |
| 6035 | 17991775 | FoxP3(+)CD4(+) regulatory T cells (Tregs) play a key role in the maintenance of peripheral self-tolerance, and it has been suggested that diabetes-susceptible nonobese diabetic (NOD) mice are defective in the generation and numbers of Tregs. |
| 6036 | 18003758 | Sphingosine-1-phosphate reduces CD4+ T-cell activation in type 1 diabetes through regulation of hypoxia-inducible factor short isoform I.1 and CD69. |
| 6037 | 18024188 | The CD4(+)CD25(+) lineage of regulatory T (Treg) cells plays a key role in controlling immune and autoimmune responses and is characterized by a unique transcriptional signature. |
| 6038 | 18024188 | We have performed a cross-sectional analysis of the Treg cell signature in Treg-like cells generated under a number of conditions, with or without Foxp3, to delineate the elements that can be ascribed to T cell activation, interleukin-2, transforming growth factor-beta (TGF-beta) signaling, or Foxp3 itself. |
| 6039 | 18025164 | The therapeutic effect of transfused activated NOD B cells correlates closely with the observed decreased islet inflammation, reduced IFN-gamma production and increased production of IL-4 and IL-10 by splenocytes and CD4(+) T cells from NOD recipients of BCR-stimulated NOD B cells relative to splenocytes and CD4(+) T cells from PBS-treated control NOD mice. |
| 6040 | 18025175 | These changes in autoreactive CD4(+) T cell activation were associated with reduced dendritic cell endocytosis and soluble Ag presentation but were not as a result of virally induced IL-10 or changes in Ag-specific regulatory T cell populations. |
| 6041 | 18029395 | Essential roles of TGF-beta in anti-CD3 antibody therapy: reversal of diabetes in nonobese diabetic mice independent of Foxp3+CD4+ regulatory T cells. |
| 6042 | 18029395 | Furthermore, we found that anti-CD3 treatment did not increase the forkhead box p3+ (Foxp3+)CD4+ regulatory T cells (Tregs). |
| 6043 | 18029395 | Thus, our data showed a dispensable role of Foxp3+CD4+ Tregs in anti-CD3 antibody-reversed diabetes in NOD mice. |
| 6044 | 18029395 | Essential roles of TGF-beta in anti-CD3 antibody therapy: reversal of diabetes in nonobese diabetic mice independent of Foxp3+CD4+ regulatory T cells. |
| 6045 | 18029395 | Furthermore, we found that anti-CD3 treatment did not increase the forkhead box p3+ (Foxp3+)CD4+ regulatory T cells (Tregs). |
| 6046 | 18029395 | Thus, our data showed a dispensable role of Foxp3+CD4+ Tregs in anti-CD3 antibody-reversed diabetes in NOD mice. |
| 6047 | 18029395 | Essential roles of TGF-beta in anti-CD3 antibody therapy: reversal of diabetes in nonobese diabetic mice independent of Foxp3+CD4+ regulatory T cells. |
| 6048 | 18029395 | Furthermore, we found that anti-CD3 treatment did not increase the forkhead box p3+ (Foxp3+)CD4+ regulatory T cells (Tregs). |
| 6049 | 18029395 | Thus, our data showed a dispensable role of Foxp3+CD4+ Tregs in anti-CD3 antibody-reversed diabetes in NOD mice. |
| 6050 | 18063685 | Although GLP-1R mRNA transcripts were detected in spleen, thymus, and lymph nodes from nonobese diabetic mice, Ex-4 treatment was not associated with significant changes in the numbers of CD4+ or CD8+ T cells or B cells in the spleen. |
| 6051 | 18063685 | However, Ex-4 treatment resulted in an increase in the number of CD4+ and CD8+ T cells in the lymph nodes and a reduction in the numbers of CD4+CD25+Foxp3+ regulatory T cells in the thymus but not in lymph nodes. |
| 6052 | 18063685 | Although GLP-1R mRNA transcripts were detected in spleen, thymus, and lymph nodes from nonobese diabetic mice, Ex-4 treatment was not associated with significant changes in the numbers of CD4+ or CD8+ T cells or B cells in the spleen. |
| 6053 | 18063685 | However, Ex-4 treatment resulted in an increase in the number of CD4+ and CD8+ T cells in the lymph nodes and a reduction in the numbers of CD4+CD25+Foxp3+ regulatory T cells in the thymus but not in lymph nodes. |
| 6054 | 18075857 | Our data showed that the surface expressions of MHC II and CD86 on NOD-derived DC were increased after insulin treatment compared with those on PBS controlled mice. |
| 6055 | 18075857 | The dendritic cells with a mature phenotype and increased MLR stimulation adoptively transferred immune tolerogenic effects in secondary NOD-SCID mice, which were associated with significant greater IL-10, TGF-beta production and CD4(+)CD25(+)T differentiation from splenocytes compared with NOD-SCID control recipients. |
| 6056 | 18087999 | These data demonstrate that simultaneous targeting of LFA-1, CD154, and CD4 molecules can be effective in inducing long-term islet xenograft survival and function in autoimmune-prone NOD mice. |
| 6057 | 18091354 | We tested the hypothesis that formula feeding during the neonatal period accelerates the development of T1D in diabetes-prone BioBreeding (BBDP) rats through regulation of CD4+CD25+ regulatory T lymphocytes (T(reg)) and anti-inflammatory cytokines. |
| 6058 | 18091354 | The spleen and thymus were analyzed for Foxp3-expressing CD4+/CD25+ T cells. |
| 6059 | 18091354 | Multiplex enzyme-linked immunosorbent assays (ELISAs) were performed to measure cytokine-induced neutrophil chemoattractant (CINC), tumor necrosis factor alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin (IL)-4, IL-10, and IL-18. |
| 6060 | 18091354 | There were no differences in ileal cytokine concentrations of 75-d-old rats, but the formula-fed rats had greater liver TNF-alpha (p < 0.001), IFN-gamma, and IL-4 (p < 0.01) and lower IL-10 (p = 0.002) compared with MF animals. |
| 6061 | 18091354 | We tested the hypothesis that formula feeding during the neonatal period accelerates the development of T1D in diabetes-prone BioBreeding (BBDP) rats through regulation of CD4+CD25+ regulatory T lymphocytes (T(reg)) and anti-inflammatory cytokines. |
| 6062 | 18091354 | The spleen and thymus were analyzed for Foxp3-expressing CD4+/CD25+ T cells. |
| 6063 | 18091354 | Multiplex enzyme-linked immunosorbent assays (ELISAs) were performed to measure cytokine-induced neutrophil chemoattractant (CINC), tumor necrosis factor alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin (IL)-4, IL-10, and IL-18. |
| 6064 | 18091354 | There were no differences in ileal cytokine concentrations of 75-d-old rats, but the formula-fed rats had greater liver TNF-alpha (p < 0.001), IFN-gamma, and IL-4 (p < 0.01) and lower IL-10 (p = 0.002) compared with MF animals. |
| 6065 | 18093919 | To address this, a mouse CD20 antibody that depletes >95% of mature B cells in mice with otherwise intact immune systems was used to assess the role of B cells in CD4(+) and CD8(+) T cell activation and expansion in vivo. |
| 6066 | 18093919 | B cell depletion had no direct effect on T cell subsets or the activation status of CD4(+) and CD8(+) T cells in naive mice. |
| 6067 | 18093919 | However, B cell depletion impaired CD4(+) T cell activation and clonal expansion in response to protein antigens and pathogen challenge, whereas CD8(+) T cell activation was not affected. |
| 6068 | 18093919 | Most importantly, B cell depletion inhibited antigen-specific CD4(+) T cell expansion in both collagen-induced arthritis and autoimmune diabetes mouse models. |
| 6069 | 18093919 | To address this, a mouse CD20 antibody that depletes >95% of mature B cells in mice with otherwise intact immune systems was used to assess the role of B cells in CD4(+) and CD8(+) T cell activation and expansion in vivo. |
| 6070 | 18093919 | B cell depletion had no direct effect on T cell subsets or the activation status of CD4(+) and CD8(+) T cells in naive mice. |
| 6071 | 18093919 | However, B cell depletion impaired CD4(+) T cell activation and clonal expansion in response to protein antigens and pathogen challenge, whereas CD8(+) T cell activation was not affected. |
| 6072 | 18093919 | Most importantly, B cell depletion inhibited antigen-specific CD4(+) T cell expansion in both collagen-induced arthritis and autoimmune diabetes mouse models. |
| 6073 | 18093919 | To address this, a mouse CD20 antibody that depletes >95% of mature B cells in mice with otherwise intact immune systems was used to assess the role of B cells in CD4(+) and CD8(+) T cell activation and expansion in vivo. |
| 6074 | 18093919 | B cell depletion had no direct effect on T cell subsets or the activation status of CD4(+) and CD8(+) T cells in naive mice. |
| 6075 | 18093919 | However, B cell depletion impaired CD4(+) T cell activation and clonal expansion in response to protein antigens and pathogen challenge, whereas CD8(+) T cell activation was not affected. |
| 6076 | 18093919 | Most importantly, B cell depletion inhibited antigen-specific CD4(+) T cell expansion in both collagen-induced arthritis and autoimmune diabetes mouse models. |
| 6077 | 18093919 | To address this, a mouse CD20 antibody that depletes >95% of mature B cells in mice with otherwise intact immune systems was used to assess the role of B cells in CD4(+) and CD8(+) T cell activation and expansion in vivo. |
| 6078 | 18093919 | B cell depletion had no direct effect on T cell subsets or the activation status of CD4(+) and CD8(+) T cells in naive mice. |
| 6079 | 18093919 | However, B cell depletion impaired CD4(+) T cell activation and clonal expansion in response to protein antigens and pathogen challenge, whereas CD8(+) T cell activation was not affected. |
| 6080 | 18093919 | Most importantly, B cell depletion inhibited antigen-specific CD4(+) T cell expansion in both collagen-induced arthritis and autoimmune diabetes mouse models. |
| 6081 | 18157812 | Functional inhibition related to structure of a highly potent insulin-specific CD8 T cell clone using altered peptide ligands. |
| 6082 | 18157812 | Insulin-reactive CD8 T cells are amongst the earliest islet-infiltrating CD8 T cells in NOD mice. |
| 6083 | 18157812 | This is important in considering the therapeutic use of peptides as APL that encompass both CD4 and CD8 epitopes of insulin. |
| 6084 | 18178847 | Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes. |
| 6085 | 18178847 | NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes 1 (Idd5) and 3 (Idd3) derived from the nondiabetic strains B10 and B6, respectively. |
| 6086 | 18178847 | To test the hypothesis that candidate Idd genes can be identified by differential gene expression between activated CD4+ T cells from the diabetes-susceptible NOD strain and the diabetes-resistant NOD.Idd3/5 congenic strain, genome-wide microarray expression analysis was performed using an empirical Bayes method. |
| 6087 | 18178847 | The two genes with the greatest differential RNA expression on chromosome 1 were those encoding decay-accelerating factor (DAF, also known as CD55) and acyl-coenzyme A dehydrogenase, long chain, which are located in the Idd5.4 and Idd5.3 regions, respectively. |
| 6088 | 18178847 | In the case of DAF, differential expression of mRNA was extended to the protein level; NOD CD4+ T cells expressed higher levels of cell surface DAF compared with NOD.Idd3/5 CD4+ T cells following activation with anti-CD3 and -CD28. |
| 6089 | 18178847 | DAF up-regulation was IL-4 dependent and blocked under Th1 conditions. |
| 6090 | 18178847 | Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes. |
| 6091 | 18178847 | NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes 1 (Idd5) and 3 (Idd3) derived from the nondiabetic strains B10 and B6, respectively. |
| 6092 | 18178847 | To test the hypothesis that candidate Idd genes can be identified by differential gene expression between activated CD4+ T cells from the diabetes-susceptible NOD strain and the diabetes-resistant NOD.Idd3/5 congenic strain, genome-wide microarray expression analysis was performed using an empirical Bayes method. |
| 6093 | 18178847 | The two genes with the greatest differential RNA expression on chromosome 1 were those encoding decay-accelerating factor (DAF, also known as CD55) and acyl-coenzyme A dehydrogenase, long chain, which are located in the Idd5.4 and Idd5.3 regions, respectively. |
| 6094 | 18178847 | In the case of DAF, differential expression of mRNA was extended to the protein level; NOD CD4+ T cells expressed higher levels of cell surface DAF compared with NOD.Idd3/5 CD4+ T cells following activation with anti-CD3 and -CD28. |
| 6095 | 18178847 | DAF up-regulation was IL-4 dependent and blocked under Th1 conditions. |
| 6096 | 18178847 | Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes. |
| 6097 | 18178847 | NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes 1 (Idd5) and 3 (Idd3) derived from the nondiabetic strains B10 and B6, respectively. |
| 6098 | 18178847 | To test the hypothesis that candidate Idd genes can be identified by differential gene expression between activated CD4+ T cells from the diabetes-susceptible NOD strain and the diabetes-resistant NOD.Idd3/5 congenic strain, genome-wide microarray expression analysis was performed using an empirical Bayes method. |
| 6099 | 18178847 | The two genes with the greatest differential RNA expression on chromosome 1 were those encoding decay-accelerating factor (DAF, also known as CD55) and acyl-coenzyme A dehydrogenase, long chain, which are located in the Idd5.4 and Idd5.3 regions, respectively. |
| 6100 | 18178847 | In the case of DAF, differential expression of mRNA was extended to the protein level; NOD CD4+ T cells expressed higher levels of cell surface DAF compared with NOD.Idd3/5 CD4+ T cells following activation with anti-CD3 and -CD28. |
| 6101 | 18178847 | DAF up-regulation was IL-4 dependent and blocked under Th1 conditions. |
| 6102 | 18200031 | Moreover, these SNPs segregate with differential production of IL-2 by CD4(+) T cells as well as susceptibility alleles at Idd3 and Eae3, QTL controlling insulin-dependent diabetes mellitus and experimental allergic encephalomyelitis. |
| 6103 | 18200031 | These are the first SNPs identified within the extended murine IL2 promoter that control differential IL-2 transcription in CD4(+) T cells, and, as such, they are not only candidates for Aod2, but are also candidates for a shared autoimmune disease-susceptibility locus underlying Idd3 and Eae3. |
| 6104 | 18200031 | Moreover, these SNPs segregate with differential production of IL-2 by CD4(+) T cells as well as susceptibility alleles at Idd3 and Eae3, QTL controlling insulin-dependent diabetes mellitus and experimental allergic encephalomyelitis. |
| 6105 | 18200031 | These are the first SNPs identified within the extended murine IL2 promoter that control differential IL-2 transcription in CD4(+) T cells, and, as such, they are not only candidates for Aod2, but are also candidates for a shared autoimmune disease-susceptibility locus underlying Idd3 and Eae3. |
| 6106 | 18226498 | We also find that beta cell antigen-specific IL-10-producing CD4+ T cells are induced in the presence of apoptotic splenic stromal cells. |
| 6107 | 18248531 | CD 127- and FoxP3+ expression on CD25+CD4+ T regulatory cells upon specific diabetogeneic stimulation in high-risk relatives of type 1 diabetes mellitus patients. |
| 6108 | 18248531 | Abnormalities in CD4+CD25+ regulatory T cells (Treg) may contribute to type 1 diabetes (T1D) development. |
| 6109 | 18248531 | Using two novel markers of CD4+CD25+ Treg (CD127- and FoxP3+ respectively), we evaluated number and function of Treg after specific stimulation with diabetogeneic autoantigens in 11 high-risk (according to HLA-linked risk) relatives of T1D patients and 14 age-matched healthy controls using a cytokine secretion assay based on interferon-gamma (IFN-gamma) production. |
| 6110 | 18248531 | CD 127- and FoxP3+ expression on CD25+CD4+ T regulatory cells upon specific diabetogeneic stimulation in high-risk relatives of type 1 diabetes mellitus patients. |
| 6111 | 18248531 | Abnormalities in CD4+CD25+ regulatory T cells (Treg) may contribute to type 1 diabetes (T1D) development. |
| 6112 | 18248531 | Using two novel markers of CD4+CD25+ Treg (CD127- and FoxP3+ respectively), we evaluated number and function of Treg after specific stimulation with diabetogeneic autoantigens in 11 high-risk (according to HLA-linked risk) relatives of T1D patients and 14 age-matched healthy controls using a cytokine secretion assay based on interferon-gamma (IFN-gamma) production. |
| 6113 | 18248531 | CD 127- and FoxP3+ expression on CD25+CD4+ T regulatory cells upon specific diabetogeneic stimulation in high-risk relatives of type 1 diabetes mellitus patients. |
| 6114 | 18248531 | Abnormalities in CD4+CD25+ regulatory T cells (Treg) may contribute to type 1 diabetes (T1D) development. |
| 6115 | 18248531 | Using two novel markers of CD4+CD25+ Treg (CD127- and FoxP3+ respectively), we evaluated number and function of Treg after specific stimulation with diabetogeneic autoantigens in 11 high-risk (according to HLA-linked risk) relatives of T1D patients and 14 age-matched healthy controls using a cytokine secretion assay based on interferon-gamma (IFN-gamma) production. |
| 6116 | 18267303 | We analyzed the genes expressed (transcriptomes) and the proteins translated (pro- teomes) in muscle tissues and activated CD4(+) and CD8(+) T-lymphocytes (T-cells) of five Type 2 diabetes (T2DM) subjects using Affymetrix microarrays and mass spectrometry, and compared them with matched non-diabetic controls. |
| 6117 | 18267303 | Gene expressions of insulin receptor (INSR), vitamin D receptor, insulin degrading enzyme, Akt, insulin receptor substrate-1 (IRS-1), IRS-2, glucose transporter 4 (GLUT4), and enzymes of the glycolytic pathway were decreased at least 50% in T2DM than in controls. |
| 6118 | 18267303 | The gene silencing for INSR or TNFalpha resulted in the inhibition or stimulation of GLUT4, respectively. |
| 6119 | 18283119 | The AKT-mTOR axis regulates de novo differentiation of CD4+Foxp3+ cells. |
| 6120 | 18283119 | CD4(+)Foxp3(+) regulatory T (T reg) cells play an essential role in maintaining immunological tolerance via their suppressive function on conventional CD4(+) T (Tconv) cells. |
| 6121 | 18283119 | Expression of active AKT at a stage before Foxp3 turn on during normal T reg differentiation in the thymus selectively impaired differentiation of CD4(+)Foxp3(+) cells without any alteration in the positive selection of Tconv. |
| 6122 | 18283119 | The AKT-mTOR axis regulates de novo differentiation of CD4+Foxp3+ cells. |
| 6123 | 18283119 | CD4(+)Foxp3(+) regulatory T (T reg) cells play an essential role in maintaining immunological tolerance via their suppressive function on conventional CD4(+) T (Tconv) cells. |
| 6124 | 18283119 | Expression of active AKT at a stage before Foxp3 turn on during normal T reg differentiation in the thymus selectively impaired differentiation of CD4(+)Foxp3(+) cells without any alteration in the positive selection of Tconv. |
| 6125 | 18283119 | The AKT-mTOR axis regulates de novo differentiation of CD4+Foxp3+ cells. |
| 6126 | 18283119 | CD4(+)Foxp3(+) regulatory T (T reg) cells play an essential role in maintaining immunological tolerance via their suppressive function on conventional CD4(+) T (Tconv) cells. |
| 6127 | 18283119 | Expression of active AKT at a stage before Foxp3 turn on during normal T reg differentiation in the thymus selectively impaired differentiation of CD4(+)Foxp3(+) cells without any alteration in the positive selection of Tconv. |
| 6128 | 18283628 | Here we report on the IN VITRO findings of a vaccination trial in five MTC patients, who were treated with a new DC generation protocol consisting of granulocyte-macrophage colony-stimulating factor and interferon-alpha (IFN-DCs). |
| 6129 | 18283628 | In two patients who responded to therapy we found a large increase (in mean 2.9+/-1.9%) of antigen-specific IFN-gamma-secreting CD4+ cells as well as an increase of granzyme B positive CD8+ cells (mean 2.2+/-0.2%) in the peripheral blood. |
| 6130 | 18283628 | In parallel, a decrease of CD4+/CD25+/FoxP3+ regulatory T cells was seen. |
| 6131 | 18283628 | Here we report on the IN VITRO findings of a vaccination trial in five MTC patients, who were treated with a new DC generation protocol consisting of granulocyte-macrophage colony-stimulating factor and interferon-alpha (IFN-DCs). |
| 6132 | 18283628 | In two patients who responded to therapy we found a large increase (in mean 2.9+/-1.9%) of antigen-specific IFN-gamma-secreting CD4+ cells as well as an increase of granzyme B positive CD8+ cells (mean 2.2+/-0.2%) in the peripheral blood. |
| 6133 | 18283628 | In parallel, a decrease of CD4+/CD25+/FoxP3+ regulatory T cells was seen. |
| 6134 | 18283631 | They are usually controlled by a network of regulatory mechanisms including CD4+CD25+Foxp3+ regulatory T cells (Tregs). |
| 6135 | 18287017 | CD4 T cells, lymphopenia, and IL-7 in a multistep pathway to autoimmunity. |
| 6136 | 18287017 | We show in a model of beta-islet cell self-reactivity that the transfer of activated autoreactive CD4 T cells can prime and expand endogenous autoreactive CD8 T cells in a CD28- and CD40-dependent manner through the licensing of dendritic cells. |
| 6137 | 18287017 | Autoimmune diabetes rapidly ensued with CD4 help and the subsequent activation of CD8 T cells, which contributed to disease progression. |
| 6138 | 18287017 | With the advent of many biologicals targeting TNFalpha, IL-6, and IL-1 and their effective use in the treatment of autoimmune diseases, we propose that IL-7 and its receptor may be promising targets for biological agents in the treatment of autoimmunity. |
| 6139 | 18287017 | CD4 T cells, lymphopenia, and IL-7 in a multistep pathway to autoimmunity. |
| 6140 | 18287017 | We show in a model of beta-islet cell self-reactivity that the transfer of activated autoreactive CD4 T cells can prime and expand endogenous autoreactive CD8 T cells in a CD28- and CD40-dependent manner through the licensing of dendritic cells. |
| 6141 | 18287017 | Autoimmune diabetes rapidly ensued with CD4 help and the subsequent activation of CD8 T cells, which contributed to disease progression. |
| 6142 | 18287017 | With the advent of many biologicals targeting TNFalpha, IL-6, and IL-1 and their effective use in the treatment of autoimmune diseases, we propose that IL-7 and its receptor may be promising targets for biological agents in the treatment of autoimmunity. |
| 6143 | 18287017 | CD4 T cells, lymphopenia, and IL-7 in a multistep pathway to autoimmunity. |
| 6144 | 18287017 | We show in a model of beta-islet cell self-reactivity that the transfer of activated autoreactive CD4 T cells can prime and expand endogenous autoreactive CD8 T cells in a CD28- and CD40-dependent manner through the licensing of dendritic cells. |
| 6145 | 18287017 | Autoimmune diabetes rapidly ensued with CD4 help and the subsequent activation of CD8 T cells, which contributed to disease progression. |
| 6146 | 18287017 | With the advent of many biologicals targeting TNFalpha, IL-6, and IL-1 and their effective use in the treatment of autoimmune diseases, we propose that IL-7 and its receptor may be promising targets for biological agents in the treatment of autoimmunity. |
| 6147 | 18292508 | Rather, impaired CD4+ and CD8+ T cell activation in the lymph nodes of B cell-depleted NOD mice may delay diabetes onset. |
| 6148 | 18295332 | Here we show that antibodies to CD1d, when given during early thymic development, induce specific increases in surface TCR of developing NOD and C57BL/6 CD4(+)CD8(+) (DP) invariant NKT (iNKT) cells. |
| 6149 | 18297721 | Compared with controls on day 7 p.i., cytofluorometric analyses on cells from CV-B4 E2-infected foetal thymus organ cultures displayed a marked increase in the percentage of the most immature CD3(-)CD4(-)CD8(-) thymocytes, and a decrease in the percentage of immature CD3(-)CD4(+)CD8(+) cells, together with an increase in the percentage of mature CD3(+)CD4(+) and CD3(+)CD8(+) cells. |
| 6150 | 18299186 | Reduced CD4+T cell activation in children with type 1 diabetes carrying the PTPN22/Lyp 620Trp variant. |
| 6151 | 18299186 | We found a decreased proliferation and IL-2 production of CD4(+)T cells after anti-CD3/anti-CD28 stimulation (p=0.04 for IL-2) among T1D patients. |
| 6152 | 18299186 | In conclusion, the LYP 620Trp variant is associated with reduced activation, proliferation and IL-2 production in CD4(+)T cells among T1D patients. |
| 6153 | 18299186 | Reduced CD4+T cell activation in children with type 1 diabetes carrying the PTPN22/Lyp 620Trp variant. |
| 6154 | 18299186 | We found a decreased proliferation and IL-2 production of CD4(+)T cells after anti-CD3/anti-CD28 stimulation (p=0.04 for IL-2) among T1D patients. |
| 6155 | 18299186 | In conclusion, the LYP 620Trp variant is associated with reduced activation, proliferation and IL-2 production in CD4(+)T cells among T1D patients. |
| 6156 | 18299186 | Reduced CD4+T cell activation in children with type 1 diabetes carrying the PTPN22/Lyp 620Trp variant. |
| 6157 | 18299186 | We found a decreased proliferation and IL-2 production of CD4(+)T cells after anti-CD3/anti-CD28 stimulation (p=0.04 for IL-2) among T1D patients. |
| 6158 | 18299186 | In conclusion, the LYP 620Trp variant is associated with reduced activation, proliferation and IL-2 production in CD4(+)T cells among T1D patients. |
| 6159 | 18300057 | The two possibilities to explain the pathogenic basis of stiff-person syndrome (SPS) are intrathecal sensitization of GAD65-reactive CD4+T cells and synthesis of GAD65-specific autoantibodies within the CNS [Rakocevic et al., Arch. |
| 6160 | 18308198 | Recent data suggest that the proinsulin cleavage product C-peptide could play a causal role in atherogenesis by promoting monocyte and CD4-positive lymphocyte recruitment in early arteriosclerotic lesions and by inducing the proliferation of vascular smooth muscle cells. |
| 6161 | 18317533 | Immunodysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is a rare disorder caused by mutations in the FOXP3 gene that result in the defective development of CD4+CD25+ regulatory T cells which constitute an important T cell subset involved in immune homeostasis and protection against autoimmunity. |
| 6162 | 18317533 | Apart from its clinical implications, IPEX illustrates the importance of immunoregulatory cells such as CD4+CD25+ regulatory T cells. |
| 6163 | 18317533 | Immunodysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is a rare disorder caused by mutations in the FOXP3 gene that result in the defective development of CD4+CD25+ regulatory T cells which constitute an important T cell subset involved in immune homeostasis and protection against autoimmunity. |
| 6164 | 18317533 | Apart from its clinical implications, IPEX illustrates the importance of immunoregulatory cells such as CD4+CD25+ regulatory T cells. |
| 6165 | 18319580 | In the diabetic dogs, the counts of CD3(+) (T cells), CD4(+) (Helper T cells) and CD21(+) (B cells) cells and the peripheral lymphocytes CD4/CD8 ratio were significantly lower than those in the control dogs. |
| 6166 | 18322192 | We used insulinomas transfected with the CIITA transactivator, which resulted in their expression of class II histocompatibility molecules and activation of diabetogenic CD4 T cells. |
| 6167 | 18351019 | Cellular infiltrate in successful grafts revealed CD4 T cells and macrophages along the periphery and within the grafts, and very few CD8 T cells. |
| 6168 | 18351019 | Conversely, examination of unsuccessful grafts, harvested from hyperglycemic recipients at the time of rejection, revealed the presence of SC arranged randomly with islets adjacent to the Sertoli cells, when present, and massive CD4 and CD8 T cell as well as macrophage cell infiltration. |
| 6169 | 18351019 | Cellular infiltrate in successful grafts revealed CD4 T cells and macrophages along the periphery and within the grafts, and very few CD8 T cells. |
| 6170 | 18351019 | Conversely, examination of unsuccessful grafts, harvested from hyperglycemic recipients at the time of rejection, revealed the presence of SC arranged randomly with islets adjacent to the Sertoli cells, when present, and massive CD4 and CD8 T cell as well as macrophage cell infiltration. |
| 6171 | 18351394 | A retrospective analysis revealed that tubulointerstitial infiltrates present in the biopsies prior to treatment with rituximab contained numerous CD20+ and CD3+ (CD4 > CD8) lymphocyte aggregates. |
| 6172 | 18354167 | Autoimmunity to both proinsulin and IGRP is required for diabetes in nonobese diabetic 8.3 TCR transgenic mice. |
| 6173 | 18354167 | T cells specific for proinsulin and islet-specific glucose-6-phosphatase catalytic subunit related protein (IGRP) induce diabetes in nonobese diabetic (NOD) mice. |
| 6174 | 18354167 | TCR transgenic mice with CD8(+) T cells specific for IGRP(206-214) (NOD8.3 mice) develop accelerated diabetes that requires CD4(+) T cell help. |
| 6175 | 18354167 | We previously showed that immune responses against proinsulin are necessary for IGRP(206-214)-specific CD8(+) T cells to expand. |
| 6176 | 18354167 | This indicates that immunity to proinsulin is even required in the great majority of NOD8.3 mice that have a pre-existing repertoire of IGRP(206-214)-specific cells. |
| 6177 | 18354167 | This suggests that islet inflammation can substitute for proinsulin-specific CD4(+) T cell help to activate IGRP(206-214)-specific T cells. |
| 6178 | 18354167 | Autoimmunity to both proinsulin and IGRP is required for diabetes in nonobese diabetic 8.3 TCR transgenic mice. |
| 6179 | 18354167 | T cells specific for proinsulin and islet-specific glucose-6-phosphatase catalytic subunit related protein (IGRP) induce diabetes in nonobese diabetic (NOD) mice. |
| 6180 | 18354167 | TCR transgenic mice with CD8(+) T cells specific for IGRP(206-214) (NOD8.3 mice) develop accelerated diabetes that requires CD4(+) T cell help. |
| 6181 | 18354167 | We previously showed that immune responses against proinsulin are necessary for IGRP(206-214)-specific CD8(+) T cells to expand. |
| 6182 | 18354167 | This indicates that immunity to proinsulin is even required in the great majority of NOD8.3 mice that have a pre-existing repertoire of IGRP(206-214)-specific cells. |
| 6183 | 18354167 | This suggests that islet inflammation can substitute for proinsulin-specific CD4(+) T cell help to activate IGRP(206-214)-specific T cells. |
| 6184 | 18383041 | Marked attenuation in cellularity of the CD4+ single-positive thymocyte compartment in ADAP-deficient BDC/B6g7/b animals suggests a mechanism for induction of the lymphopenia. |
| 6185 | 18385016 | CD4+ T cells from type 1 diabetic and healthy subjects exhibit different thresholds of activation to a naturally processed proinsulin epitope. |
| 6186 | 18387839 | Effects of an oral superoxide dismutase enzyme supplementation on indices of oxidative stress, proviral load, and CD4:CD8 ratios in asymptomatic FIV-infected cats. |
| 6187 | 18387839 | The CD4+ to CD8+ ratio increased significantly (0.66-0.88) in the SOD supplemented FIV-infected cats but not in the unsupplemented FIV-infected cats. |
| 6188 | 18387839 | Effects of an oral superoxide dismutase enzyme supplementation on indices of oxidative stress, proviral load, and CD4:CD8 ratios in asymptomatic FIV-infected cats. |
| 6189 | 18387839 | The CD4+ to CD8+ ratio increased significantly (0.66-0.88) in the SOD supplemented FIV-infected cats but not in the unsupplemented FIV-infected cats. |
| 6190 | 18390000 | In diabetic subjects, increased CD19 and CD23 expressions were observed before exercise. |
| 6191 | 18390000 | In both groups (diabetic/control) CD3, CD4 expressions and CD4/CD8 ratio were decreased following the exercise, however expression of natural killer (NK) cells increased. |
| 6192 | 18390698 | The treatment caused long-term desensitization in treated animals to hen OVA via a dexamethasone-dependent tolerogenic mechanism that blocks maturation of dendritic cells and expands OVA(323-339)-specific CD4(+)CD25(+)Foxp3(+) regulatory T cells in vivo. |
| 6193 | 18417224 | Interleukin-2 (IL-2) plays an established role in T-cell regulation through binding to the high-affinity IL-2 receptor (IL-2R). |
| 6194 | 18417224 | The non-redundant role of IL-2 and its receptor in etiology of T1D could be particularly attributable to the regulation of CD4+ CD25+ regulatory T cells, whose function is critical in maintaining immune homeostasis. |
| 6195 | 18453575 | Preferential costimulation by CD80 results in IL-10-dependent TGF-beta1(+) -adaptive regulatory T cell generation. |
| 6196 | 18453575 | Costimulatory ligands CD80 and CD86 have different binding preferences and affinities to their receptors, CD28 and CTLA-4. |
| 6197 | 18453575 | Earlier, we demonstrated that CD80 binds to CTLA-4 with higher affinity and has a role in suppressing T cell response. |
| 6198 | 18453575 | These T cells showed TGF-beta1 on their surface and secreted TGF-beta1 and IL-10 upon restimulation. |
| 6199 | 18453575 | Although blockade of CTLA-4 and neutralization of IL-10 profoundly inhibited the induction of these TGF-beta1(+) T cells, their ability to suppress the effector T cell proliferation was abrogated by neutralization of TGF-beta1 alone. |
| 6200 | 18453575 | Induction of TGF-beta1(+) and IL-10(+) T cells was found to be independent of natural CD4(+)CD25(+) regulatory T cells, demonstrating that preferential ligation of CTLA-4 by CD80 induced IL-10 production by effector T cells, which in turn promoted the secretion of TGF-beta1. |
| 6201 | 18453575 | Treatment of prediabetic NOD mice with islet beta cell Ag-pulsed CD86(-/-) DCs, but not CD80(-/-) DCs, resulted in the induction of TGF-beta1- and IL-10-producing cells, significant suppression of insulitis, and delay of the onset of hyperglycemia. |
| 6202 | 18453575 | These observations demonstrate not only that CD80 preferentially binds to CTLA-4 but also that interaction during Ag presentation can result in IL-10-dependent TGF-beta1(+) regulatory T cell induction, reinstating the potential of approaches to preferentially engage CTLA-4 through CD80 during self-Ag presentation in suppressing autoimmunity. |
| 6203 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6204 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6205 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6206 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6207 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6208 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6209 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6210 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6211 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6212 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6213 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6214 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6215 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6216 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6217 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6218 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6219 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6220 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6221 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6222 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6223 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6224 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6225 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6226 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6227 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6228 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6229 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6230 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6231 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6232 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6233 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6234 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6235 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6236 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6237 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6238 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6239 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6240 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6241 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6242 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6243 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6244 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6245 | 18465023 | Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide. |
| 6246 | 18465023 | CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. |
| 6247 | 18465023 | Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. |
| 6248 | 18465023 | We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner. |
| 6249 | 18465023 | We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells. |
| 6250 | 18465023 | Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide. |
| 6251 | 18465023 | Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes. |
| 6252 | 18468463 | The dynamics of CD4(+) effector T cells (Teff cells) and CD4(+)Foxp3(+) regulatory T cells (Treg cells) during diabetes progression in nonobese diabetic mice was investigated to determine whether an imbalance of Treg cells and Teff cells contributes to the development of type 1 diabetes. |
| 6253 | 18468463 | Intra-islet Treg cells expressed reduced amounts of CD25 and Bcl-2, suggesting that their decline was due to increased apoptosis. |
| 6254 | 18469093 | Disruption of the homeostatic balance between autoaggressive (CD4+CD40+) and regulatory (CD4+CD25+FoxP3+) T cells promotes diabetes. |
| 6255 | 18469093 | Importantly, these cells are present in pancreata of prediabetic and diabetic NOD mice, and Th40 cells but not CD4+CD40(-) T cells transfer progressive insulitis and diabetes to NOD.scid recipients. |
| 6256 | 18469093 | NOD mice have statistically equal numbers of CD4+CD25+forkhead box P3+intrinsic Tregs compared with NOR or nonautoimmune BALB/c mice, and NOD Tregs are equally as suppressive as NOR Tregs. |
| 6257 | 18469093 | CD40 engagement of Th40 cells induces Fas expression but further confers resistance to Fas-mediated cell death in NOD mice. |
| 6258 | 18469093 | Disruption of the homeostatic balance between autoaggressive (CD4+CD40+) and regulatory (CD4+CD25+FoxP3+) T cells promotes diabetes. |
| 6259 | 18469093 | Importantly, these cells are present in pancreata of prediabetic and diabetic NOD mice, and Th40 cells but not CD4+CD40(-) T cells transfer progressive insulitis and diabetes to NOD.scid recipients. |
| 6260 | 18469093 | NOD mice have statistically equal numbers of CD4+CD25+forkhead box P3+intrinsic Tregs compared with NOR or nonautoimmune BALB/c mice, and NOD Tregs are equally as suppressive as NOR Tregs. |
| 6261 | 18469093 | CD40 engagement of Th40 cells induces Fas expression but further confers resistance to Fas-mediated cell death in NOD mice. |
| 6262 | 18469093 | Disruption of the homeostatic balance between autoaggressive (CD4+CD40+) and regulatory (CD4+CD25+FoxP3+) T cells promotes diabetes. |
| 6263 | 18469093 | Importantly, these cells are present in pancreata of prediabetic and diabetic NOD mice, and Th40 cells but not CD4+CD40(-) T cells transfer progressive insulitis and diabetes to NOD.scid recipients. |
| 6264 | 18469093 | NOD mice have statistically equal numbers of CD4+CD25+forkhead box P3+intrinsic Tregs compared with NOR or nonautoimmune BALB/c mice, and NOD Tregs are equally as suppressive as NOR Tregs. |
| 6265 | 18469093 | CD40 engagement of Th40 cells induces Fas expression but further confers resistance to Fas-mediated cell death in NOD mice. |
| 6266 | 18482207 | Indeed, mTEC have been found to express promiscuous self-antigens, used directly or through thymic dendritic cells to drive either negative selection of insulin-reacting precursors or their differentiation into naturally occurring regulatory Foxp3+ CD4+ CD25+ T cells. |
| 6267 | 18482207 | In the periphery, naturally occurring Foxp3+ CD4+ CD25+regulatory T (Treg) cells represent the master cells in dominant peripheral T-cell tolerance. |
| 6268 | 18482207 | The development and function of Treg cells are ultimately linked to IL-2 and Foxp3 expression. |
| 6269 | 18482207 | Indeed, mTEC have been found to express promiscuous self-antigens, used directly or through thymic dendritic cells to drive either negative selection of insulin-reacting precursors or their differentiation into naturally occurring regulatory Foxp3+ CD4+ CD25+ T cells. |
| 6270 | 18482207 | In the periphery, naturally occurring Foxp3+ CD4+ CD25+regulatory T (Treg) cells represent the master cells in dominant peripheral T-cell tolerance. |
| 6271 | 18482207 | The development and function of Treg cells are ultimately linked to IL-2 and Foxp3 expression. |
| 6272 | 18523243 | NOD mouse AIP was associated with severe periductal and parenchymal inflammation of the exocrine pancreas by CD4(+) T cells, CD8(+) T cells, and B cells. |
| 6273 | 18550852 | In vivo-activated CD103+CD4+ regulatory T cells ameliorate ongoing chronic graft-versus-host disease. |
| 6274 | 18550852 | CD103 (alphaEbeta7) has been shown to be an excellent marker for identifying in vivo-activated FoxP3(+)CD4(+) regulatory T (Treg) cells. |
| 6275 | 18550852 | In vivo-activated CD103+CD4+ regulatory T cells ameliorate ongoing chronic graft-versus-host disease. |
| 6276 | 18550852 | CD103 (alphaEbeta7) has been shown to be an excellent marker for identifying in vivo-activated FoxP3(+)CD4(+) regulatory T (Treg) cells. |
| 6277 | 18560422 | Moreover, expression of mIL-4 also maintained the level of CD4(+)CD25(+)FoxP3(+) cells, and adoptive transfer of splenocytes from nondiabetic dsAAV8-mIP-IL-4 mice to NODscid mice was able to block the diabetes induced by splenocytes co-adoptively transferred from nondiabetic dsAAV-mIP-eGFP mice. |
| 6278 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 6279 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 6280 | 18566388 | IL-2- and IL-2R-deficient mice are not completely devoid of Foxp3+ cells, but rather lack population of mature CD4+CD25+Foxp3high Treg cells and contain few immature CD4+CD25-Foxp3low T cells. |
| 6281 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 6282 | 18566388 | The present study was undertaken to determine whether the gammac-cytokines IL-7 or IL-15 normally contribute to expression of Foxp3 and Treg cell production. |
| 6283 | 18566388 | These studies revealed that mice double deficient in IL-2Rbeta and IL-7Ralpha contained a striking lack in the CD4+Foxp3+ population and the Treg cell defect recapitulated the gammac knockout mice. |
| 6284 | 18566388 | In the absence of IL-7R signaling, IL-15/IL-15R interaction is dispensable for the production of CD4+CD25+Foxp3+ Treg cells, indicating that normal thymic Treg cell production likely depends on signaling through both IL-2 and IL-7 receptors. |
| 6285 | 18566388 | Selective thymic reconstitution of IL-2Rbeta in mice double deficient in IL-2Rbeta and IL-7Ralpha established that IL-2Rbeta is dominant and sufficient to restore production of Treg cells. |
| 6286 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 6287 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 6288 | 18566388 | IL-2- and IL-2R-deficient mice are not completely devoid of Foxp3+ cells, but rather lack population of mature CD4+CD25+Foxp3high Treg cells and contain few immature CD4+CD25-Foxp3low T cells. |
| 6289 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 6290 | 18566388 | The present study was undertaken to determine whether the gammac-cytokines IL-7 or IL-15 normally contribute to expression of Foxp3 and Treg cell production. |
| 6291 | 18566388 | These studies revealed that mice double deficient in IL-2Rbeta and IL-7Ralpha contained a striking lack in the CD4+Foxp3+ population and the Treg cell defect recapitulated the gammac knockout mice. |
| 6292 | 18566388 | In the absence of IL-7R signaling, IL-15/IL-15R interaction is dispensable for the production of CD4+CD25+Foxp3+ Treg cells, indicating that normal thymic Treg cell production likely depends on signaling through both IL-2 and IL-7 receptors. |
| 6293 | 18566388 | Selective thymic reconstitution of IL-2Rbeta in mice double deficient in IL-2Rbeta and IL-7Ralpha established that IL-2Rbeta is dominant and sufficient to restore production of Treg cells. |
| 6294 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 6295 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 6296 | 18566388 | IL-2- and IL-2R-deficient mice are not completely devoid of Foxp3+ cells, but rather lack population of mature CD4+CD25+Foxp3high Treg cells and contain few immature CD4+CD25-Foxp3low T cells. |
| 6297 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 6298 | 18566388 | The present study was undertaken to determine whether the gammac-cytokines IL-7 or IL-15 normally contribute to expression of Foxp3 and Treg cell production. |
| 6299 | 18566388 | These studies revealed that mice double deficient in IL-2Rbeta and IL-7Ralpha contained a striking lack in the CD4+Foxp3+ population and the Treg cell defect recapitulated the gammac knockout mice. |
| 6300 | 18566388 | In the absence of IL-7R signaling, IL-15/IL-15R interaction is dispensable for the production of CD4+CD25+Foxp3+ Treg cells, indicating that normal thymic Treg cell production likely depends on signaling through both IL-2 and IL-7 receptors. |
| 6301 | 18566388 | Selective thymic reconstitution of IL-2Rbeta in mice double deficient in IL-2Rbeta and IL-7Ralpha established that IL-2Rbeta is dominant and sufficient to restore production of Treg cells. |
| 6302 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 6303 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 6304 | 18566388 | IL-2- and IL-2R-deficient mice are not completely devoid of Foxp3+ cells, but rather lack population of mature CD4+CD25+Foxp3high Treg cells and contain few immature CD4+CD25-Foxp3low T cells. |
| 6305 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 6306 | 18566388 | The present study was undertaken to determine whether the gammac-cytokines IL-7 or IL-15 normally contribute to expression of Foxp3 and Treg cell production. |
| 6307 | 18566388 | These studies revealed that mice double deficient in IL-2Rbeta and IL-7Ralpha contained a striking lack in the CD4+Foxp3+ population and the Treg cell defect recapitulated the gammac knockout mice. |
| 6308 | 18566388 | In the absence of IL-7R signaling, IL-15/IL-15R interaction is dispensable for the production of CD4+CD25+Foxp3+ Treg cells, indicating that normal thymic Treg cell production likely depends on signaling through both IL-2 and IL-7 receptors. |
| 6309 | 18566388 | Selective thymic reconstitution of IL-2Rbeta in mice double deficient in IL-2Rbeta and IL-7Ralpha established that IL-2Rbeta is dominant and sufficient to restore production of Treg cells. |
| 6310 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 6311 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 6312 | 18566388 | IL-2- and IL-2R-deficient mice are not completely devoid of Foxp3+ cells, but rather lack population of mature CD4+CD25+Foxp3high Treg cells and contain few immature CD4+CD25-Foxp3low T cells. |
| 6313 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 6314 | 18566388 | The present study was undertaken to determine whether the gammac-cytokines IL-7 or IL-15 normally contribute to expression of Foxp3 and Treg cell production. |
| 6315 | 18566388 | These studies revealed that mice double deficient in IL-2Rbeta and IL-7Ralpha contained a striking lack in the CD4+Foxp3+ population and the Treg cell defect recapitulated the gammac knockout mice. |
| 6316 | 18566388 | In the absence of IL-7R signaling, IL-15/IL-15R interaction is dispensable for the production of CD4+CD25+Foxp3+ Treg cells, indicating that normal thymic Treg cell production likely depends on signaling through both IL-2 and IL-7 receptors. |
| 6317 | 18566388 | Selective thymic reconstitution of IL-2Rbeta in mice double deficient in IL-2Rbeta and IL-7Ralpha established that IL-2Rbeta is dominant and sufficient to restore production of Treg cells. |
| 6318 | 18599122 | Diabetes is not prevented by Foxp3-transduced CD4(+)T cells under the IL-12Rbeta2 promoter control. |
| 6319 | 18599122 | Our previous studies have shown that Foxp3 under the control of IFN-gamma promoter (IgammaP-Foxp3) converts pathogenic CD4(+)Th1 cells into regulatory T cells (Tregs), which control diabetes in non-obese diabetic (NOD) mice. |
| 6320 | 18599122 | Foxp3, under the control of IL-12Rbeta2 promoter (Ibeta2P), was lentivirally transduced into naïve CD4(+)T cells from NOD mice. |
| 6321 | 18599122 | Furthermore, we found that Ibeta2P-Foxp3-transduced CD4(+)T cells, stimulated by a high dose of autoantigen, did not suppress CD4(+)T cell activation, produce CD4(+)Foxp3(+)Tregs, and up-regulate CTLA4 expression. |
| 6322 | 18599122 | Diabetes is not prevented by Foxp3-transduced CD4(+)T cells under the IL-12Rbeta2 promoter control. |
| 6323 | 18599122 | Our previous studies have shown that Foxp3 under the control of IFN-gamma promoter (IgammaP-Foxp3) converts pathogenic CD4(+)Th1 cells into regulatory T cells (Tregs), which control diabetes in non-obese diabetic (NOD) mice. |
| 6324 | 18599122 | Foxp3, under the control of IL-12Rbeta2 promoter (Ibeta2P), was lentivirally transduced into naïve CD4(+)T cells from NOD mice. |
| 6325 | 18599122 | Furthermore, we found that Ibeta2P-Foxp3-transduced CD4(+)T cells, stimulated by a high dose of autoantigen, did not suppress CD4(+)T cell activation, produce CD4(+)Foxp3(+)Tregs, and up-regulate CTLA4 expression. |
| 6326 | 18599122 | Diabetes is not prevented by Foxp3-transduced CD4(+)T cells under the IL-12Rbeta2 promoter control. |
| 6327 | 18599122 | Our previous studies have shown that Foxp3 under the control of IFN-gamma promoter (IgammaP-Foxp3) converts pathogenic CD4(+)Th1 cells into regulatory T cells (Tregs), which control diabetes in non-obese diabetic (NOD) mice. |
| 6328 | 18599122 | Foxp3, under the control of IL-12Rbeta2 promoter (Ibeta2P), was lentivirally transduced into naïve CD4(+)T cells from NOD mice. |
| 6329 | 18599122 | Furthermore, we found that Ibeta2P-Foxp3-transduced CD4(+)T cells, stimulated by a high dose of autoantigen, did not suppress CD4(+)T cell activation, produce CD4(+)Foxp3(+)Tregs, and up-regulate CTLA4 expression. |
| 6330 | 18599122 | Diabetes is not prevented by Foxp3-transduced CD4(+)T cells under the IL-12Rbeta2 promoter control. |
| 6331 | 18599122 | Our previous studies have shown that Foxp3 under the control of IFN-gamma promoter (IgammaP-Foxp3) converts pathogenic CD4(+)Th1 cells into regulatory T cells (Tregs), which control diabetes in non-obese diabetic (NOD) mice. |
| 6332 | 18599122 | Foxp3, under the control of IL-12Rbeta2 promoter (Ibeta2P), was lentivirally transduced into naïve CD4(+)T cells from NOD mice. |
| 6333 | 18599122 | Furthermore, we found that Ibeta2P-Foxp3-transduced CD4(+)T cells, stimulated by a high dose of autoantigen, did not suppress CD4(+)T cell activation, produce CD4(+)Foxp3(+)Tregs, and up-regulate CTLA4 expression. |
| 6334 | 18675407 | After TGF-beta blockade, CD4+ T cells differentiated along a route favoring development of Th17, but not Treg cells. |
| 6335 | 18675592 | Whereas intramuscular injection of pGAD65 promoted a predominant type 1 CD4(+) T cell response and failed to suppress ongoing beta cell autoimmunity, gene gun vaccination preferentially induced IL-4 secreting CD4(+) T cells and significantly delayed the onset of diabetes. |
| 6336 | 18708940 | Subcutaneous panniculitis-like T-cell lymphoma (SPTL) is defined as a rare cytotoxic alpha/beta T-cell lymphoma characterized by primary involvement of subcutaneous tissue mimicking panniculitis and a predominant CD3+/CD4-/CD8+ phenotype in 2005 World Health Organization-European Organization for Research and Treatment of Cancer (WHO-EORTC) classification for cutaneous lymphomas. |
| 6337 | 18708940 | Besides the common features described before, unusual CD4+/CD8- and CD4-/CD8- T-cell phenotypes were noted in 2 of our cases, respectively. |
| 6338 | 18708940 | The frequency of rearranged TCRB, TCRG, and TCRD genes detected by BIOMED-2 multiplex polymerase chain reaction tubes was 80%, 67%, and 13%, respectively, with a total clonality detection rate of 100%. |
| 6339 | 18708940 | We conclude that SPTL as a cytotoxic lymphoma derived from alpha/beta T cell has a predominant CD4-/CD8+ phenotype, but unusual CD4+/CD8- and CD4-/CD8- phenotypes do exist. |
| 6340 | 18708940 | Subcutaneous panniculitis-like T-cell lymphoma (SPTL) is defined as a rare cytotoxic alpha/beta T-cell lymphoma characterized by primary involvement of subcutaneous tissue mimicking panniculitis and a predominant CD3+/CD4-/CD8+ phenotype in 2005 World Health Organization-European Organization for Research and Treatment of Cancer (WHO-EORTC) classification for cutaneous lymphomas. |
| 6341 | 18708940 | Besides the common features described before, unusual CD4+/CD8- and CD4-/CD8- T-cell phenotypes were noted in 2 of our cases, respectively. |
| 6342 | 18708940 | The frequency of rearranged TCRB, TCRG, and TCRD genes detected by BIOMED-2 multiplex polymerase chain reaction tubes was 80%, 67%, and 13%, respectively, with a total clonality detection rate of 100%. |
| 6343 | 18708940 | We conclude that SPTL as a cytotoxic lymphoma derived from alpha/beta T cell has a predominant CD4-/CD8+ phenotype, but unusual CD4+/CD8- and CD4-/CD8- phenotypes do exist. |
| 6344 | 18708940 | Subcutaneous panniculitis-like T-cell lymphoma (SPTL) is defined as a rare cytotoxic alpha/beta T-cell lymphoma characterized by primary involvement of subcutaneous tissue mimicking panniculitis and a predominant CD3+/CD4-/CD8+ phenotype in 2005 World Health Organization-European Organization for Research and Treatment of Cancer (WHO-EORTC) classification for cutaneous lymphomas. |
| 6345 | 18708940 | Besides the common features described before, unusual CD4+/CD8- and CD4-/CD8- T-cell phenotypes were noted in 2 of our cases, respectively. |
| 6346 | 18708940 | The frequency of rearranged TCRB, TCRG, and TCRD genes detected by BIOMED-2 multiplex polymerase chain reaction tubes was 80%, 67%, and 13%, respectively, with a total clonality detection rate of 100%. |
| 6347 | 18708940 | We conclude that SPTL as a cytotoxic lymphoma derived from alpha/beta T cell has a predominant CD4-/CD8+ phenotype, but unusual CD4+/CD8- and CD4-/CD8- phenotypes do exist. |
| 6348 | 18716002 | Moreover, blockade of IFN-alpha receptor 1 in NOD mice by a neutralizing antibody at 2-3 weeks of age significantly delayed the onset and decreased the incidence of type 1 diabetes, increased the relative number of immature dendritic cells in the PLNs, and enhanced the ability of spleen CD4(+) T cells to produce IL-4 and IL-10. |
| 6349 | 18755894 | We isolated highly pure CD4 or CD8 T cells from patients with type 1 diabetes (n = 675), other AI diseases, and healthy controls (n = 512). |
| 6350 | 18755894 | Using two cell death assays, we found that a subpopulation of CD8, but not CD4, T cells in patients' blood was vulnerable to TNF or TNF agonist-induced death. |
| 6351 | 18755894 | In type 1 diabetes, the subpopulation of T cells susceptible to TNF or TNFR2 agonist-induced death was traced specifically to autoreactive T cells to insulin, a known autoantigen. |
| 6352 | 18755894 | We isolated highly pure CD4 or CD8 T cells from patients with type 1 diabetes (n = 675), other AI diseases, and healthy controls (n = 512). |
| 6353 | 18755894 | Using two cell death assays, we found that a subpopulation of CD8, but not CD4, T cells in patients' blood was vulnerable to TNF or TNF agonist-induced death. |
| 6354 | 18755894 | In type 1 diabetes, the subpopulation of T cells susceptible to TNF or TNFR2 agonist-induced death was traced specifically to autoreactive T cells to insulin, a known autoantigen. |
| 6355 | 18807145 | The Langerhans' cells contained interdigitated nuclei, exhibiting rather clear nucleoplasm and cytoplasm; they were positive for S-100 protein, CD1a, and also CD4. |
| 6356 | 18825752 | Disease progression in experimental autoimmune encephalomyelitis (EAE) is regulated by programmed death receptor 1 (PD-1) and its ligands, B7-H1 (programmed death ligand 1 (PD-L1)) and B7-DC (PD-L2). |
| 6357 | 18825752 | B7-H1 and B7-DC have negative regulatory effects upon binding PD-1 on activated T cells and B7-H1 deficiency increases severity of both diabetes and EAE. |
| 6358 | 18825752 | Our data show that the majority of CNS CD4+ T cells isolated during acute EAE are PD-1+, and T cells specific for relapse-associated epitopes express PD-1 upon antigen stimulation in the CNS. |
| 6359 | 18825752 | B7-H1 and B7-DC are differentially expressed on discrete APC populations in the inflamed CNS. |
| 6360 | 18825752 | B7-H1 and PD-1 have mainly inhibitory functions on CNS T cells. |
| 6361 | 18825752 | B7-H1 negatively regulates the stimulation of activated PD-1+ T(H) cells, in co-cultures with microglia and different CNS-infiltrating APC presenting endogenously processed peptides. |
| 6362 | 18825752 | The preponderance of IFN-gamma+ versus IL-17+ T cells in the CNS of B7-H1(-/-) mice suggests that B7-H1 more selectively suppresses T(H)-1 than T(H)-17 responses in vivo. |
| 6363 | 18848698 | The role of interferon gamma in regulation of CD4+ T-cells and its clinical implications. |
| 6364 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6365 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6366 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6367 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6368 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6369 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6370 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6371 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6372 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6373 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6374 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6375 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6376 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6377 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6378 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6379 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6380 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6381 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6382 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6383 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6384 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6385 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6386 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6387 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6388 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6389 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6390 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6391 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6392 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6393 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6394 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6395 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6396 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6397 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6398 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6399 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6400 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6401 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6402 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6403 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6404 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6405 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6406 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6407 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6408 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6409 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6410 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6411 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6412 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6413 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6414 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6415 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6416 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6417 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6418 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6419 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6420 | 18855194 | Active CD4+ helper T cells directly stimulate CD8+ cytotoxic T lymphocyte responses in wild-type and MHC II gene knockout C57BL/6 mice and transgenic RIP-mOVA mice expressing islet beta-cell ovalbumin antigen leading to diabetes. |
| 6421 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 6422 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 6423 | 18855194 | We previously demonstrated that CD4+ Th cells can acquire ovalbumin (OVA) peptide/major histocompatibility complex (pMHC I) and costimulatory CD80 by OVA-pulsed DC (DC(OVA)) stimulation, and then stimulate OVA-specific CD8+ CTL responses in C57BL/6 mice. |
| 6424 | 18855194 | In this study, we further investigated CD4+ Th cell's effect on stimulation of CD8 CTL responses in major histocompatibility complex (MHC II) gene knockout (KO) mice and transgenic rat insulin promoter (RIP)-mOVA mice with moderate expression of self OVA by using CD4+ Th cells or Th cells with various gene deficiency. |
| 6425 | 18855194 | We demonstrated that the in vitro DC(OVA)-activated CD4+ Th cells (3 x 10(6) cells/mouse) can directly stimulate OVA-specific CD8+ T-cell responses in wild-type C57BL/6 mice and MHC II gene KO mice lacking CD4+ T cells. |
| 6426 | 18855194 | A large amount of CD4+ Th cells (12 x 10(6) cells/mouse) can even overcome OVA-specific immune tolerance in transgenic RIP-mOVA mice, leading to CD8+ CTL-mediated mouse pancreatic islet destruction and diabetes. |
| 6427 | 18855194 | The stimulatory effect of CD4+ Th cells is mediated by its IL-2 secretion and CD40L and CD80 costimulations, and is specifically delivered to OVA-specific CD8+ T cells in vivo via its acquired pMHC I complexes. |
| 6428 | 18925576 | Increased diabetes development and decreased function of CD4+CD25+ Treg in the absence of a functional DAP12 adaptor protein. |
| 6429 | 18925576 | Transferred BDC2.5 T cells proliferated more efficiently in the PLN of DAP12-deficient B6g7 recipients, which correlated with a decreased impact of co-transferred BDC2.5+CD4+CD25+ T cells. |
| 6430 | 18925576 | Increased diabetes development and decreased function of CD4+CD25+ Treg in the absence of a functional DAP12 adaptor protein. |
| 6431 | 18925576 | Transferred BDC2.5 T cells proliferated more efficiently in the PLN of DAP12-deficient B6g7 recipients, which correlated with a decreased impact of co-transferred BDC2.5+CD4+CD25+ T cells. |
| 6432 | 18941200 | Freshly isolated human islet ECs constitutively expressed CD86 (B7-2) and ICOS ligand but not CD80 (B7-1) or CD40 costimulatory molecules. |
| 6433 | 18941200 | The functional activity of islet EC-expressed CD86 was examined by coculture of resting islet ECs with CD4 T cells stimulated by CD3 ligation alone. |
| 6434 | 18941200 | In keeping with this, adhesion/transmigration of activated (CD3 ligated) memory (CD45R0(+)) CD4 T cells across islet ECs was completely inhibited in the presence of CD86 blocking mAb. |
| 6435 | 18941200 | Identical results were obtained for T cell adhesion using either CTLA-4 blocking mAb or CTLA-4Ig (abatacept), indicating CTLA-4 as the T cell ligand for these CD86-mediated effects. |
| 6436 | 18941200 | These data suggest a novel role for CD86 expression on the microvasculature, whereby ligation of CTLA-4 on CD4 T cells by CD86 on islet ECs is key to the adhesion of recently activated T cells. |
| 6437 | 18941200 | Freshly isolated human islet ECs constitutively expressed CD86 (B7-2) and ICOS ligand but not CD80 (B7-1) or CD40 costimulatory molecules. |
| 6438 | 18941200 | The functional activity of islet EC-expressed CD86 was examined by coculture of resting islet ECs with CD4 T cells stimulated by CD3 ligation alone. |
| 6439 | 18941200 | In keeping with this, adhesion/transmigration of activated (CD3 ligated) memory (CD45R0(+)) CD4 T cells across islet ECs was completely inhibited in the presence of CD86 blocking mAb. |
| 6440 | 18941200 | Identical results were obtained for T cell adhesion using either CTLA-4 blocking mAb or CTLA-4Ig (abatacept), indicating CTLA-4 as the T cell ligand for these CD86-mediated effects. |
| 6441 | 18941200 | These data suggest a novel role for CD86 expression on the microvasculature, whereby ligation of CTLA-4 on CD4 T cells by CD86 on islet ECs is key to the adhesion of recently activated T cells. |
| 6442 | 18941200 | Freshly isolated human islet ECs constitutively expressed CD86 (B7-2) and ICOS ligand but not CD80 (B7-1) or CD40 costimulatory molecules. |
| 6443 | 18941200 | The functional activity of islet EC-expressed CD86 was examined by coculture of resting islet ECs with CD4 T cells stimulated by CD3 ligation alone. |
| 6444 | 18941200 | In keeping with this, adhesion/transmigration of activated (CD3 ligated) memory (CD45R0(+)) CD4 T cells across islet ECs was completely inhibited in the presence of CD86 blocking mAb. |
| 6445 | 18941200 | Identical results were obtained for T cell adhesion using either CTLA-4 blocking mAb or CTLA-4Ig (abatacept), indicating CTLA-4 as the T cell ligand for these CD86-mediated effects. |
| 6446 | 18941200 | These data suggest a novel role for CD86 expression on the microvasculature, whereby ligation of CTLA-4 on CD4 T cells by CD86 on islet ECs is key to the adhesion of recently activated T cells. |
| 6447 | 18941219 | Impact of protective IL-2 allelic variants on CD4+ Foxp3+ regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. |
| 6448 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 6449 | 18941219 | The protective function of the Idd3 locus is confined to the Il2 gene, whose expression is critical for naturally occurring CD4(+)Foxp3(+) regulatory T (nT(reg)) cell development and function. |
| 6450 | 18941219 | We show that resistance to T1D in NOD.B6 Idd3 congenic mice correlates with increased levels of IL-2 mRNA and protein production in Ag-activated diabetogenic CD4(+) T cells. |
| 6451 | 18941219 | We also observe that protective IL2 allelic variants (Idd3(B6) resistance allele) also favor the expansion and suppressive functions of CD4(+)Foxp3(+) nT(reg) cells in vitro, as well as restrain the proliferation, IL-17 production, and pathogenicity of diabetogenic CD4(+) T cells in vivo more efficiently than control do nT(reg) cells. |
| 6452 | 18941219 | Lastly, the resistance to T1D in Idd3 congenic mice does not correlate with an augmented systemic frequency of CD4(+)Foxp3(+) nT(reg) cells but more so with the ability of protective IL2 allelic variants to promote the expansion of CD4(+)Foxp3(+) nT(reg) cells directly in the target organ undergoing autoimmune attack. |
| 6453 | 18941219 | Thus, protective, IL2 allelic variants impinge the development of organ-specific autoimmunity by bolstering the IL-2 producing capacity of self-reactive CD4(+) T cells and, in turn, favor the function and homeostasis of CD4(+)Foxp3(+) nT(reg) cells in vivo. |
| 6454 | 18941219 | Impact of protective IL-2 allelic variants on CD4+ Foxp3+ regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. |
| 6455 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 6456 | 18941219 | The protective function of the Idd3 locus is confined to the Il2 gene, whose expression is critical for naturally occurring CD4(+)Foxp3(+) regulatory T (nT(reg)) cell development and function. |
| 6457 | 18941219 | We show that resistance to T1D in NOD.B6 Idd3 congenic mice correlates with increased levels of IL-2 mRNA and protein production in Ag-activated diabetogenic CD4(+) T cells. |
| 6458 | 18941219 | We also observe that protective IL2 allelic variants (Idd3(B6) resistance allele) also favor the expansion and suppressive functions of CD4(+)Foxp3(+) nT(reg) cells in vitro, as well as restrain the proliferation, IL-17 production, and pathogenicity of diabetogenic CD4(+) T cells in vivo more efficiently than control do nT(reg) cells. |
| 6459 | 18941219 | Lastly, the resistance to T1D in Idd3 congenic mice does not correlate with an augmented systemic frequency of CD4(+)Foxp3(+) nT(reg) cells but more so with the ability of protective IL2 allelic variants to promote the expansion of CD4(+)Foxp3(+) nT(reg) cells directly in the target organ undergoing autoimmune attack. |
| 6460 | 18941219 | Thus, protective, IL2 allelic variants impinge the development of organ-specific autoimmunity by bolstering the IL-2 producing capacity of self-reactive CD4(+) T cells and, in turn, favor the function and homeostasis of CD4(+)Foxp3(+) nT(reg) cells in vivo. |
| 6461 | 18941219 | Impact of protective IL-2 allelic variants on CD4+ Foxp3+ regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. |
| 6462 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 6463 | 18941219 | The protective function of the Idd3 locus is confined to the Il2 gene, whose expression is critical for naturally occurring CD4(+)Foxp3(+) regulatory T (nT(reg)) cell development and function. |
| 6464 | 18941219 | We show that resistance to T1D in NOD.B6 Idd3 congenic mice correlates with increased levels of IL-2 mRNA and protein production in Ag-activated diabetogenic CD4(+) T cells. |
| 6465 | 18941219 | We also observe that protective IL2 allelic variants (Idd3(B6) resistance allele) also favor the expansion and suppressive functions of CD4(+)Foxp3(+) nT(reg) cells in vitro, as well as restrain the proliferation, IL-17 production, and pathogenicity of diabetogenic CD4(+) T cells in vivo more efficiently than control do nT(reg) cells. |
| 6466 | 18941219 | Lastly, the resistance to T1D in Idd3 congenic mice does not correlate with an augmented systemic frequency of CD4(+)Foxp3(+) nT(reg) cells but more so with the ability of protective IL2 allelic variants to promote the expansion of CD4(+)Foxp3(+) nT(reg) cells directly in the target organ undergoing autoimmune attack. |
| 6467 | 18941219 | Thus, protective, IL2 allelic variants impinge the development of organ-specific autoimmunity by bolstering the IL-2 producing capacity of self-reactive CD4(+) T cells and, in turn, favor the function and homeostasis of CD4(+)Foxp3(+) nT(reg) cells in vivo. |
| 6468 | 18941219 | Impact of protective IL-2 allelic variants on CD4+ Foxp3+ regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. |
| 6469 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 6470 | 18941219 | The protective function of the Idd3 locus is confined to the Il2 gene, whose expression is critical for naturally occurring CD4(+)Foxp3(+) regulatory T (nT(reg)) cell development and function. |
| 6471 | 18941219 | We show that resistance to T1D in NOD.B6 Idd3 congenic mice correlates with increased levels of IL-2 mRNA and protein production in Ag-activated diabetogenic CD4(+) T cells. |
| 6472 | 18941219 | We also observe that protective IL2 allelic variants (Idd3(B6) resistance allele) also favor the expansion and suppressive functions of CD4(+)Foxp3(+) nT(reg) cells in vitro, as well as restrain the proliferation, IL-17 production, and pathogenicity of diabetogenic CD4(+) T cells in vivo more efficiently than control do nT(reg) cells. |
| 6473 | 18941219 | Lastly, the resistance to T1D in Idd3 congenic mice does not correlate with an augmented systemic frequency of CD4(+)Foxp3(+) nT(reg) cells but more so with the ability of protective IL2 allelic variants to promote the expansion of CD4(+)Foxp3(+) nT(reg) cells directly in the target organ undergoing autoimmune attack. |
| 6474 | 18941219 | Thus, protective, IL2 allelic variants impinge the development of organ-specific autoimmunity by bolstering the IL-2 producing capacity of self-reactive CD4(+) T cells and, in turn, favor the function and homeostasis of CD4(+)Foxp3(+) nT(reg) cells in vivo. |
| 6475 | 18941219 | Impact of protective IL-2 allelic variants on CD4+ Foxp3+ regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. |
| 6476 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 6477 | 18941219 | The protective function of the Idd3 locus is confined to the Il2 gene, whose expression is critical for naturally occurring CD4(+)Foxp3(+) regulatory T (nT(reg)) cell development and function. |
| 6478 | 18941219 | We show that resistance to T1D in NOD.B6 Idd3 congenic mice correlates with increased levels of IL-2 mRNA and protein production in Ag-activated diabetogenic CD4(+) T cells. |
| 6479 | 18941219 | We also observe that protective IL2 allelic variants (Idd3(B6) resistance allele) also favor the expansion and suppressive functions of CD4(+)Foxp3(+) nT(reg) cells in vitro, as well as restrain the proliferation, IL-17 production, and pathogenicity of diabetogenic CD4(+) T cells in vivo more efficiently than control do nT(reg) cells. |
| 6480 | 18941219 | Lastly, the resistance to T1D in Idd3 congenic mice does not correlate with an augmented systemic frequency of CD4(+)Foxp3(+) nT(reg) cells but more so with the ability of protective IL2 allelic variants to promote the expansion of CD4(+)Foxp3(+) nT(reg) cells directly in the target organ undergoing autoimmune attack. |
| 6481 | 18941219 | Thus, protective, IL2 allelic variants impinge the development of organ-specific autoimmunity by bolstering the IL-2 producing capacity of self-reactive CD4(+) T cells and, in turn, favor the function and homeostasis of CD4(+)Foxp3(+) nT(reg) cells in vivo. |
| 6482 | 18941219 | Impact of protective IL-2 allelic variants on CD4+ Foxp3+ regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. |
| 6483 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 6484 | 18941219 | The protective function of the Idd3 locus is confined to the Il2 gene, whose expression is critical for naturally occurring CD4(+)Foxp3(+) regulatory T (nT(reg)) cell development and function. |
| 6485 | 18941219 | We show that resistance to T1D in NOD.B6 Idd3 congenic mice correlates with increased levels of IL-2 mRNA and protein production in Ag-activated diabetogenic CD4(+) T cells. |
| 6486 | 18941219 | We also observe that protective IL2 allelic variants (Idd3(B6) resistance allele) also favor the expansion and suppressive functions of CD4(+)Foxp3(+) nT(reg) cells in vitro, as well as restrain the proliferation, IL-17 production, and pathogenicity of diabetogenic CD4(+) T cells in vivo more efficiently than control do nT(reg) cells. |
| 6487 | 18941219 | Lastly, the resistance to T1D in Idd3 congenic mice does not correlate with an augmented systemic frequency of CD4(+)Foxp3(+) nT(reg) cells but more so with the ability of protective IL2 allelic variants to promote the expansion of CD4(+)Foxp3(+) nT(reg) cells directly in the target organ undergoing autoimmune attack. |
| 6488 | 18941219 | Thus, protective, IL2 allelic variants impinge the development of organ-specific autoimmunity by bolstering the IL-2 producing capacity of self-reactive CD4(+) T cells and, in turn, favor the function and homeostasis of CD4(+)Foxp3(+) nT(reg) cells in vivo. |
| 6489 | 18951762 | CD40 on NOD CD4 T cells contributes to their activation and pathogenicity. |
| 6490 | 18951762 | Our goals in this study were to investigate conditions under which T cells from NOD mice express CD40 and to determine how CD40 on autoreactive CD4 T cells contributes to their pathogenicity in T1D. |
| 6491 | 18951762 | Using CD40-positive diabetogenic T cell clones and CD4 T cells from NOD mice, we examined expression of CD40 upon activation through the TCR and costimulation through either CD28 or CD40. |
| 6492 | 18951762 | Our results indicate that CD40 expression is increased upon activation with antigen/MHC and that activation of NOD CD4 T cells through TCR/CD40 rapidly induced CD40 expression. |
| 6493 | 18951762 | Furthermore, CD40 costimulation promoted T cell proliferation to the same extent as costimulation through TCR/CD28. |
| 6494 | 18951762 | Importantly, costimulation of CD4 T cells through CD40 also interfered with T cell homeostasis by altering regulation of CTLA-4 expression. |
| 6495 | 18951762 | Thus, costimulation through CD40 on NOD T cells contributes to their pathogenicity by providing additional pathways for activation and by inhibiting upregulation of CTLA-4 during T cell activation. |
| 6496 | 18951762 | CD40 on NOD CD4 T cells contributes to their activation and pathogenicity. |
| 6497 | 18951762 | Our goals in this study were to investigate conditions under which T cells from NOD mice express CD40 and to determine how CD40 on autoreactive CD4 T cells contributes to their pathogenicity in T1D. |
| 6498 | 18951762 | Using CD40-positive diabetogenic T cell clones and CD4 T cells from NOD mice, we examined expression of CD40 upon activation through the TCR and costimulation through either CD28 or CD40. |
| 6499 | 18951762 | Our results indicate that CD40 expression is increased upon activation with antigen/MHC and that activation of NOD CD4 T cells through TCR/CD40 rapidly induced CD40 expression. |
| 6500 | 18951762 | Furthermore, CD40 costimulation promoted T cell proliferation to the same extent as costimulation through TCR/CD28. |
| 6501 | 18951762 | Importantly, costimulation of CD4 T cells through CD40 also interfered with T cell homeostasis by altering regulation of CTLA-4 expression. |
| 6502 | 18951762 | Thus, costimulation through CD40 on NOD T cells contributes to their pathogenicity by providing additional pathways for activation and by inhibiting upregulation of CTLA-4 during T cell activation. |
| 6503 | 18951762 | CD40 on NOD CD4 T cells contributes to their activation and pathogenicity. |
| 6504 | 18951762 | Our goals in this study were to investigate conditions under which T cells from NOD mice express CD40 and to determine how CD40 on autoreactive CD4 T cells contributes to their pathogenicity in T1D. |
| 6505 | 18951762 | Using CD40-positive diabetogenic T cell clones and CD4 T cells from NOD mice, we examined expression of CD40 upon activation through the TCR and costimulation through either CD28 or CD40. |
| 6506 | 18951762 | Our results indicate that CD40 expression is increased upon activation with antigen/MHC and that activation of NOD CD4 T cells through TCR/CD40 rapidly induced CD40 expression. |
| 6507 | 18951762 | Furthermore, CD40 costimulation promoted T cell proliferation to the same extent as costimulation through TCR/CD28. |
| 6508 | 18951762 | Importantly, costimulation of CD4 T cells through CD40 also interfered with T cell homeostasis by altering regulation of CTLA-4 expression. |
| 6509 | 18951762 | Thus, costimulation through CD40 on NOD T cells contributes to their pathogenicity by providing additional pathways for activation and by inhibiting upregulation of CTLA-4 during T cell activation. |
| 6510 | 18951762 | CD40 on NOD CD4 T cells contributes to their activation and pathogenicity. |
| 6511 | 18951762 | Our goals in this study were to investigate conditions under which T cells from NOD mice express CD40 and to determine how CD40 on autoreactive CD4 T cells contributes to their pathogenicity in T1D. |
| 6512 | 18951762 | Using CD40-positive diabetogenic T cell clones and CD4 T cells from NOD mice, we examined expression of CD40 upon activation through the TCR and costimulation through either CD28 or CD40. |
| 6513 | 18951762 | Our results indicate that CD40 expression is increased upon activation with antigen/MHC and that activation of NOD CD4 T cells through TCR/CD40 rapidly induced CD40 expression. |
| 6514 | 18951762 | Furthermore, CD40 costimulation promoted T cell proliferation to the same extent as costimulation through TCR/CD28. |
| 6515 | 18951762 | Importantly, costimulation of CD4 T cells through CD40 also interfered with T cell homeostasis by altering regulation of CTLA-4 expression. |
| 6516 | 18951762 | Thus, costimulation through CD40 on NOD T cells contributes to their pathogenicity by providing additional pathways for activation and by inhibiting upregulation of CTLA-4 during T cell activation. |
| 6517 | 18951762 | CD40 on NOD CD4 T cells contributes to their activation and pathogenicity. |
| 6518 | 18951762 | Our goals in this study were to investigate conditions under which T cells from NOD mice express CD40 and to determine how CD40 on autoreactive CD4 T cells contributes to their pathogenicity in T1D. |
| 6519 | 18951762 | Using CD40-positive diabetogenic T cell clones and CD4 T cells from NOD mice, we examined expression of CD40 upon activation through the TCR and costimulation through either CD28 or CD40. |
| 6520 | 18951762 | Our results indicate that CD40 expression is increased upon activation with antigen/MHC and that activation of NOD CD4 T cells through TCR/CD40 rapidly induced CD40 expression. |
| 6521 | 18951762 | Furthermore, CD40 costimulation promoted T cell proliferation to the same extent as costimulation through TCR/CD28. |
| 6522 | 18951762 | Importantly, costimulation of CD4 T cells through CD40 also interfered with T cell homeostasis by altering regulation of CTLA-4 expression. |
| 6523 | 18951762 | Thus, costimulation through CD40 on NOD T cells contributes to their pathogenicity by providing additional pathways for activation and by inhibiting upregulation of CTLA-4 during T cell activation. |
| 6524 | 18981116 | Furthermore, islet-infiltrating leukocytes in the LTP mice contained Foxp3(+)CD4 T cells. |
| 6525 | 18981116 | The LTP was abolished if mice were treated with either Ab-depleting CD4 T cells or a neutralizing Ab to CTLA-4, in this case, only at a late stage. |
| 6526 | 18981116 | Neutralization of IL-10, TGF-beta, glucocorticoid-induced TNF receptor (GITR), or CD25 had no effect. |
| 6527 | 18981116 | Hence, using monoclonal CD4 T cells, IFN-gamma can have a wide diversity of roles, depending on the setting of the immune process. |
| 6528 | 18981116 | Furthermore, islet-infiltrating leukocytes in the LTP mice contained Foxp3(+)CD4 T cells. |
| 6529 | 18981116 | The LTP was abolished if mice were treated with either Ab-depleting CD4 T cells or a neutralizing Ab to CTLA-4, in this case, only at a late stage. |
| 6530 | 18981116 | Neutralization of IL-10, TGF-beta, glucocorticoid-induced TNF receptor (GITR), or CD25 had no effect. |
| 6531 | 18981116 | Hence, using monoclonal CD4 T cells, IFN-gamma can have a wide diversity of roles, depending on the setting of the immune process. |
| 6532 | 18981116 | Furthermore, islet-infiltrating leukocytes in the LTP mice contained Foxp3(+)CD4 T cells. |
| 6533 | 18981116 | The LTP was abolished if mice were treated with either Ab-depleting CD4 T cells or a neutralizing Ab to CTLA-4, in this case, only at a late stage. |
| 6534 | 18981116 | Neutralization of IL-10, TGF-beta, glucocorticoid-induced TNF receptor (GITR), or CD25 had no effect. |
| 6535 | 18981116 | Hence, using monoclonal CD4 T cells, IFN-gamma can have a wide diversity of roles, depending on the setting of the immune process. |
| 6536 | 18981158 | The effector T cells of diabetic subjects are resistant to regulation via CD4+ FOXP3+ regulatory T cells. |
| 6537 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6538 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6539 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6540 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6541 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6542 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6543 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6544 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6545 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6546 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6547 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6548 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6549 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6550 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6551 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6552 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6553 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6554 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6555 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6556 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6557 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6558 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6559 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6560 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6561 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6562 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6563 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6564 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6565 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6566 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6567 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6568 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6569 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6570 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6571 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6572 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6573 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6574 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6575 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6576 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6577 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6578 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6579 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6580 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6581 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6582 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6583 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6584 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6585 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6586 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6587 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6588 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6589 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6590 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6591 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6592 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6593 | 18985367 | CD4(+)CD25 (+) regulatory T cells in human lupus erythematosus. |
| 6594 | 18985367 | Natural CD4(+)CD25(+) regulatory T cells (T(reg)) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. |
| 6595 | 18985367 | For example, aberrant numbers of circulating CD4(+)CD25(+) T(reg) have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. |
| 6596 | 18985367 | Moreover, increased numbers of functionally active CD4(+)CD25(+) T(reg) have been detected in the synovial fluid of patients with rheumatoid arthritis. |
| 6597 | 18985367 | In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T(reg) in human autoimmune diseases have been presented in the literature. |
| 6598 | 18985367 | Decreased numbers of peripheral blood T(reg) have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T(reg) numbers have also been described. |
| 6599 | 18985367 | Analysis of CD4(+)FoxP3(+) T(reg) in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T(reg) numbers in the affected tissue. |
| 6600 | 18985367 | In this review, we discuss the role of CD4(+)CD25(+) T(reg) in autoimmunity and recent published data on SLE. |
| 6601 | 19006694 | CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. |
| 6602 | 19006694 | We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. |
| 6603 | 19006694 | These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. |
| 6604 | 19006694 | CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. |
| 6605 | 19006694 | We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. |
| 6606 | 19006694 | These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. |
| 6607 | 19006694 | CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. |
| 6608 | 19006694 | We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. |
| 6609 | 19006694 | These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. |
| 6610 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6611 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6612 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6613 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6614 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6615 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6616 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6617 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6618 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6619 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6620 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6621 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6622 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6623 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6624 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6625 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6626 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6627 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6628 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6629 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6630 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6631 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6632 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6633 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6634 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6635 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6636 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6637 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6638 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6639 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6640 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6641 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6642 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6643 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6644 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6645 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6646 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6647 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6648 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6649 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6650 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6651 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6652 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6653 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6654 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6655 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6656 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6657 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6658 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6659 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6660 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6661 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6662 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6663 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6664 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6665 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6666 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6667 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6668 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6669 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6670 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6671 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6672 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6673 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 6674 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 6675 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 6676 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 6677 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 6678 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 6679 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 6680 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 6681 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 6682 | 19011680 | APC activation restores functional CD4(+)CD25(+) regulatory T cells in NOD mice that can prevent diabetes development. |
| 6683 | 19018006 | Moreover, in vivo BLyS neutralization: 1) restored negative selection at the TR-->FO checkpoint, 2) abrogated serum insulin autoantibodies, 3) reduced the severity of islet inflammation, 4) significantly reduced the incidence of spontaneous diabetes, 5) arrested the terminal stages of islet cell destruction, and 6) disrupted CD4 T cell activation in NOD mice. |
| 6684 | 19034003 | Pancreatic islets induce CD4(+) [corrected] CD25(-)Foxp3(+) [corrected] T-cell regulated tolerance to HY-mismatched skin grafts. |
| 6685 | 19036642 | It is widely believed that CD4(+)CD25(+) regulatory T cells (Treg) are defective in type 1 diabetes (T1D) and other autoimmune diseases. |
| 6686 | 19036642 | The frequencies of CD4(+)CD25(+) and CD4(+)CD25(hi) T cells were found to increase with age in normal controls but not in T1D patients, resulting in significantly higher frequencies of CD4(+)CD25(+) (p=0.001) and CD4(+)CD25(hi) (p=0.009) T cells in young T1D subjects than age-matched controls but slightly lower CD4(+)CD25(+) (p=0.003) and CD4(+)CD25(hi) (p=0.08) T cells in old T1D subjects than age-matched controls. |
| 6687 | 19036642 | It is widely believed that CD4(+)CD25(+) regulatory T cells (Treg) are defective in type 1 diabetes (T1D) and other autoimmune diseases. |
| 6688 | 19036642 | The frequencies of CD4(+)CD25(+) and CD4(+)CD25(hi) T cells were found to increase with age in normal controls but not in T1D patients, resulting in significantly higher frequencies of CD4(+)CD25(+) (p=0.001) and CD4(+)CD25(hi) (p=0.009) T cells in young T1D subjects than age-matched controls but slightly lower CD4(+)CD25(+) (p=0.003) and CD4(+)CD25(hi) (p=0.08) T cells in old T1D subjects than age-matched controls. |
| 6689 | 19044032 | He was given a clinical diagnosis of central neurosarcoidosis with panhypopituitarism because of the presence of an abnormal lung shadow, positive gallium scintigram in bilateral hilar lymph nodes, negative tuberculin skin test, lymphocytosis and a high CD4/8 ratio in bronchoalveolar lavage fluid. |
| 6690 | 19050246 | Therapeutic administration of proinsulin DNA was accompanied by a rapid decrease in the number of insulin-specific IFN-gamma-producing T cells, whereas prophylactic treatment was accompanied by enhanced IFN-gamma-secreting cells and a decrease in insulin autoantibodies. |
| 6691 | 19050246 | Adoptive transfer experiments demonstrated that the protection was not mediated by induction of CD25(+)/CD4(+) T regulatory cells. |
| 6692 | 19050249 | Exposure of APCs of NOD mice to zymosan, a fungal cell wall component that interacts with TLR2 and dectin 1, resulted in the release of significant amounts of IL-10, TGF-beta1, IL-2, and TNF-alpha. |
| 6693 | 19050249 | Zymosan treatment induced suppression of T1D was associated with an increase in the L-selectin(high) T cell frequencies and enhanced suppressor function of CD4(+)CD25(+) T regulatory cells. |
| 6694 | 19050249 | Further, activation by anti-CD3-Ab induced larger amounts of TGF-beta1 and/or IL-10 production by CD4(+)CD25(+) and CD4(+)CD25(-) T cells from zymosan-treated mice. |
| 6695 | 19050249 | Exposure of APCs of NOD mice to zymosan, a fungal cell wall component that interacts with TLR2 and dectin 1, resulted in the release of significant amounts of IL-10, TGF-beta1, IL-2, and TNF-alpha. |
| 6696 | 19050249 | Zymosan treatment induced suppression of T1D was associated with an increase in the L-selectin(high) T cell frequencies and enhanced suppressor function of CD4(+)CD25(+) T regulatory cells. |
| 6697 | 19050249 | Further, activation by anti-CD3-Ab induced larger amounts of TGF-beta1 and/or IL-10 production by CD4(+)CD25(+) and CD4(+)CD25(-) T cells from zymosan-treated mice. |
| 6698 | 19062254 | Autologous bone marrow-derived rat mesenchymal stem cells promote PDX-1 and insulin expression in the islets, alter T cell cytokine pattern and preserve regulatory T cells in the periphery and induce sustained normoglycemia. |
| 6699 | 19062254 | MSC were CD45(-)/CD44(+)/CD54(+)/CD90(+)/CD106(+). |
| 6700 | 19062254 | MSC spontaneously secreted IL-6, HGF, TGF-beta1 and expressed high levels of SDF-1 and low levels of VEGF, IL-1beta and PGE(2), but no EGF, insulin or glucagon. |
| 6701 | 19062254 | Interestingly, immunohistochemistry demonstrated that, the islets from MSC-treated rats expressed high levels of PDX-1 and that these cells were also positive for insulin staining. |
| 6702 | 19062254 | In addition, peripheral T cells from MSC-treated rats exhibited a shift toward IL-10/IL-13 production and higher frequencies of CD4(+)/CD8(+) Foxp3(+) T cells compared to the PBS-treated rats. |
| 6703 | 19076626 | The primary antibodies used were monoclonal antibody to S100, CD1a, CD34, HLA-DR, PCNA, CD45Ro, CD40, and langerin. |
| 6704 | 19076626 | Cells CD1a+ and S100+ infiltrated the epidermic and were dispersed over the infiltrates as well as in clusters, and around the vessels. |
| 6705 | 19076626 | A considerable number of CD40-expressing cells were restricted to CD1a+ LCH cells. |
| 6706 | 19076626 | Histopathologic examination of the lesion evidences a mixture of Langerhans cell histiocytes (CD1a+, S100+, HLADr+, CD207+, CD 40+), lymphocytes (predominantly helper [CD4] CD 45 Ro+), eosinophils, and macrophages. |
| 6707 | 19111164 | Type 1 diabetes (T1D), an autoimmune disease once thought to be mediated exclusively by beta cell-specific CD4+ T cells, is now recognized as one in which autoreactive CD8+ T cells play a fundamental role. |
| 6708 | 19111528 | Although the PTPRC gene has a significant role in regulating CD4+ and CD8+ autoreactive T-cells, interferon-beta responsiveness, and potentially other important processes, our study does not support a role for the two tested variants of this gene in MS susceptibility in the Australian population. |
| 6709 | 19120285 | We report that TLR agonists prevent the generation of mixed chimerism by breaking tolerance in the alloreactive CD4(+) and CD8(+) T cell compartments, and that type I interferon (IFN) is important in this process. |
| 6710 | 19120288 | Furthermore, TCR-transgenic CD4(+) T cells primed by the antigens to which they were specific in the presence of UVB-irradiated stromal cells were rendered unresponsive to the antigen restimulation, a result that was partially attributed to the induced IL-10-producing regulatory T cells. |
| 6711 | 19120290 | Of interest, Ad-hTGFbeta transduction in CD4(+)CD25(-) T cells resulted in a significant enhanced expression of CD25 and a regulatory T cell-specific transcription factor, Foxp3. |
| 6712 | 19120290 | Although we found favorable in vitro results, such as decrease in islet apoptosis, enhanced proliferation and differentiation, and increase in the level of CD4(+)CD25(+) regulatory T cells, there was no difference in reduction of the development of T1D between controls and Ad-hTGFbeta-injected mice. |
| 6713 | 19120290 | Of interest, Ad-hTGFbeta transduction in CD4(+)CD25(-) T cells resulted in a significant enhanced expression of CD25 and a regulatory T cell-specific transcription factor, Foxp3. |
| 6714 | 19120290 | Although we found favorable in vitro results, such as decrease in islet apoptosis, enhanced proliferation and differentiation, and increase in the level of CD4(+)CD25(+) regulatory T cells, there was no difference in reduction of the development of T1D between controls and Ad-hTGFbeta-injected mice. |
| 6715 | 19120302 | Administration of a humanized monoclonal anti-CD3 antibody (mAb) to patients with type 1 diabetes (T1D) increases their C-peptide responses and the CD8/CD4 ratio. |
| 6716 | 19120302 | Incubation of human peripheral blood mononuclear cells (PBMC) with mAb in vitro has been shown to induce CD8(+) regulatory T cells (Tregs) capable of inhibiting proliferation of CD4(+) T cells. |
| 6717 | 19120302 | Administration of a humanized monoclonal anti-CD3 antibody (mAb) to patients with type 1 diabetes (T1D) increases their C-peptide responses and the CD8/CD4 ratio. |
| 6718 | 19120302 | Incubation of human peripheral blood mononuclear cells (PBMC) with mAb in vitro has been shown to induce CD8(+) regulatory T cells (Tregs) capable of inhibiting proliferation of CD4(+) T cells. |
| 6719 | 19120311 | The sentinel role of CD8 T cells in regulating CD4 T cell responses to proinsulin in beta-islet cell autoimmunity. |
| 6720 | 19120311 | Circulating CD4 T cells specific for peptide epitopes of proinsulin and other autoantigens are markers of autoimmune beta cell destruction in type 1 diabetes, while the role of CD8 T cells is still largely unknown. |
| 6721 | 19120311 | Here we show that CD8 T cells of a diabetic patient--after rechallange with proinsulin peptides--secrete IFNgamma and granzyme B, markers of their effector capacity. |
| 6722 | 19120311 | On the other hand, CD8 T cells of the same patient in a "cross-talk" with proinsulin-specific CD4 T cells suppress their proliferation. |
| 6723 | 19120311 | The sentinel role of CD8 T cells in regulating CD4 T cell responses to proinsulin in beta-islet cell autoimmunity. |
| 6724 | 19120311 | Circulating CD4 T cells specific for peptide epitopes of proinsulin and other autoantigens are markers of autoimmune beta cell destruction in type 1 diabetes, while the role of CD8 T cells is still largely unknown. |
| 6725 | 19120311 | Here we show that CD8 T cells of a diabetic patient--after rechallange with proinsulin peptides--secrete IFNgamma and granzyme B, markers of their effector capacity. |
| 6726 | 19120311 | On the other hand, CD8 T cells of the same patient in a "cross-talk" with proinsulin-specific CD4 T cells suppress their proliferation. |
| 6727 | 19120311 | The sentinel role of CD8 T cells in regulating CD4 T cell responses to proinsulin in beta-islet cell autoimmunity. |
| 6728 | 19120311 | Circulating CD4 T cells specific for peptide epitopes of proinsulin and other autoantigens are markers of autoimmune beta cell destruction in type 1 diabetes, while the role of CD8 T cells is still largely unknown. |
| 6729 | 19120311 | Here we show that CD8 T cells of a diabetic patient--after rechallange with proinsulin peptides--secrete IFNgamma and granzyme B, markers of their effector capacity. |
| 6730 | 19120311 | On the other hand, CD8 T cells of the same patient in a "cross-talk" with proinsulin-specific CD4 T cells suppress their proliferation. |
| 6731 | 19120313 | CD4(+)CD25(+) T cells (Tregs) play a critical role in maintaining dominant peripheral tolerance, and pathogenic autoreactive T cells may be frequent in the CD25-negative fraction of peripheral blood mononuclear cells (PBMCs) from patients with autoimmune disease. |
| 6732 | 19120313 | The frequency of CD4(+)CD25(+) T cells was not different among patients with newly developed T1D, established T1D, and healthy controls. |
| 6733 | 19120313 | The CD25 positive cell-depleted fraction was obtained by negative selection with antihuman CD25 magnetic beads, reducing the number of CD4(+)CD25(+) T cells from 4-5% to less than 1%. |
| 6734 | 19120313 | CD4(+)CD25(+) T cells (Tregs) play a critical role in maintaining dominant peripheral tolerance, and pathogenic autoreactive T cells may be frequent in the CD25-negative fraction of peripheral blood mononuclear cells (PBMCs) from patients with autoimmune disease. |
| 6735 | 19120313 | The frequency of CD4(+)CD25(+) T cells was not different among patients with newly developed T1D, established T1D, and healthy controls. |
| 6736 | 19120313 | The CD25 positive cell-depleted fraction was obtained by negative selection with antihuman CD25 magnetic beads, reducing the number of CD4(+)CD25(+) T cells from 4-5% to less than 1%. |
| 6737 | 19120313 | CD4(+)CD25(+) T cells (Tregs) play a critical role in maintaining dominant peripheral tolerance, and pathogenic autoreactive T cells may be frequent in the CD25-negative fraction of peripheral blood mononuclear cells (PBMCs) from patients with autoimmune disease. |
| 6738 | 19120313 | The frequency of CD4(+)CD25(+) T cells was not different among patients with newly developed T1D, established T1D, and healthy controls. |
| 6739 | 19120313 | The CD25 positive cell-depleted fraction was obtained by negative selection with antihuman CD25 magnetic beads, reducing the number of CD4(+)CD25(+) T cells from 4-5% to less than 1%. |
| 6740 | 19130584 | To understand the function of Th17 cells in IDDM, we differentiated islet-reactive BDC2.5 TcR transgenic CD4(+) cells in vitro into Th17 cells and transferred them into NOD.scid and neonate NOD mice. |
| 6741 | 19130584 | Surprisingly, BDC2.5(+) cells recovered from diabetic NOD.scid mice, in comparison with those from neonate NOD mice, showed predominant IFN-gamma over IL-17 expression, indicating conversion of donor cells into Th1 cells. |
| 6742 | 19130584 | Moreover, diabetes progression in NOD.scid recipients was dependent on IFN-gamma while anti-IL-17 treatment reduced insulitic inflammation. |
| 6743 | 19130584 | These results indicate that islet-reactive Th17 cells promote pancreatic inflammation, but only induce IDDM upon conversion into IFN-gamma producers. |
| 6744 | 19136960 | Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells. |
| 6745 | 19136960 | Interleukin 7 (IL-7) and T cell antigen receptor signals have been proposed to be the main drivers of homeostatic T cell proliferation. |
| 6746 | 19136960 | However, it is not known why CD4(+) T cells undergo less-efficient homeostatic proliferation than CD8(+) T cells do. |
| 6747 | 19136960 | Here we show that systemic IL-7 concentrations increased during lymphopenia because of diminished use of IL-7 but that IL-7 signaling on IL-7 receptor-alpha-positive (IL-7Ralpha(+)) dendritic cells (DCs) in lymphopenic settings paradoxically diminished the homeostatic proliferation of CD4(+) T cells. |
| 6748 | 19136960 | This effect was mediated at least in part by IL-7-mediated downregulation of the expression of major histocompatibility complex class II on IL-7Ralpha(+) DCs. |
| 6749 | 19136960 | Our results indicate that IL-7Ralpha(+) DCs are regulators of the peripheral CD4(+) T cell niche and that IL-7 signals in DCs prevent uncontrolled CD4(+) T cell population expansion in vivo. |
| 6750 | 19136960 | Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells. |
| 6751 | 19136960 | Interleukin 7 (IL-7) and T cell antigen receptor signals have been proposed to be the main drivers of homeostatic T cell proliferation. |
| 6752 | 19136960 | However, it is not known why CD4(+) T cells undergo less-efficient homeostatic proliferation than CD8(+) T cells do. |
| 6753 | 19136960 | Here we show that systemic IL-7 concentrations increased during lymphopenia because of diminished use of IL-7 but that IL-7 signaling on IL-7 receptor-alpha-positive (IL-7Ralpha(+)) dendritic cells (DCs) in lymphopenic settings paradoxically diminished the homeostatic proliferation of CD4(+) T cells. |
| 6754 | 19136960 | This effect was mediated at least in part by IL-7-mediated downregulation of the expression of major histocompatibility complex class II on IL-7Ralpha(+) DCs. |
| 6755 | 19136960 | Our results indicate that IL-7Ralpha(+) DCs are regulators of the peripheral CD4(+) T cell niche and that IL-7 signals in DCs prevent uncontrolled CD4(+) T cell population expansion in vivo. |
| 6756 | 19136960 | Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells. |
| 6757 | 19136960 | Interleukin 7 (IL-7) and T cell antigen receptor signals have been proposed to be the main drivers of homeostatic T cell proliferation. |
| 6758 | 19136960 | However, it is not known why CD4(+) T cells undergo less-efficient homeostatic proliferation than CD8(+) T cells do. |
| 6759 | 19136960 | Here we show that systemic IL-7 concentrations increased during lymphopenia because of diminished use of IL-7 but that IL-7 signaling on IL-7 receptor-alpha-positive (IL-7Ralpha(+)) dendritic cells (DCs) in lymphopenic settings paradoxically diminished the homeostatic proliferation of CD4(+) T cells. |
| 6760 | 19136960 | This effect was mediated at least in part by IL-7-mediated downregulation of the expression of major histocompatibility complex class II on IL-7Ralpha(+) DCs. |
| 6761 | 19136960 | Our results indicate that IL-7Ralpha(+) DCs are regulators of the peripheral CD4(+) T cell niche and that IL-7 signals in DCs prevent uncontrolled CD4(+) T cell population expansion in vivo. |
| 6762 | 19136960 | Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells. |
| 6763 | 19136960 | Interleukin 7 (IL-7) and T cell antigen receptor signals have been proposed to be the main drivers of homeostatic T cell proliferation. |
| 6764 | 19136960 | However, it is not known why CD4(+) T cells undergo less-efficient homeostatic proliferation than CD8(+) T cells do. |
| 6765 | 19136960 | Here we show that systemic IL-7 concentrations increased during lymphopenia because of diminished use of IL-7 but that IL-7 signaling on IL-7 receptor-alpha-positive (IL-7Ralpha(+)) dendritic cells (DCs) in lymphopenic settings paradoxically diminished the homeostatic proliferation of CD4(+) T cells. |
| 6766 | 19136960 | This effect was mediated at least in part by IL-7-mediated downregulation of the expression of major histocompatibility complex class II on IL-7Ralpha(+) DCs. |
| 6767 | 19136960 | Our results indicate that IL-7Ralpha(+) DCs are regulators of the peripheral CD4(+) T cell niche and that IL-7 signals in DCs prevent uncontrolled CD4(+) T cell population expansion in vivo. |
| 6768 | 19162441 | Here we report that CD103 had no significant impact on the development of primary and memory CD8(+) or CD4(+) responses after acute lymphocytic choriomeningitis virus (LCMV) infection. |
| 6769 | 19162441 | In addition, CD103 was found to be dispensable for T1D progression in a rapid, CD8-mediated virally-induced T1D model (the rat insulin promoter [RIP]-LCMV), suggesting that its previous efficacy in the NOD mouse model may not be related to its effect on the generation, memory conversion and/or effector function of CD8(+) or CD4(+) T cells. |
| 6770 | 19162441 | Here we report that CD103 had no significant impact on the development of primary and memory CD8(+) or CD4(+) responses after acute lymphocytic choriomeningitis virus (LCMV) infection. |
| 6771 | 19162441 | In addition, CD103 was found to be dispensable for T1D progression in a rapid, CD8-mediated virally-induced T1D model (the rat insulin promoter [RIP]-LCMV), suggesting that its previous efficacy in the NOD mouse model may not be related to its effect on the generation, memory conversion and/or effector function of CD8(+) or CD4(+) T cells. |
| 6772 | 19180473 | CD4(+)CD25(+)FOXP3(+) Treg cells require TCR engagement for suppressive function, thus ensuring that suppression occurs only in the presence of specific antigens; however, to date no studies have addressed the function of self-antigen-specific Treg in humans. |
| 6773 | 19180473 | Islet antigen-specific adaptive Treg were induced in vitro by activation of CD4(+)FOXP3(-) T cells with glutamic acid decarboxylase and islet-specific glucose-6-phosphate catalytic subunit-related protein peptides in the context of T1D-associated HLA-DRbeta alleles. |
| 6774 | 19180473 | CD4(+)CD25(+)FOXP3(+) Treg cells require TCR engagement for suppressive function, thus ensuring that suppression occurs only in the presence of specific antigens; however, to date no studies have addressed the function of self-antigen-specific Treg in humans. |
| 6775 | 19180473 | Islet antigen-specific adaptive Treg were induced in vitro by activation of CD4(+)FOXP3(-) T cells with glutamic acid decarboxylase and islet-specific glucose-6-phosphate catalytic subunit-related protein peptides in the context of T1D-associated HLA-DRbeta alleles. |
| 6776 | 19188932 | Induction of CD4+CD25+Foxp3+ regulatory T cell response by glatiramer acetate in type 1 diabetes. |
| 6777 | 19188932 | Treatment with GA significantly reduced the diabetic rate in the mice and ameliorated insulitis, which coincided with increased CD4+CD25+Foxp3+ T cell response in treated mice. |
| 6778 | 19188932 | IL-4 was found to maintain Foxp3 expression and regulatory function of CD4+CD25+ regulatory T cells (Tregs). |
| 6779 | 19188932 | Induction of CD4+CD25+Foxp3+ regulatory T cell response by glatiramer acetate in type 1 diabetes. |
| 6780 | 19188932 | Treatment with GA significantly reduced the diabetic rate in the mice and ameliorated insulitis, which coincided with increased CD4+CD25+Foxp3+ T cell response in treated mice. |
| 6781 | 19188932 | IL-4 was found to maintain Foxp3 expression and regulatory function of CD4+CD25+ regulatory T cells (Tregs). |
| 6782 | 19188932 | Induction of CD4+CD25+Foxp3+ regulatory T cell response by glatiramer acetate in type 1 diabetes. |
| 6783 | 19188932 | Treatment with GA significantly reduced the diabetic rate in the mice and ameliorated insulitis, which coincided with increased CD4+CD25+Foxp3+ T cell response in treated mice. |
| 6784 | 19188932 | IL-4 was found to maintain Foxp3 expression and regulatory function of CD4+CD25+ regulatory T cells (Tregs). |
| 6785 | 19189134 | This report describes a 5-year-old boy with IPEX syndrome with a 3 bp deletion in the FOXP3 gene (c.748-750delAAG, p.250K.del) and a paucity of CD4(+) CD25(+) FOXP3(+) T cells. |
| 6786 | 19209463 | A very significant fraction of islet-associated CD8 T cells in NOD mice recognize epitopes of islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP), a non-essential endoplasmic reticulum-resident protein of unclear function. |
| 6787 | 19209463 | IGRP is also a target of CD8 T cell responses in human T1D patients. |
| 6788 | 19209463 | In NOD mice, most IGRP-reactive CD8 T cells target the IGRP(206-214) epitope and are diabetogenic. |
| 6789 | 19209463 | In mice, Il2 polymorphisms control a negative feedback mechanism initiated by activated, IL2-producing autoreactive T cells in the pancreatic lymph nodes that increases the regulatory activity of CD4+CD25+ T cells. |
| 6790 | 19209463 | Not all IGRP-reactive CD8 T cell clones are pathogenic, however, and we have evidence that some of these clonotypes are actually anti-diabetogenic. |
| 6791 | 19209463 | We had previously shown that administration of altered peptide ligands (APL) targeting IGRP(206-214)-reactive CD8 T cells resulted in diabetes protection only at doses that did not delete low-avidity clones, suggesting a protective role for these clonotypes. |
| 6792 | 19209463 | Here I briefly summarize work done by us and others indicating that a prevalent subset of autoreactive CD8 T-cells in the NOD mouse are major (albeit likely dispensable) players in the pathogenesis of spontaneous autoimmune diabetes in the NOD mouse; that these T cells are targets of genetic elements affording autoimmune disease susceptibility and resistance; that they can either be diabetogenic or anti-diabetogenic according to their avidity for peptide/MHC; and that they can serve as useful targets for therapeutic intervention. |
| 6793 | 19211146 | Prevention of T1D was associated with reduced emergence of primed (autoreactive) CD4(+) CD25(+) T cells, but not with the emergence of Foxp3(+) Treg in the peripheral compartments. |
| 6794 | 19211146 | However, administration of ATRA to NOD mice in which the proportion and function of CD4(+)Foxp3(+) Treg cells was abrogated by cyclophosphamide (CY), failed to permit progression to T1D. |
| 6795 | 19211146 | Prevention of T1D was associated with reduced emergence of primed (autoreactive) CD4(+) CD25(+) T cells, but not with the emergence of Foxp3(+) Treg in the peripheral compartments. |
| 6796 | 19211146 | However, administration of ATRA to NOD mice in which the proportion and function of CD4(+)Foxp3(+) Treg cells was abrogated by cyclophosphamide (CY), failed to permit progression to T1D. |
| 6797 | 19214972 | Control of type 1 diabetes by CD4+Foxp3+ regulatory T cells: lessons from mouse models and implications for human disease. |
| 6798 | 19214972 | In this review, we summarize research from various laboratories, including our own, showing that CD4(+)Foxp3(+) T(reg) cells are critical in the control of type 1 diabetes (T1D) in mouse models and humans. |
| 6799 | 19214972 | In this review, we also discuss cellular and molecular determinants that impact CD4(+)Foxp3(+) T(reg) cell development and function and consequential resistance to organ-specific autoimmune disease. |
| 6800 | 19214972 | Recent advances in the use of CD4(+)Foxp3(+) T(reg) cellular therapy to promote immunological tolerance in the absence of long-term generalized immunosuppression are also presented. |
| 6801 | 19214972 | Control of type 1 diabetes by CD4+Foxp3+ regulatory T cells: lessons from mouse models and implications for human disease. |
| 6802 | 19214972 | In this review, we summarize research from various laboratories, including our own, showing that CD4(+)Foxp3(+) T(reg) cells are critical in the control of type 1 diabetes (T1D) in mouse models and humans. |
| 6803 | 19214972 | In this review, we also discuss cellular and molecular determinants that impact CD4(+)Foxp3(+) T(reg) cell development and function and consequential resistance to organ-specific autoimmune disease. |
| 6804 | 19214972 | Recent advances in the use of CD4(+)Foxp3(+) T(reg) cellular therapy to promote immunological tolerance in the absence of long-term generalized immunosuppression are also presented. |
| 6805 | 19214972 | Control of type 1 diabetes by CD4+Foxp3+ regulatory T cells: lessons from mouse models and implications for human disease. |
| 6806 | 19214972 | In this review, we summarize research from various laboratories, including our own, showing that CD4(+)Foxp3(+) T(reg) cells are critical in the control of type 1 diabetes (T1D) in mouse models and humans. |
| 6807 | 19214972 | In this review, we also discuss cellular and molecular determinants that impact CD4(+)Foxp3(+) T(reg) cell development and function and consequential resistance to organ-specific autoimmune disease. |
| 6808 | 19214972 | Recent advances in the use of CD4(+)Foxp3(+) T(reg) cellular therapy to promote immunological tolerance in the absence of long-term generalized immunosuppression are also presented. |
| 6809 | 19214972 | Control of type 1 diabetes by CD4+Foxp3+ regulatory T cells: lessons from mouse models and implications for human disease. |
| 6810 | 19214972 | In this review, we summarize research from various laboratories, including our own, showing that CD4(+)Foxp3(+) T(reg) cells are critical in the control of type 1 diabetes (T1D) in mouse models and humans. |
| 6811 | 19214972 | In this review, we also discuss cellular and molecular determinants that impact CD4(+)Foxp3(+) T(reg) cell development and function and consequential resistance to organ-specific autoimmune disease. |
| 6812 | 19214972 | Recent advances in the use of CD4(+)Foxp3(+) T(reg) cellular therapy to promote immunological tolerance in the absence of long-term generalized immunosuppression are also presented. |
| 6813 | 19217258 | T cells from recipients transplanted with allogeneic islets +MSC produced low levels of IFN-gamma and TNF-alpha upon ex-vivo activation, and this transplantation protocol promoted the generation of IL-10-secreting CD4(+) T cells. |
| 6814 | 19218134 | [Role of CD4+CD25+Foxp3+ regulatory T cells in type 2 diabetic nephropathy]. |
| 6815 | 19221395 | This abrupt disease was associated with the production of interferon gamma by P0-specific T cells and a lack of CD4(+) Foxp3(+) regulatory T cells. |
| 6816 | 19224710 | A profound and progressive infiltration with CD4(+), CD8(+) cells, natural killer cells, and macrophages was identified in adenovirus transduced grafts, which paralleled a decline in beta-gal expression. |
| 6817 | 19224710 | Intragraft interferon (IFN)-gamma and RANTES mRNA expression was not different between transduced and untransduced islet grafts, despite an increased expression of CC chemokine receptor 5 (CCR5). |
| 6818 | 19224710 | No significant splenocyte IFN-gamma and interleukin (IL)-4 production or serum anti-adenoviral antibodies were discovered albeit IgM antibody was detected in transduced grafts. |
| 6819 | 19234158 | We demonstrated that in nonobese diabetic (NOD) mice, gal-1 therapy reduces significantly the amount of Th1 cells, augments the number of T cells secreting IL-4 or IL-10 specific for islet cell Ag, and causes peripheral deletion of beta-cell-reactive T cells. |
| 6820 | 19234158 | Preventive gal-1 therapy shifted the composition of the insulitis into an infiltrate that did not invade the islets and that contained a significantly reduced number of Th1 cells and a higher percentage of CD4(+) T cells with content of IL-4, IL-5, or IL-10. |
| 6821 | 19255186 | To investigate the role of suppressor of cytokine signaling (SOCS) molecules in periodontal immunity and RANKL-mediated dendritic cell (DC)-associated osteoclastogenesis, we analyzed SOCS expression profiles in CD4(+) T cells and the effect of SOCS3 expression in CD11c(+) DCs during periodontal inflammation-induced osteoclastogenesis and bone loss in nonobese diabetic (NOD) versus humanized NOD/SCID mice. |
| 6822 | 19255186 | Our results of ex vivo and in vitro analyses showed that (i) there is significantly higher SOCS3 expression associated with RANKL(+) T-cell-mediated bone loss in correlation with increased CD11c(+) DC-mediated osteoclastogenesis; (ii) the transfection of CD11c(+) DC using an adenoviral vector carrying a dominant negative SOCS3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP expression, bone resorption, and SOCS3 activity are not associated with any detectable change in the expression levels of TRAF6 and mitogen-activated protein kinase signaling adaptors (i.e., Erk, Jnk, p38, and Akt) in RANKL(+) T cells. |
| 6823 | 19261537 | Interleukin-21 (IL-21)-mediated pathways in T cell-mediated disease. |
| 6824 | 19261537 | Interleukin-21 (IL-21) is produced mostly by activated CD4+ T cells and controls the differentiation and functional activity of effector T helper cells, counteracts the suppressive effects of regulatory T cells, and stimulates non-immune cells to make inflammatory mediators. |
| 6825 | 19261537 | Therefore new treatment modalities to neutralise IL-21 in vivo would be a valuable addition to the therapeutic armamentarium to combat immune-mediated inflammation. |
| 6826 | 19261537 | Here we describe the emerging role of IL-21 in the initiation and progress of the tissue-damaging inflammatory response in immune-mediated pathologies. |
| 6827 | 19275768 | However, it was not until the discovery that CD4(+)CD25(+) T-cells had suppressive capabilities both in vitro and in vivo that this concept regained credibility and developed into one of the most active research areas in immunology today. |
| 6828 | 19291704 | Foxp3 induction requires the presence of DC, which we also show are modified by SEA to upregulate C-type lectins, IL-10 and IL-2. |
| 6829 | 19291704 | Our studies show that SEA can have a direct effect on CD4(+) T cells increasing expression of TGF-beta, integrin beta8 and galectins. |
| 6830 | 19292763 | The A-chain of insulin is a hot-spot for CD4+ T cell epitopes in human type 1 diabetes. |
| 6831 | 19292763 | Human CD4(+) T cells from the pancreatic lymph nodes of subjects with T1D respond to the first 15 amino acids of the insulin A-chain. |
| 6832 | 19292763 | Here we describe the analysis of a CD4(+) T cell clone, isolated from a subject with T1D, which recognizes a new HLR-DR4-restricted epitope (KRGIVEQCCTSICS) that overlaps the insulin A1-13 epitope. |
| 6833 | 19292763 | The finding of a further CD4(+) T cell epitope in the N-terminal A-chain region of human insulin underscores the importance of this region as a target of CD4(+) T cell responses in human T1D. |
| 6834 | 19292763 | The A-chain of insulin is a hot-spot for CD4+ T cell epitopes in human type 1 diabetes. |
| 6835 | 19292763 | Human CD4(+) T cells from the pancreatic lymph nodes of subjects with T1D respond to the first 15 amino acids of the insulin A-chain. |
| 6836 | 19292763 | Here we describe the analysis of a CD4(+) T cell clone, isolated from a subject with T1D, which recognizes a new HLR-DR4-restricted epitope (KRGIVEQCCTSICS) that overlaps the insulin A1-13 epitope. |
| 6837 | 19292763 | The finding of a further CD4(+) T cell epitope in the N-terminal A-chain region of human insulin underscores the importance of this region as a target of CD4(+) T cell responses in human T1D. |
| 6838 | 19292763 | The A-chain of insulin is a hot-spot for CD4+ T cell epitopes in human type 1 diabetes. |
| 6839 | 19292763 | Human CD4(+) T cells from the pancreatic lymph nodes of subjects with T1D respond to the first 15 amino acids of the insulin A-chain. |
| 6840 | 19292763 | Here we describe the analysis of a CD4(+) T cell clone, isolated from a subject with T1D, which recognizes a new HLR-DR4-restricted epitope (KRGIVEQCCTSICS) that overlaps the insulin A1-13 epitope. |
| 6841 | 19292763 | The finding of a further CD4(+) T cell epitope in the N-terminal A-chain region of human insulin underscores the importance of this region as a target of CD4(+) T cell responses in human T1D. |
| 6842 | 19292763 | The A-chain of insulin is a hot-spot for CD4+ T cell epitopes in human type 1 diabetes. |
| 6843 | 19292763 | Human CD4(+) T cells from the pancreatic lymph nodes of subjects with T1D respond to the first 15 amino acids of the insulin A-chain. |
| 6844 | 19292763 | Here we describe the analysis of a CD4(+) T cell clone, isolated from a subject with T1D, which recognizes a new HLR-DR4-restricted epitope (KRGIVEQCCTSICS) that overlaps the insulin A1-13 epitope. |
| 6845 | 19292763 | The finding of a further CD4(+) T cell epitope in the N-terminal A-chain region of human insulin underscores the importance of this region as a target of CD4(+) T cell responses in human T1D. |
| 6846 | 19295543 | Genetic association of HLA DQB1 with CD4+CD25+(high) T-cell apoptosis in type 1 diabetes. |
| 6847 | 19295543 | We found earlier an increased apoptosis with decreased viability and function of the CD4+CD25+(high) T-cell subset (Treg) in human subjects with recent-onset T1D and in multiple autoantibody-positive, high at-risk individuals. |
| 6848 | 19295543 | In this study, we test the hypothesis that HLA DQB1 genotypes are associated with increased CD4+CD25+(high) T-cell apoptosis. |
| 6849 | 19295543 | HLA DQ-based genetic risk status was significantly associated with CD4+CD25+(high) T-cell apoptosis, after adjustment for age, gender and phenotypic status (n=83, F=4.04 (d.f.=3), P=0.01). |
| 6850 | 19295543 | Unaffected, autoantibody-negative high risk HLA DQB1 control subjects showed increased CD4+CD25+(high) apoptosis levels compared with low risk HLA DQB1 control subjects (n=26, P=0.002), confirming that the association precedes disease. |
| 6851 | 19295543 | Our study shows an association of HLA DQB1 genotypes with CD4+CD25+(high) T-cell apoptosis, which implicates CD4+CD25+(high) T-cell apoptosis as a new intermediate trait for T1D. |
| 6852 | 19295543 | Genetic association of HLA DQB1 with CD4+CD25+(high) T-cell apoptosis in type 1 diabetes. |
| 6853 | 19295543 | We found earlier an increased apoptosis with decreased viability and function of the CD4+CD25+(high) T-cell subset (Treg) in human subjects with recent-onset T1D and in multiple autoantibody-positive, high at-risk individuals. |
| 6854 | 19295543 | In this study, we test the hypothesis that HLA DQB1 genotypes are associated with increased CD4+CD25+(high) T-cell apoptosis. |
| 6855 | 19295543 | HLA DQ-based genetic risk status was significantly associated with CD4+CD25+(high) T-cell apoptosis, after adjustment for age, gender and phenotypic status (n=83, F=4.04 (d.f.=3), P=0.01). |
| 6856 | 19295543 | Unaffected, autoantibody-negative high risk HLA DQB1 control subjects showed increased CD4+CD25+(high) apoptosis levels compared with low risk HLA DQB1 control subjects (n=26, P=0.002), confirming that the association precedes disease. |
| 6857 | 19295543 | Our study shows an association of HLA DQB1 genotypes with CD4+CD25+(high) T-cell apoptosis, which implicates CD4+CD25+(high) T-cell apoptosis as a new intermediate trait for T1D. |
| 6858 | 19295543 | Genetic association of HLA DQB1 with CD4+CD25+(high) T-cell apoptosis in type 1 diabetes. |
| 6859 | 19295543 | We found earlier an increased apoptosis with decreased viability and function of the CD4+CD25+(high) T-cell subset (Treg) in human subjects with recent-onset T1D and in multiple autoantibody-positive, high at-risk individuals. |
| 6860 | 19295543 | In this study, we test the hypothesis that HLA DQB1 genotypes are associated with increased CD4+CD25+(high) T-cell apoptosis. |
| 6861 | 19295543 | HLA DQ-based genetic risk status was significantly associated with CD4+CD25+(high) T-cell apoptosis, after adjustment for age, gender and phenotypic status (n=83, F=4.04 (d.f.=3), P=0.01). |
| 6862 | 19295543 | Unaffected, autoantibody-negative high risk HLA DQB1 control subjects showed increased CD4+CD25+(high) apoptosis levels compared with low risk HLA DQB1 control subjects (n=26, P=0.002), confirming that the association precedes disease. |
| 6863 | 19295543 | Our study shows an association of HLA DQB1 genotypes with CD4+CD25+(high) T-cell apoptosis, which implicates CD4+CD25+(high) T-cell apoptosis as a new intermediate trait for T1D. |
| 6864 | 19295543 | Genetic association of HLA DQB1 with CD4+CD25+(high) T-cell apoptosis in type 1 diabetes. |
| 6865 | 19295543 | We found earlier an increased apoptosis with decreased viability and function of the CD4+CD25+(high) T-cell subset (Treg) in human subjects with recent-onset T1D and in multiple autoantibody-positive, high at-risk individuals. |
| 6866 | 19295543 | In this study, we test the hypothesis that HLA DQB1 genotypes are associated with increased CD4+CD25+(high) T-cell apoptosis. |
| 6867 | 19295543 | HLA DQ-based genetic risk status was significantly associated with CD4+CD25+(high) T-cell apoptosis, after adjustment for age, gender and phenotypic status (n=83, F=4.04 (d.f.=3), P=0.01). |
| 6868 | 19295543 | Unaffected, autoantibody-negative high risk HLA DQB1 control subjects showed increased CD4+CD25+(high) apoptosis levels compared with low risk HLA DQB1 control subjects (n=26, P=0.002), confirming that the association precedes disease. |
| 6869 | 19295543 | Our study shows an association of HLA DQB1 genotypes with CD4+CD25+(high) T-cell apoptosis, which implicates CD4+CD25+(high) T-cell apoptosis as a new intermediate trait for T1D. |
| 6870 | 19295543 | Genetic association of HLA DQB1 with CD4+CD25+(high) T-cell apoptosis in type 1 diabetes. |
| 6871 | 19295543 | We found earlier an increased apoptosis with decreased viability and function of the CD4+CD25+(high) T-cell subset (Treg) in human subjects with recent-onset T1D and in multiple autoantibody-positive, high at-risk individuals. |
| 6872 | 19295543 | In this study, we test the hypothesis that HLA DQB1 genotypes are associated with increased CD4+CD25+(high) T-cell apoptosis. |
| 6873 | 19295543 | HLA DQ-based genetic risk status was significantly associated with CD4+CD25+(high) T-cell apoptosis, after adjustment for age, gender and phenotypic status (n=83, F=4.04 (d.f.=3), P=0.01). |
| 6874 | 19295543 | Unaffected, autoantibody-negative high risk HLA DQB1 control subjects showed increased CD4+CD25+(high) apoptosis levels compared with low risk HLA DQB1 control subjects (n=26, P=0.002), confirming that the association precedes disease. |
| 6875 | 19295543 | Our study shows an association of HLA DQB1 genotypes with CD4+CD25+(high) T-cell apoptosis, which implicates CD4+CD25+(high) T-cell apoptosis as a new intermediate trait for T1D. |
| 6876 | 19295543 | Genetic association of HLA DQB1 with CD4+CD25+(high) T-cell apoptosis in type 1 diabetes. |
| 6877 | 19295543 | We found earlier an increased apoptosis with decreased viability and function of the CD4+CD25+(high) T-cell subset (Treg) in human subjects with recent-onset T1D and in multiple autoantibody-positive, high at-risk individuals. |
| 6878 | 19295543 | In this study, we test the hypothesis that HLA DQB1 genotypes are associated with increased CD4+CD25+(high) T-cell apoptosis. |
| 6879 | 19295543 | HLA DQ-based genetic risk status was significantly associated with CD4+CD25+(high) T-cell apoptosis, after adjustment for age, gender and phenotypic status (n=83, F=4.04 (d.f.=3), P=0.01). |
| 6880 | 19295543 | Unaffected, autoantibody-negative high risk HLA DQB1 control subjects showed increased CD4+CD25+(high) apoptosis levels compared with low risk HLA DQB1 control subjects (n=26, P=0.002), confirming that the association precedes disease. |
| 6881 | 19295543 | Our study shows an association of HLA DQB1 genotypes with CD4+CD25+(high) T-cell apoptosis, which implicates CD4+CD25+(high) T-cell apoptosis as a new intermediate trait for T1D. |
| 6882 | 19336675 | CD4(+)CD25(+) T-cells control autoimmunity in the absence of B-cells. |
| 6883 | 19342624 | Our results thus demonstrate an important role for BTLA in the induction of peripheral tolerance of both CD4(+) and CD8(+) T cells in vivo. |
| 6884 | 19347338 | Recent data suggest that the proinsulin cleavage product C-peptide could play a causal role in atherogenesis by promoting monocyte and CD4-positive lymphocyte recruitment in early arteriosclerotic lesions and by inducing the proliferation of vascular smooth muscle cells. |
| 6885 | 19349464 | AAMacs are defined by the expression of Arginase 1, chitinase-like molecules, and resistin-like molecule (RELM) alpha/FIZZ1; however, the influence of these molecules on the development, progression, or resolution of inflammatory diseases is unknown. |
| 6886 | 19349464 | Consistent with immunoregulatory properties, recombinant RELM-alpha could bind to macrophages and effector CD4(+) Th2 cells and inhibited Th2 cytokine production in a Bruton's tyrosine kinase-dependent manner. |
| 6887 | 19380803 | LPS mediates its effects via a mechanism that involves both CD4(+) and CD8(+) T cells and results from signaling through either the MyD88 or the type I IFN receptor pathways. |
| 6888 | 19478458 | Delayed T1D onset was due to transient upregulation of programmed cell death-1 ligand 1 (PD-L1) on lymphoid cells, which prevented the expansion of diabetogenic CD8+ T cells expressing programmed cell death-1 (PD-1). |
| 6889 | 19478458 | Reduced T1D incidence was caused by increased numbers of invigorated CD4+CD25+ Tregs, which produced TGF-beta and maintained long-term tolerance. |
| 6890 | 19478458 | Full protection from T1D resulted from synergy between PD-L1 and CD4+CD25+ Tregs. |
| 6891 | 19478458 | Delayed T1D onset was due to transient upregulation of programmed cell death-1 ligand 1 (PD-L1) on lymphoid cells, which prevented the expansion of diabetogenic CD8+ T cells expressing programmed cell death-1 (PD-1). |
| 6892 | 19478458 | Reduced T1D incidence was caused by increased numbers of invigorated CD4+CD25+ Tregs, which produced TGF-beta and maintained long-term tolerance. |
| 6893 | 19478458 | Full protection from T1D resulted from synergy between PD-L1 and CD4+CD25+ Tregs. |
| 6894 | 19482555 | We compared CD4+ T cell avidities for the diabetes-associated autoantigen glutamic acid decarboxylase 555-567 (GAD 555) among serial samples from autoantibody-positive subjects at high risk of progression to type 1 diabetes (T1D). |
| 6895 | 19494813 | T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes. |
| 6896 | 19494813 | Here we show that mouse effector and memory CD4(+) T cells abolish macrophage inflammasome-mediated caspase-1 activation and subsequent interleukin 1beta release in a cognate manner. |
| 6897 | 19494813 | Inflammasome inhibition is observed for all tested NLRP1 (commonly called NALP1) and NLRP3 (NALP3 or cryopyrin) activators, whereas NLRC4 (IPAF) inflammasome function and release of other inflammatory mediators such as CXCL2, interleukin 6 and tumour necrosis factor are not affected. |
| 6898 | 19494813 | Suppression of the NLRP3 inflammasome requires cell-to-cell contact and can be mimicked by macrophage stimulation with selected ligands of the tumour necrosis factor family, such as CD40L (also known as CD40LG). |
| 6899 | 19494813 | In a NLRP3-dependent peritonitis model, effector CD4(+) T cells are responsible for decreasing neutrophil recruitment in an antigen-dependent manner. |
| 6900 | 19494813 | T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes. |
| 6901 | 19494813 | Here we show that mouse effector and memory CD4(+) T cells abolish macrophage inflammasome-mediated caspase-1 activation and subsequent interleukin 1beta release in a cognate manner. |
| 6902 | 19494813 | Inflammasome inhibition is observed for all tested NLRP1 (commonly called NALP1) and NLRP3 (NALP3 or cryopyrin) activators, whereas NLRC4 (IPAF) inflammasome function and release of other inflammatory mediators such as CXCL2, interleukin 6 and tumour necrosis factor are not affected. |
| 6903 | 19494813 | Suppression of the NLRP3 inflammasome requires cell-to-cell contact and can be mimicked by macrophage stimulation with selected ligands of the tumour necrosis factor family, such as CD40L (also known as CD40LG). |
| 6904 | 19494813 | In a NLRP3-dependent peritonitis model, effector CD4(+) T cells are responsible for decreasing neutrophil recruitment in an antigen-dependent manner. |
| 6905 | 19497561 | Costimulation via the PD-1 and B7-H1/B7-DC pathway regulates immunity. |
| 6906 | 19497561 | A progressive increase in the expression of PD-1 and B7-H1/B7-DC on T cells and APC, respectively, was observed in the pancreatic lymph nodes of female non-obese diabetic (NOD) mice as they developed diabetes. |
| 6907 | 19497561 | A significantly decreased expression of PD-1 and B7-H1/B7-DC on T cells and APC, respectively, was observed in the periphery of prediabetic NOD mice versus non-diabetic C57BL/6 strain. |
| 6908 | 19497561 | In vivo blocking studies in NOD/B7-2KONOD mice revealed that B7-H1 and B7-DC positively costimulate autoreactive CD4 and CD8 T cells and may co-operate with B7-2 to augment priming and expansion of naïve autoreactive T cells. |
| 6909 | 19507278 | The effects of PHC on postprandial blood glucose concentrations, plasmatic insulin levels, morphology of pancreatic beta cells and CD4(+) T cells proliferation after 28-day treatment were monitored. |
| 6910 | 19547759 | Diminished expression of ICOS, GITR and CTLA-4 at the mRNA level in T regulatory cells of children with newly diagnosed type 1 diabetes. |
| 6911 | 19547759 | The percentages of CD4(+)CD25(high)CD127(dim/-) were very low and did not differ between T1DM and control children. |
| 6912 | 19547759 | We did not observe any statistically significant differences between healthy and diabetic children in mRNA expression for FoxP3, IL-7R (CD127), IL-8RA, IL-10RA, IL-12A, IL-2RA (CD25), IL-21, STAT1, STAT3, SOCS2, SOCS3, TGF-beta1-R1, TGF-beta-R2 and TBX-21 genes. |
| 6913 | 19547759 | Interestingly the mRNA level for CTLA-4, ICOS1, IL-23, IL-27, SMAD3 and GITR were lower in Treg cells of children with diabetes compared to the control patients. |
| 6914 | 19554034 | Redirecting human CD4+CD25+ regulatory T cells from the peripheral blood with pre-defined target specificity. |
| 6915 | 19557879 | We found that the onset of type 1 diabetes in NOD mice was associated with an imbalance of CD4(+)CD25(+)FoxP3(+) regulatory T (Treg) cells and IL-17 producing Th17 cells. |
| 6916 | 19587699 | Finally, we report the results of expression studies demonstrating that CDKAL1 transcripts are virtually absent from skin keratinocytes, but are abundantly expressed in immune cells, especially in CD4+ and CD19+ lymphocytes. |
| 6917 | 19616319 | Recent studies indicate that interleukin (IL)-21, a cytokine produced mostly by activated CD4+ T cells, participates in the tissue damage in various tissues, owing to its ability to regulate the function of immune and non-immune cells. |
| 6918 | 19616319 | For instance, IL-21 controls the differentiation and functional activity of T cells, B cells and NK cells, limits the differentiation of inducible regulatory T cells (Tregs), and makes T cells resistant to the Treg-mediated immunesuppression. |
| 6919 | 19616319 | Here, we focus on data supporting the pathogenic role of IL-21 in human inflammatory diseases and discuss pre-clinical studies that suggest that neutralization of IL-21 in vivo could be a new biological therapy to combat immune-mediated pathologies, such as inflammatory bowel diseases, diabetes, rheumatoid arthritis and systemic lupus erythematosus. |
| 6920 | 19633131 | Vasoactive intestinal peptide (VIP) is a neuroimmunopeptide that has anti-inflammatory effects, promotes Th2 cytokines and CD4(+)CD25(+)FOXP3(+) Treg activation, and stimulates exocrine secretion, smooth muscle relaxation, and vasodilatation favoring uterus quiescence. |
| 6921 | 19633131 | VIP receptors, Vipr1 and Vipr2 (Vpac1 and Vpac2), were expressed at the implantation sites and VIP induced leukemia inhibitory factor (LIF) and Treg marker expression in both strains; however, a reduced Vip expression was found in NOD implantation sites. |
| 6922 | 19633656 | CD4(+) Foxp3(+) T regulatory (T(reg)) cells with a unique phenotype were highly enriched in the abdominal fat of normal mice, but their numbers were strikingly and specifically reduced at this site in insulin-resistant models of obesity. |
| 6923 | 19635924 | By analyzing the T cell development in anti-CTLA-4 scFv/Th1/Th2 triple transgenic mice, we found that beta cell-specific expression of CTLA-4 agonist did not affect the development of Th1/Th2 or CD4(+)CD25(+) regulatory T cells. |
| 6924 | 19652940 | Lymphocyte imbalance in vitiligo patients indicated by elevated CD4+/CD8+ T-cell ratio. |
| 6925 | 19652940 | To investigate the mechanisms of cellular immunity, peripheral blood cell count and lymphocyte subtype analysis by flow cytometry were done. sTNF-RI, IL-6 and CIC serum levels were in the normal range. |
| 6926 | 19652940 | The ratio of CD4+/CD8+ T-cells had an elevated median value of 2.6 [quartiles 2.0; 3.1]. 61% of the vitiligo patients had a ratio higher than 2.4, which was the normal cut-off point. |
| 6927 | 19652940 | Lymphocyte imbalance in vitiligo patients indicated by elevated CD4+/CD8+ T-cell ratio. |
| 6928 | 19652940 | To investigate the mechanisms of cellular immunity, peripheral blood cell count and lymphocyte subtype analysis by flow cytometry were done. sTNF-RI, IL-6 and CIC serum levels were in the normal range. |
| 6929 | 19652940 | The ratio of CD4+/CD8+ T-cells had an elevated median value of 2.6 [quartiles 2.0; 3.1]. 61% of the vitiligo patients had a ratio higher than 2.4, which was the normal cut-off point. |
| 6930 | 19654878 | Apoptosis of CD4+ CD25(high) T cells in type 1 diabetes may be partially mediated by IL-2 deprivation. |
| 6931 | 19658094 | Temporal analysis demonstrated that unlike CD4(+) T cells that are primed in the draining pancreatic lymph nodes, initial proliferation of transferred CD8(+) T cells was detected in the islets. |
| 6932 | 19658094 | Furthermore, ectopic expression of CD80 by beta cells accelerated the onset of insulitis mediated by beta-cell-specific CD8(+) T cells, but had no effect on CD4(+) T-cell-mediated diabetes, suggesting an antigenic interaction between beta cells and naive CD8(+) T cells. |
| 6933 | 19658094 | Temporal analysis demonstrated that unlike CD4(+) T cells that are primed in the draining pancreatic lymph nodes, initial proliferation of transferred CD8(+) T cells was detected in the islets. |
| 6934 | 19658094 | Furthermore, ectopic expression of CD80 by beta cells accelerated the onset of insulitis mediated by beta-cell-specific CD8(+) T cells, but had no effect on CD4(+) T-cell-mediated diabetes, suggesting an antigenic interaction between beta cells and naive CD8(+) T cells. |
| 6935 | 19667061 | CD4(+)CD25(+)Foxp3(+) natural regulatory T cells (T reg cells) maintain self-tolerance and suppress autoimmune diseases such as type 1 diabetes and inflammatory bowel disease (IBD). |
| 6936 | 19667061 | The DC-dependent loss in T reg cells leads to an increase in the number of T cells producing inflammatory cytokines, such as interferon gamma and interleukin 17. |
| 6937 | 19684036 | Resistin: a newly identified chemokine for human CD4-positive lymphocytes. |
| 6938 | 19684511 | Blastic plasmacytoid dendritic cell (BPDC) neoplasm, formerly called blastic natural killer cell lymphoma or CD4+/CD56+ hematodermic neoplasm, is a rare tumor entity, now regarded to be derived from the plasmacytoid dendritic cell (PDC) lineage. |
| 6939 | 19690518 | Efficacy was associated with an expansion of bystander suppressor regulatory T cells (Tregs) recognizing the C-terminal region of GAD65 and secreting interleukin-10 (IL-10), transforming growth factor-beta (TGF-beta), and interferon-gamma (IFN-gamma). |
| 6940 | 19690518 | In addition, we found that frequency and epitope specificity of GAD65-reactive CD4(+) T cells during antigen priming at diabetes onset and Tregs detected after CT correlated. |
| 6941 | 19690518 | Consequently, NOD mice harbored significantly lower levels of GAD65-reactive CD4(+) T cells than RIP-LCMV-GP before and after treatment. |
| 6942 | 19690518 | Efficacy was associated with an expansion of bystander suppressor regulatory T cells (Tregs) recognizing the C-terminal region of GAD65 and secreting interleukin-10 (IL-10), transforming growth factor-beta (TGF-beta), and interferon-gamma (IFN-gamma). |
| 6943 | 19690518 | In addition, we found that frequency and epitope specificity of GAD65-reactive CD4(+) T cells during antigen priming at diabetes onset and Tregs detected after CT correlated. |
| 6944 | 19690518 | Consequently, NOD mice harbored significantly lower levels of GAD65-reactive CD4(+) T cells than RIP-LCMV-GP before and after treatment. |
| 6945 | 19743458 | That is because their primary genetic associations are mostly with certain human leukocyte antigen class II alleles, whose gene products present antigens to CD4(+) T cells. |
| 6946 | 19752032 | Helminth infection can reduce insulitis and type 1 diabetes through CD25- and IL-10-independent mechanisms. |
| 6947 | 19752032 | Interleukin-4 (IL-4), IL-10, and IL-13 expression and the frequency of CD4(+) CD25(+) FoxP3(+) regulatory T cells were elevated in mesenteric and pancreatic lymph nodes. |
| 6948 | 19752032 | Depletion of CD4(+) CD25(+) T cells in vivo did not abrogate H. polygyrus-induced T1D protection, nor did anti-IL-10 receptor blocking antibody. |
| 6949 | 19752032 | These findings suggest that infection with H. polygyrus significantly inhibits T1D in NOD mice through CD25- and IL-10-independent mechanisms and also reduces the severity of T1D when administered late after the onset of insulitis. |
| 6950 | 19752032 | Helminth infection can reduce insulitis and type 1 diabetes through CD25- and IL-10-independent mechanisms. |
| 6951 | 19752032 | Interleukin-4 (IL-4), IL-10, and IL-13 expression and the frequency of CD4(+) CD25(+) FoxP3(+) regulatory T cells were elevated in mesenteric and pancreatic lymph nodes. |
| 6952 | 19752032 | Depletion of CD4(+) CD25(+) T cells in vivo did not abrogate H. polygyrus-induced T1D protection, nor did anti-IL-10 receptor blocking antibody. |
| 6953 | 19752032 | These findings suggest that infection with H. polygyrus significantly inhibits T1D in NOD mice through CD25- and IL-10-independent mechanisms and also reduces the severity of T1D when administered late after the onset of insulitis. |
| 6954 | 19752238 | Furthermore, suppression of T1D was dependent on beta cell-specific IL-10-secreting CD4+ T cells, although the frequency of GAD65-specific FoxP3-expressing CD4+ T cells was also increased in sIA(g7)-pGAD65 dimer vaccinated NOD mice. |
| 6955 | 19759824 | Glutamic acid decarboxylase-derived epitopes with specific domains expand CD4(+)CD25(+) regulatory T cells. |
| 6956 | 19783679 | Idd5.1 regulates T1D susceptibility in nonobese diabetic (NOD) mice and has two notable candidate genes, Ctla4 and Icos. |
| 6957 | 19783679 | However, further support of this hypothesis is required since the Idd5.1 haplotypes of the diabetes-susceptible NOD and the resistant B10 strains differ throughout Ctla4 and Icos. |
| 6958 | 19783679 | Using haplotype analysis and the generation of novel Idd5.1-congenic strains that differ at the disease-associated Ctla4 exon 2 single-nucleotide polymorphism, we demonstrate that increased expression of liCTLA-4 correlates with reduced T1D susceptibility. |
| 6959 | 19783679 | CTLA-4(-/-) mice expressing liCTLA-4 accumulated fewer activated effector/memory CD4(+) T cells than CTLA-4(-/-) mice and the transgenic mice were partially rescued from the multiorgan inflammation and early lethality caused by the disruption of Ctla4. |
| 6960 | 19788384 | We further show that the inhibitory function is due to the induction of TGF-beta-producing CD4(+)CD25(-) islet-specific iTreg cells against the onset of T1D in NOD mice. |
| 6961 | 19788505 | Disengaging the IL-2 receptor with daclizumab enhances IL-7-mediated proliferation of CD4(+) and CD8(+) T cells. |
| 6962 | 19788505 | Allograft rejection is mainly driven by the production of IL-2, which expands T cells by linking the IL-2 receptor (IL-2R) composed of three subunits: CD25, CD122 and CD132. |
| 6963 | 19788505 | Daclizumab, widely used in immunosuppression, is a humanized anti-CD25 antibody that disrupts IL-2 signaling by binding to CD25 and preventing the assembly of the high-affinity IL-2R. |
| 6964 | 19788505 | Here we show that Daclizumab, while blocking the T-cell response to IL-2, increases CD4(+) and CD8(+) T-cell proliferative response to the homeostatic cytokine IL-7. |
| 6965 | 19788505 | The IL-7R shares CD132 with the IL-2R and blocking of CD25 by Daclizumab results in the enhanced formation of the IL-7R that in turn allows IL-7 to bind more efficiently on the cell surface. |
| 6966 | 19788505 | In addition, treatment with Daclizumab delays the internalization of CD127 upon IL-7 treatment, retaining T-cell sensitivity to IL-7 for a prolonged time. |
| 6967 | 19788505 | Disengaging the IL-2 receptor with daclizumab enhances IL-7-mediated proliferation of CD4(+) and CD8(+) T cells. |
| 6968 | 19788505 | Allograft rejection is mainly driven by the production of IL-2, which expands T cells by linking the IL-2 receptor (IL-2R) composed of three subunits: CD25, CD122 and CD132. |
| 6969 | 19788505 | Daclizumab, widely used in immunosuppression, is a humanized anti-CD25 antibody that disrupts IL-2 signaling by binding to CD25 and preventing the assembly of the high-affinity IL-2R. |
| 6970 | 19788505 | Here we show that Daclizumab, while blocking the T-cell response to IL-2, increases CD4(+) and CD8(+) T-cell proliferative response to the homeostatic cytokine IL-7. |
| 6971 | 19788505 | The IL-7R shares CD132 with the IL-2R and blocking of CD25 by Daclizumab results in the enhanced formation of the IL-7R that in turn allows IL-7 to bind more efficiently on the cell surface. |
| 6972 | 19788505 | In addition, treatment with Daclizumab delays the internalization of CD127 upon IL-7 treatment, retaining T-cell sensitivity to IL-7 for a prolonged time. |
| 6973 | 19801514 | Dominant role of antigen dose in CD4+Foxp3+ regulatory T cell induction and expansion. |
| 6974 | 19801514 | In this study, islet-specific CD4(+) T cells from BDC2.5 TCR-transgenic mice were stimulated in the absence of exogenous cytokine with iDC or mDC pulsed with high- or low-affinity antigenic peptides and examined for Treg induction. |
| 6975 | 19801514 | Both iDC and mDC presenting low peptide doses induced weak TCR signaling via the Akt/mammalian target of rapamycin (mTOR) pathway, resulting in significant expansion of Foxp3(+) Treg. |
| 6976 | 19801514 | The inverse correlation of Foxp3 and Akt/mTOR signaling was also observed in DO11.10 and OT-II TCR-transgenic T cells and was recapitulated with anti-CD3/CD28 stimulation in the absence of DC. |
| 6977 | 19801514 | Dominant role of antigen dose in CD4+Foxp3+ regulatory T cell induction and expansion. |
| 6978 | 19801514 | In this study, islet-specific CD4(+) T cells from BDC2.5 TCR-transgenic mice were stimulated in the absence of exogenous cytokine with iDC or mDC pulsed with high- or low-affinity antigenic peptides and examined for Treg induction. |
| 6979 | 19801514 | Both iDC and mDC presenting low peptide doses induced weak TCR signaling via the Akt/mammalian target of rapamycin (mTOR) pathway, resulting in significant expansion of Foxp3(+) Treg. |
| 6980 | 19801514 | The inverse correlation of Foxp3 and Akt/mTOR signaling was also observed in DO11.10 and OT-II TCR-transgenic T cells and was recapitulated with anti-CD3/CD28 stimulation in the absence of DC. |
| 6981 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 6982 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 6983 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 6984 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 6985 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 6986 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 6987 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 6988 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 6989 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 6990 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 6991 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 6992 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 6993 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 6994 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 6995 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 6996 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 6997 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 6998 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 6999 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 7000 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 7001 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 7002 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 7003 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 7004 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 7005 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 7006 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 7007 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 7008 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 7009 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 7010 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 7011 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 7012 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 7013 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 7014 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 7015 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 7016 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 7017 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 7018 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 7019 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 7020 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 7021 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 7022 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 7023 | 19806239 | Type 1 diabetes development requires both CD4+ and CD8+ T cells and can be reversed by non-depleting antibodies targeting both T cell populations. |
| 7024 | 19806239 | Type 1 diabetes development in NOD mice appears to require both CD4(+) and CD8(+) T cells. |
| 7025 | 19806239 | However, there are some situations where it has been suggested that either CD4(+) or CD8(+) T cells are able to mediate diabetes in the absence of the other population. |
| 7026 | 19806239 | Therefore, we have re-examined the need for both CD4(+) and CD8(+) T cell populations in diabetes development in NOD mice using an antibody to CD8beta. |
| 7027 | 19806239 | In accordance with some other reports, we found that CD4(+) T cells appeared to be able to access the pancreas more readily than CD8(+) T cells. |
| 7028 | 19806239 | Despite the ability of CD4(+) T cells to recruit CD11b class II positive cells, diabetes did not develop in the absence of CD8(+) T cells. |
| 7029 | 19806239 | As both T cell populations are clearly implicated in diabetes development, we have used a combination of non-depleting antibodies to target both CD4-positive and CD8-positive cells and found that this antibody combination was able to reverse diabetes onset in NOD mice as effectively as anti-CD3 antibodies. |
| 7030 | 19833887 | Idd9.1 locus controls the suppressive activity of FoxP3+CD4+CD25+ regulatory T-cells. |
| 7031 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7032 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7033 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7034 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7035 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7036 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7037 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7038 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7039 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7040 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7041 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7042 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7043 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7044 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7045 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7046 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7047 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7048 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7049 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7050 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7051 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7052 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7053 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7054 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7055 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7056 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7057 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7058 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7059 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7060 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7061 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7062 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7063 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7064 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7065 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7066 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7067 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7068 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7069 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7070 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7071 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7072 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7073 | 19841877 | Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice. |
| 7074 | 19841877 | CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. |
| 7075 | 19841877 | During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. |
| 7076 | 19841877 | In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. |
| 7077 | 19841877 | DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. |
| 7078 | 19841877 | Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. |
| 7079 | 19841877 | Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases. |
| 7080 | 19855244 | Treatment group showed increased serum interleukin (IL)-10 (twofold) and decreased inducible protein-10 and IL-4 (threefold) in luminex. |
| 7081 | 19855244 | Significantly reduced frequency of interferon-gamma (4.5-fold), IL-4 (3.5-fold), IL-2 (2.3-fold), and IL-17 (fourfold) producing T-cell populations were found in ELISPOT. |
| 7082 | 19855244 | OA-treated grafts had significant reduced and delayed infiltration of CD4+ and CD8+ T cells. |
| 7083 | 19875613 | Defects in IL-2R signaling contribute to diminished maintenance of FOXP3 expression in CD4(+)CD25(+) regulatory T-cells of type 1 diabetic subjects. |
| 7084 | 19886740 | Unexpectedly, the ratio of CD4(+):CD8(+) T cells was tightly controlled in the islets throughout diabetogenesis. |
| 7085 | 19886740 | The frequency of IL-4(+) CD4(+) T cells started high but quickly fell to 3% of the population that was maintained with increasing inflammation. |
| 7086 | 19886740 | A significant portion of the CD8(+) T cells were islet-specific glucose-6-phosphatase catalytic subunit-related protein specific in both male and female NOD mice and this population was antigen experienced and increased at high levels of islet inflammation. |
| 7087 | 19886740 | Unexpectedly, the ratio of CD4(+):CD8(+) T cells was tightly controlled in the islets throughout diabetogenesis. |
| 7088 | 19886740 | The frequency of IL-4(+) CD4(+) T cells started high but quickly fell to 3% of the population that was maintained with increasing inflammation. |
| 7089 | 19886740 | A significant portion of the CD8(+) T cells were islet-specific glucose-6-phosphatase catalytic subunit-related protein specific in both male and female NOD mice and this population was antigen experienced and increased at high levels of islet inflammation. |
| 7090 | 19912978 | The FOXP3 molecule is crucial for the generation and maturation of regulatory T cells (Treg) expressing CD4+ and CD25+ molecules. |
| 7091 | 19917704 | Type 1 diabetes is an autoimmune disease mediated by beta cell-specific CD4(+) and CD8(+) T cells. |
| 7092 | 19917704 | TCR-beta and CDR-beta gene usage of single islet-infiltrating g7-mBDC(+) CD4(+) T cells from individual NOD mice showed a restricted repertoire dominated by one or two clones typically expressing TCR beta-chain variable TRBV-15. |
| 7093 | 19917704 | Type 1 diabetes is an autoimmune disease mediated by beta cell-specific CD4(+) and CD8(+) T cells. |
| 7094 | 19917704 | TCR-beta and CDR-beta gene usage of single islet-infiltrating g7-mBDC(+) CD4(+) T cells from individual NOD mice showed a restricted repertoire dominated by one or two clones typically expressing TCR beta-chain variable TRBV-15. |
| 7095 | 19934031 | This report describes population pharmacokinetics/pharmacodynamic (PK/PD) modeling of serum otelixizumab concentrations, changes in CD4+ and CD8+ T-cell counts, and modulation and saturation of CD3/T-cell receptors (TCR) (determined by flow cytometry) after IV administration of otelixizumab in subjects with either type 1 diabetes or psoriasis. |
| 7096 | 19934031 | In diabetic subjects, the otelixizumab serum concentration producing a 50% decrease in peripheral blood counts was 0.0187 microg/mL for CD4+ T cells and 0.0120 microg/mL for CD8+ T cells. |
| 7097 | 19934031 | Corresponding values for psoriatic subjects were much lower: 0.000533 for CD4+ T cells and 0.000269 microg/mL for CD8+ T cells. |
| 7098 | 19934031 | This report describes population pharmacokinetics/pharmacodynamic (PK/PD) modeling of serum otelixizumab concentrations, changes in CD4+ and CD8+ T-cell counts, and modulation and saturation of CD3/T-cell receptors (TCR) (determined by flow cytometry) after IV administration of otelixizumab in subjects with either type 1 diabetes or psoriasis. |
| 7099 | 19934031 | In diabetic subjects, the otelixizumab serum concentration producing a 50% decrease in peripheral blood counts was 0.0187 microg/mL for CD4+ T cells and 0.0120 microg/mL for CD8+ T cells. |
| 7100 | 19934031 | Corresponding values for psoriatic subjects were much lower: 0.000533 for CD4+ T cells and 0.000269 microg/mL for CD8+ T cells. |
| 7101 | 19934031 | This report describes population pharmacokinetics/pharmacodynamic (PK/PD) modeling of serum otelixizumab concentrations, changes in CD4+ and CD8+ T-cell counts, and modulation and saturation of CD3/T-cell receptors (TCR) (determined by flow cytometry) after IV administration of otelixizumab in subjects with either type 1 diabetes or psoriasis. |
| 7102 | 19934031 | In diabetic subjects, the otelixizumab serum concentration producing a 50% decrease in peripheral blood counts was 0.0187 microg/mL for CD4+ T cells and 0.0120 microg/mL for CD8+ T cells. |
| 7103 | 19934031 | Corresponding values for psoriatic subjects were much lower: 0.000533 for CD4+ T cells and 0.000269 microg/mL for CD8+ T cells. |
| 7104 | 19934373 | The non-obese diabetic mouse (NOD) is the most characterized model used to study insulin-dependent type 1 diabetes mellitus (IDDM) and Sjoögren's syndrome (SS). |
| 7105 | 19934373 | In a previous report, we found NOD.E2f1(-/-) mice show a greater progressive development to IDDM and SS compared to NOD mice. |
| 7106 | 19934373 | Our previous data indicated a progressive decrease in regulatory T cells (CD4(+)CD25(+)) and a decrease in the systemic secretion systems for insulin, and saliva was associated with the progression of IDDM and SS. |
| 7107 | 19934373 | Therefore, to define the mechanism of early-onset IDDM SS in E2F-1 deficient NOD mice required further investigation by producing E2F-1 deficient NOD/SCID mice in which the T and B cells do not develop. |
| 7108 | 19934373 | The purpose here was to analyze the essential function of the E2F-1 molecule in the development of IDDM and SS; and the dysfunction of the pancreas islet and salivary gland in the NOD background using NOD/SCID mice. |
| 7109 | 19934373 | We produced NOD/SCID.E2f1(-/-) mice using homologous recombination; determined diabetes development; measured saliva and insulin production; and performed a histological analysis. |
| 7110 | 19934373 | Therefore, we considered a deficiency in E2F-1 induces a decrease in regulatory T cells and an increase in auto-reactive T cells; however, the E2F-1 deficiency is not associated with T and B cells-independent dysfunction of pancreatic beta cell in insulin secretion. |
| 7111 | 19954774 | microRNA-342, microRNA-191 and microRNA-510 are differentially expressed in T regulatory cells of type 1 diabetic patients. |
| 7112 | 19954774 | Tregs were isolated according to CD3+, CD4+, CD25(hi)+ and CD127- by flow cytometry, and miRNA expression profiling was performed using TaqMan Array Human MicroRNA Panel-1 (384-well low density array). |
| 7113 | 20000848 | Here we describe an alternative approach that uses arrays of subnanoliter wells coated with recombinant peptide-loaded MHC class II monomers to isolate and stimulate individual CD4+ T cells in an antigen-specific manner. |
| 7114 | 20000848 | In these experiments, activation was monitored using microengraving to capture two cytokines (IFNgamma and IL-17) released from single cells. |
| 7115 | 20012396 | It has long been appreciated that within the MHC, particular unusual class II genes contribute to the development of T1D in both humans and NOD mice by allowing for the development and functional activation of beta-cell autoreactive CD4 T cells. |
| 7116 | 20012396 | However, studies in NOD mice have revealed that through interactions with other background susceptibility genes, the quite common class I variants (K(d), D(b)) characterizing this strain's H2 ( g7 ) MHC haplotype aberrantly acquire an ability to support the development of beta cell autoreactive CD8 T-cell responses also essential to T1D development. |
| 7117 | 20045101 | Quantitative trait loci for CD4:CD8 lymphocyte ratio are associated with risk of type 1 diabetes and HIV-1 immune control. |
| 7118 | 20045101 | We tested 2.3 million variants for association with five lymphocyte subsets, measured in 2538 individuals from the general population, including CD4+ T cells, CD8+ T cells, CD56+ natural killer (NK) cells, and the derived measure CD4:CD8 ratio. |
| 7119 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 7120 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 7121 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 7122 | 20045101 | Jointly, both QTL explained 8% of the variance in CD4:CD8 ratio. |
| 7123 | 20045101 | Quantitative trait loci for CD4:CD8 lymphocyte ratio are associated with risk of type 1 diabetes and HIV-1 immune control. |
| 7124 | 20045101 | We tested 2.3 million variants for association with five lymphocyte subsets, measured in 2538 individuals from the general population, including CD4+ T cells, CD8+ T cells, CD56+ natural killer (NK) cells, and the derived measure CD4:CD8 ratio. |
| 7125 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 7126 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 7127 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 7128 | 20045101 | Jointly, both QTL explained 8% of the variance in CD4:CD8 ratio. |
| 7129 | 20045101 | Quantitative trait loci for CD4:CD8 lymphocyte ratio are associated with risk of type 1 diabetes and HIV-1 immune control. |
| 7130 | 20045101 | We tested 2.3 million variants for association with five lymphocyte subsets, measured in 2538 individuals from the general population, including CD4+ T cells, CD8+ T cells, CD56+ natural killer (NK) cells, and the derived measure CD4:CD8 ratio. |
| 7131 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 7132 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 7133 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 7134 | 20045101 | Jointly, both QTL explained 8% of the variance in CD4:CD8 ratio. |
| 7135 | 20045101 | Quantitative trait loci for CD4:CD8 lymphocyte ratio are associated with risk of type 1 diabetes and HIV-1 immune control. |
| 7136 | 20045101 | We tested 2.3 million variants for association with five lymphocyte subsets, measured in 2538 individuals from the general population, including CD4+ T cells, CD8+ T cells, CD56+ natural killer (NK) cells, and the derived measure CD4:CD8 ratio. |
| 7137 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 7138 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 7139 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 7140 | 20045101 | Jointly, both QTL explained 8% of the variance in CD4:CD8 ratio. |
| 7141 | 20045101 | Quantitative trait loci for CD4:CD8 lymphocyte ratio are associated with risk of type 1 diabetes and HIV-1 immune control. |
| 7142 | 20045101 | We tested 2.3 million variants for association with five lymphocyte subsets, measured in 2538 individuals from the general population, including CD4+ T cells, CD8+ T cells, CD56+ natural killer (NK) cells, and the derived measure CD4:CD8 ratio. |
| 7143 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 7144 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 7145 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 7146 | 20045101 | Jointly, both QTL explained 8% of the variance in CD4:CD8 ratio. |
| 7147 | 20045101 | Quantitative trait loci for CD4:CD8 lymphocyte ratio are associated with risk of type 1 diabetes and HIV-1 immune control. |
| 7148 | 20045101 | We tested 2.3 million variants for association with five lymphocyte subsets, measured in 2538 individuals from the general population, including CD4+ T cells, CD8+ T cells, CD56+ natural killer (NK) cells, and the derived measure CD4:CD8 ratio. |
| 7149 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 7150 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 7151 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 7152 | 20045101 | Jointly, both QTL explained 8% of the variance in CD4:CD8 ratio. |
| 7153 | 20054344 | We have directly analyzed peripheral CD4+ proinsulin (PI) 76-90 (SLQPLALEGSLQKRG)-specific T cells using soluble fluorescent major histocompatibility complex class II tetramers. |
| 7154 | 20059577 | We evaluated lower-dose regimens of monoclonal anti-CD3 F(ab')(2) in diabetic NOD mice for their efficacy and associated pharmacodynamic (PD) effects, including CD3-T-cell receptor (TCR) complex modulation, complete blood counts and proportions of circulating CD4(+), CD8(+) and CD4(+) FoxP3(+) T cells. |
| 7155 | 20059577 | In treated mice, the proportions of circulating CD4(+) and CD8(+) T cells decreased, whereas the proportions of CD4(+) FoxP3(+) T cells increased; these effects were transient. |
| 7156 | 20059577 | We evaluated lower-dose regimens of monoclonal anti-CD3 F(ab')(2) in diabetic NOD mice for their efficacy and associated pharmacodynamic (PD) effects, including CD3-T-cell receptor (TCR) complex modulation, complete blood counts and proportions of circulating CD4(+), CD8(+) and CD4(+) FoxP3(+) T cells. |
| 7157 | 20059577 | In treated mice, the proportions of circulating CD4(+) and CD8(+) T cells decreased, whereas the proportions of CD4(+) FoxP3(+) T cells increased; these effects were transient. |
| 7158 | 20061825 | NKG2D is a surface receptor expressed on NK cells but also on CD8(+) T cells, gammadelta T cells, and auto-reactive CD4(+)/CD28(-) T cells of patients with rheumatoid arthritis. |
| 7159 | 20061825 | MAb E4 potently antagonized the cytolytic activity of NKL cells against BaF/3-MICA cells expressing NKG2D ligand, and blocked the NKG2D ligand-induced secretion of TNFalpha, IFNgamma and GM-CSF, as well as surface expression of CRTAM by NK cells cultured on immobilized MICA or ULBP-1 ligands. |
| 7160 | 20066510 | A major question is why lymphoproliferation caused by the lpr mutation of Fas and gld mutation of FasL ligand (FasL) is dominated by CD4(-) and CD8(-) double-negative alphabeta T cells (DN T cells) that are otherwise rare components of the peripheral T cell repertoire. |
| 7161 | 20093428 | These findings are consistent with the requirement for both CD4(+) and CD8(+) T cells in the pathogenesis of T1D. |
| 7162 | 20093428 | We have found that H-2K(wm7) molecules are predominantly occupied by the single self-peptide VNDIFERI, derived from the ubiquitous protein histone H2B. |
| 7163 | 20097866 | Functionally significant differences in expression of disease-associated IL-7 receptor alpha haplotypes in CD4 T cells and dendritic cells. |
| 7164 | 20097866 | Common genetic variants of IL-7 receptor alpha (IL-7Ralpha) have recently been shown to affect susceptibility to multiple sclerosis (MS) and type 1 diabetes, and survival following bone marrow transplantation. |
| 7165 | 20097866 | The TSLP/IL-7Ralpha interaction on DCs is known to be critical for production of thymic regulatory T cells, and reduced production of these cells in MS susceptibility haplotypes may be a basis for its association with this disease. |
| 7166 | 20138735 | CD47 and signal regulatory protein (SIRP) interactions have been proposed to take part in autoimmune disease susceptibility. |
| 7167 | 20138735 | Importantly, a recent genome-wide association study for type 1 diabetes susceptibility highlighted the association of the 20p13 region comprising the SIRP cluster, where some of the SIRP proteins encode functional ligands to CD47. |
| 7168 | 20138735 | Interestingly, CD47-deficient mice show a severe reduction in the number of mature CD4(-)CD8(-) T cells, and passive transfer of these CD4(-)CD8(-) T cells is sufficient to restore immune tolerance and prevent diabetes progression. |
| 7169 | 20138735 | Together, these findings constitute an in vivo demonstration that CD47 is involved in diabetes susceptibility and controls the homeostatic regulation of CD4(-)CD8(-) T cells. |
| 7170 | 20138735 | CD47 and signal regulatory protein (SIRP) interactions have been proposed to take part in autoimmune disease susceptibility. |
| 7171 | 20138735 | Importantly, a recent genome-wide association study for type 1 diabetes susceptibility highlighted the association of the 20p13 region comprising the SIRP cluster, where some of the SIRP proteins encode functional ligands to CD47. |
| 7172 | 20138735 | Interestingly, CD47-deficient mice show a severe reduction in the number of mature CD4(-)CD8(-) T cells, and passive transfer of these CD4(-)CD8(-) T cells is sufficient to restore immune tolerance and prevent diabetes progression. |
| 7173 | 20138735 | Together, these findings constitute an in vivo demonstration that CD47 is involved in diabetes susceptibility and controls the homeostatic regulation of CD4(-)CD8(-) T cells. |
| 7174 | 20139986 | In the nonobese diabetic (NOD) mouse model of type 1 diabetes, we have identified the peptide WE14 from chromogranin A (ChgA) as the antigen for highly diabetogenic CD4(+) T cell clones. |
| 7175 | 20143240 | CD4+CD25+(high) regulatory T cells (Tregs) play a pivotal role in the control of the immune response. |
| 7176 | 20143240 | We showed that iTregs from RO T1D subjects had increased expression of Foxp3, E3 ubiquitin ligase (ITCH) and TGF-beta-inducible early gene 1 (TIEG1) compared with control and LS T1D subjects. |
| 7177 | 20146898 | The prevalence of CD4(+), CD8(+), CD25(+) and CD69(+) cells at baseline and after 3 months of add-on therapy was determined. |
| 7178 | 20146898 | The prevalence of regulatory T-cells was detected by two different approaches: forkhead box P3 (FoxP3) positivity; and the number of CD4(+)CD25(+high) cells. |
| 7179 | 20146898 | Simultaneously, the prevalence of activated T-cells (CD4(+)CD69(+) and CD8(+)CD69(+) cells) decreased, whereas that of regulatory T-cells increased. |
| 7180 | 20146898 | The prevalence of CD4(+), CD8(+), CD25(+) and CD69(+) cells at baseline and after 3 months of add-on therapy was determined. |
| 7181 | 20146898 | The prevalence of regulatory T-cells was detected by two different approaches: forkhead box P3 (FoxP3) positivity; and the number of CD4(+)CD25(+high) cells. |
| 7182 | 20146898 | Simultaneously, the prevalence of activated T-cells (CD4(+)CD69(+) and CD8(+)CD69(+) cells) decreased, whereas that of regulatory T-cells increased. |
| 7183 | 20146898 | The prevalence of CD4(+), CD8(+), CD25(+) and CD69(+) cells at baseline and after 3 months of add-on therapy was determined. |
| 7184 | 20146898 | The prevalence of regulatory T-cells was detected by two different approaches: forkhead box P3 (FoxP3) positivity; and the number of CD4(+)CD25(+high) cells. |
| 7185 | 20146898 | Simultaneously, the prevalence of activated T-cells (CD4(+)CD69(+) and CD8(+)CD69(+) cells) decreased, whereas that of regulatory T-cells increased. |
| 7186 | 20155453 | The CFU-GM count in AA group and control group was (74.50+/-9.50)/10(4) cells and (124.25+/-19.80)/10(4) cells respectively under an inverted microscope (P<0.01), and the expression levels of CyclinD3 mRNA and protein in cord blood CD34(+) cells were both down-regulated induced by BM CD4(+) T cell culture supernatant in AA patients. |
| 7187 | 20155453 | BM CD4(+) T cells in AA patients can secret some soluble cytokines that can inhibit proliferation of hematopoietic stem cells by suppressing the expression of Cyclin D3, resulting in hematopoiesis failure. |
| 7188 | 20155453 | The CFU-GM count in AA group and control group was (74.50+/-9.50)/10(4) cells and (124.25+/-19.80)/10(4) cells respectively under an inverted microscope (P<0.01), and the expression levels of CyclinD3 mRNA and protein in cord blood CD34(+) cells were both down-regulated induced by BM CD4(+) T cell culture supernatant in AA patients. |
| 7189 | 20155453 | BM CD4(+) T cells in AA patients can secret some soluble cytokines that can inhibit proliferation of hematopoietic stem cells by suppressing the expression of Cyclin D3, resulting in hematopoiesis failure. |
| 7190 | 20167539 | Dexamethasone downmodulated inflammation and restored normal ratios between CD8(+) and CD4(+)CD25(+)Foxp3(+) cells in the spleen. |
| 7191 | 20173776 | Type 1 diabetes mellitus (T1DM) is a prototypic organ-specific autoimmune disease that results from selective destruction of insulin-secreting beta-cells by immune-mediated inflammation (insulitis), that is, the infiltration of pancreatic islets by autoreactive CD4(+) and CD8(+) T lymphocytes. |
| 7192 | 20174617 | The ligand-activated transcription factor, aryl hydrocarbon receptor (AHR), is a novel inducer of adaptive Tregs. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent AHR ligand, induces adaptive CD4+CD25+ Tregs during an acute graft-versus-host (GvH) response and prevents the generation of allospecific cytotoxic T lymphocytes. |
| 7193 | 20174617 | In this study, we show that chronic treatment of NOD mice with TCDD potently suppresses the development of autoimmune Type 1 diabetes in parallel with greatly reduced pancreatic islet insulitis and an expanded population of CD4+CD25+Foxp3+ cells in the pancreatic lymph nodes. |
| 7194 | 20174617 | The ligand-activated transcription factor, aryl hydrocarbon receptor (AHR), is a novel inducer of adaptive Tregs. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent AHR ligand, induces adaptive CD4+CD25+ Tregs during an acute graft-versus-host (GvH) response and prevents the generation of allospecific cytotoxic T lymphocytes. |
| 7195 | 20174617 | In this study, we show that chronic treatment of NOD mice with TCDD potently suppresses the development of autoimmune Type 1 diabetes in parallel with greatly reduced pancreatic islet insulitis and an expanded population of CD4+CD25+Foxp3+ cells in the pancreatic lymph nodes. |
| 7196 | 20190756 | A set of autoreactive CD4(+) T cells specific for an insulin peptide, with the noteworthy feature of not recognizing the insulin protein when processed by antigen-presenting cells (APCs), escaped thymic control, participated in diabetes and caused disease. |
| 7197 | 20299469 | Idd9.2 and Idd9.3 protective alleles function in CD4+ T-cells and nonlymphoid cells to prevent expansion of pathogenic islet-specific CD8+ T-cells. |
| 7198 | 20299476 | Naturally arising human CD4 T-cells that recognize islet autoantigens and secrete interleukin-10 regulate proinflammatory T-cell responses via linked suppression. |
| 7199 | 20309012 | On the other hand, VIP-treated NOD mice show an increase in the proportion of CD4(+)CD25(+) cells in the spleen. |
| 7200 | 20348424 | High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. |
| 7201 | 20348424 | Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells in type 1 diabetes, little is known about their role in SPS. |
| 7202 | 20348424 | In this study, we show that mice possessing a monoclonal GAD65-specific CD4(+) T cell population (4B5, PA19.9G11, or PA17.9G7) develop a lethal encephalomyelitis-like disease in the absence of any other T cells or B cells. |
| 7203 | 20348424 | GAD65-reactive CD4(+) T cells were found throughout the CNS in direct concordance with GAD65 expression and activated microglia: proximal to the circumventricular organs at the interface between the brain parenchyma and the blood-brain barrier. |
| 7204 | 20348424 | In addition, GAD65-specific CD4(+) T cells isolated from the brain were activated and produced IFN-gamma. |
| 7205 | 20348424 | These findings suggest that GAD65-reactive CD4(+) T cells alone mediate a lethal encephalomyelitis-like disease that may serve as a useful model to study GAD65-mediated diseases of the CNS. |
| 7206 | 20348424 | High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. |
| 7207 | 20348424 | Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells in type 1 diabetes, little is known about their role in SPS. |
| 7208 | 20348424 | In this study, we show that mice possessing a monoclonal GAD65-specific CD4(+) T cell population (4B5, PA19.9G11, or PA17.9G7) develop a lethal encephalomyelitis-like disease in the absence of any other T cells or B cells. |
| 7209 | 20348424 | GAD65-reactive CD4(+) T cells were found throughout the CNS in direct concordance with GAD65 expression and activated microglia: proximal to the circumventricular organs at the interface between the brain parenchyma and the blood-brain barrier. |
| 7210 | 20348424 | In addition, GAD65-specific CD4(+) T cells isolated from the brain were activated and produced IFN-gamma. |
| 7211 | 20348424 | These findings suggest that GAD65-reactive CD4(+) T cells alone mediate a lethal encephalomyelitis-like disease that may serve as a useful model to study GAD65-mediated diseases of the CNS. |
| 7212 | 20348424 | High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. |
| 7213 | 20348424 | Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells in type 1 diabetes, little is known about their role in SPS. |
| 7214 | 20348424 | In this study, we show that mice possessing a monoclonal GAD65-specific CD4(+) T cell population (4B5, PA19.9G11, or PA17.9G7) develop a lethal encephalomyelitis-like disease in the absence of any other T cells or B cells. |
| 7215 | 20348424 | GAD65-reactive CD4(+) T cells were found throughout the CNS in direct concordance with GAD65 expression and activated microglia: proximal to the circumventricular organs at the interface between the brain parenchyma and the blood-brain barrier. |
| 7216 | 20348424 | In addition, GAD65-specific CD4(+) T cells isolated from the brain were activated and produced IFN-gamma. |
| 7217 | 20348424 | These findings suggest that GAD65-reactive CD4(+) T cells alone mediate a lethal encephalomyelitis-like disease that may serve as a useful model to study GAD65-mediated diseases of the CNS. |
| 7218 | 20348424 | High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. |
| 7219 | 20348424 | Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells in type 1 diabetes, little is known about their role in SPS. |
| 7220 | 20348424 | In this study, we show that mice possessing a monoclonal GAD65-specific CD4(+) T cell population (4B5, PA19.9G11, or PA17.9G7) develop a lethal encephalomyelitis-like disease in the absence of any other T cells or B cells. |
| 7221 | 20348424 | GAD65-reactive CD4(+) T cells were found throughout the CNS in direct concordance with GAD65 expression and activated microglia: proximal to the circumventricular organs at the interface between the brain parenchyma and the blood-brain barrier. |
| 7222 | 20348424 | In addition, GAD65-specific CD4(+) T cells isolated from the brain were activated and produced IFN-gamma. |
| 7223 | 20348424 | These findings suggest that GAD65-reactive CD4(+) T cells alone mediate a lethal encephalomyelitis-like disease that may serve as a useful model to study GAD65-mediated diseases of the CNS. |
| 7224 | 20348424 | High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. |
| 7225 | 20348424 | Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells in type 1 diabetes, little is known about their role in SPS. |
| 7226 | 20348424 | In this study, we show that mice possessing a monoclonal GAD65-specific CD4(+) T cell population (4B5, PA19.9G11, or PA17.9G7) develop a lethal encephalomyelitis-like disease in the absence of any other T cells or B cells. |
| 7227 | 20348424 | GAD65-reactive CD4(+) T cells were found throughout the CNS in direct concordance with GAD65 expression and activated microglia: proximal to the circumventricular organs at the interface between the brain parenchyma and the blood-brain barrier. |
| 7228 | 20348424 | In addition, GAD65-specific CD4(+) T cells isolated from the brain were activated and produced IFN-gamma. |
| 7229 | 20348424 | These findings suggest that GAD65-reactive CD4(+) T cells alone mediate a lethal encephalomyelitis-like disease that may serve as a useful model to study GAD65-mediated diseases of the CNS. |
| 7230 | 20363968 | We injected NOD mice with mycobacterial products s.c. and analyzed the IL-17-producing cells from the draining lymph nodes and spleen by restimulating whole-cell populations or CD4(+) T cells in vitro with or without IL-17-polarizing cytokines. |
| 7231 | 20363968 | Mice receiving CFA had a concomitant rise in the level of IL-17, IL-22, IL-10, and IFN-gamma in the draining lymph node and spleen. |
| 7232 | 20363968 | Adoptive transfer of splenocytes from CFA-injected NOD mice polarized with TGF-beta plus IL-6 or IL-23 delayed the development of diabetes in recipient mice. |
| 7233 | 20363968 | Injection of CFA also changed the cytokine profile of cells in pancreatic tissue by increasing IL-17, IL-10, and IFN-gamma cytokine gene expression. |
| 7234 | 20370569 | A low antigen dose selectively promotes expansion of high-avidity autoreactive T cells with distinct phenotypic characteristics: a study of human autoreactive CD4+T cells specific for GAD65. |
| 7235 | 20370569 | We addressed the question, how antigen dose shapes the diversity of CD4+ autoreactive T cells specific for glutamate decarboxylase 65 (GAD65) in a healthy HLA-DR*0404+ individual, with a persistent GAD65-specific T-cell response. |
| 7236 | 20370569 | CD4+T cells from this subject were stimulated with decreasing concentrations of the GAD65 555-567 (557I) peptide, and T-cell clones were derived from the tetramer-binding cell population. |
| 7237 | 20370569 | High IL-13 and IL-10 production by GAD65-reactive T cells suggests a more anti-inflammatory profile of this healthy individual underlying protection from T1D. |
| 7238 | 20370569 | A low antigen dose selectively promotes expansion of high-avidity autoreactive T cells with distinct phenotypic characteristics: a study of human autoreactive CD4+T cells specific for GAD65. |
| 7239 | 20370569 | We addressed the question, how antigen dose shapes the diversity of CD4+ autoreactive T cells specific for glutamate decarboxylase 65 (GAD65) in a healthy HLA-DR*0404+ individual, with a persistent GAD65-specific T-cell response. |
| 7240 | 20370569 | CD4+T cells from this subject were stimulated with decreasing concentrations of the GAD65 555-567 (557I) peptide, and T-cell clones were derived from the tetramer-binding cell population. |
| 7241 | 20370569 | High IL-13 and IL-10 production by GAD65-reactive T cells suggests a more anti-inflammatory profile of this healthy individual underlying protection from T1D. |
| 7242 | 20370569 | A low antigen dose selectively promotes expansion of high-avidity autoreactive T cells with distinct phenotypic characteristics: a study of human autoreactive CD4+T cells specific for GAD65. |
| 7243 | 20370569 | We addressed the question, how antigen dose shapes the diversity of CD4+ autoreactive T cells specific for glutamate decarboxylase 65 (GAD65) in a healthy HLA-DR*0404+ individual, with a persistent GAD65-specific T-cell response. |
| 7244 | 20370569 | CD4+T cells from this subject were stimulated with decreasing concentrations of the GAD65 555-567 (557I) peptide, and T-cell clones were derived from the tetramer-binding cell population. |
| 7245 | 20370569 | High IL-13 and IL-10 production by GAD65-reactive T cells suggests a more anti-inflammatory profile of this healthy individual underlying protection from T1D. |
| 7246 | 20440443 | CD4+ and CD8+ T-cell infiltration and interleukin (IL)-2 mRNA levels were decreased in TMC/CsA-cotreated rats, whereas IL-10 levels were increased. |
| 7247 | 20444936 | Inhibition of dipeptidyl peptidase IV (DPP-IV) activity by NVP-DPP728, a DPP-IV inhibitor, improves the therapeutic efficacy of glucagon-like peptide-1 (GLP-1). |
| 7248 | 20444936 | Regulatory T cells in thymus and secondary lymph nodes, TGF-beta1 and GLP-1 in plasma, and the insulin content in the pancreas were measured. |
| 7249 | 20444936 | Insulitis was reduced and the percentage of CD4(+)CD25(+)FoxP3(+) regulatory T cells was increased in treated NOD mice with remission. |
| 7250 | 20444936 | Plasma TGF-beta1 and GLP-1, the insulin content, and both insulin(+) and BrdU(+) beta-cells in pancreas were also significantly increased. |
| 7251 | 20444936 | In conclusion, NVP-DPP728 treatment can reverse new-onset diabetes in NOD mice by reducing insulitis, increasing CD4(+)CD25(+)FoxP3(+) regulatory T cells, and stimulating beta-cell replication. beta-Cell replication is not associated with the degree of inflammation in NVP-DPP728-treated NOD mice. |
| 7252 | 20444936 | Inhibition of dipeptidyl peptidase IV (DPP-IV) activity by NVP-DPP728, a DPP-IV inhibitor, improves the therapeutic efficacy of glucagon-like peptide-1 (GLP-1). |
| 7253 | 20444936 | Regulatory T cells in thymus and secondary lymph nodes, TGF-beta1 and GLP-1 in plasma, and the insulin content in the pancreas were measured. |
| 7254 | 20444936 | Insulitis was reduced and the percentage of CD4(+)CD25(+)FoxP3(+) regulatory T cells was increased in treated NOD mice with remission. |
| 7255 | 20444936 | Plasma TGF-beta1 and GLP-1, the insulin content, and both insulin(+) and BrdU(+) beta-cells in pancreas were also significantly increased. |
| 7256 | 20444936 | In conclusion, NVP-DPP728 treatment can reverse new-onset diabetes in NOD mice by reducing insulitis, increasing CD4(+)CD25(+)FoxP3(+) regulatory T cells, and stimulating beta-cell replication. beta-Cell replication is not associated with the degree of inflammation in NVP-DPP728-treated NOD mice. |
| 7257 | 20445103 | Leptin-deficient ob/ob mice are overweight, develop insulin resistance, and serve as a model for type 2 diabetes (T2D). |
| 7258 | 20445103 | We induced TGF-beta-dependent CD4(+) latency-associated peptide (LAP)-positive Tregs by oral administration of anti-CD3 antibody plus beta-glucosylceramide. |
| 7259 | 20445103 | Adoptive transfer of orally induced CD4(+)LAP(+) Tregs ameliorated metabolic and cytokine abnormalities. |
| 7260 | 20445103 | Leptin-deficient ob/ob mice are overweight, develop insulin resistance, and serve as a model for type 2 diabetes (T2D). |
| 7261 | 20445103 | We induced TGF-beta-dependent CD4(+) latency-associated peptide (LAP)-positive Tregs by oral administration of anti-CD3 antibody plus beta-glucosylceramide. |
| 7262 | 20445103 | Adoptive transfer of orally induced CD4(+)LAP(+) Tregs ameliorated metabolic and cytokine abnormalities. |
| 7263 | 20491795 | The model uses ordinary differential and algebraic equations to represent the pancreas and PLN as well as dynamic interactions of multiple cell types (e.g. dendritic cells, macrophages, CD4+ T lymphocytes, CD8+ T lymphocytes, regulatory T cells, beta cells). |
| 7264 | 20503254 | Both CD4(+) and CD8(+) T lymphocytes play a crucial role in the autoimmune process leading to T1D. |
| 7265 | 20503259 | Characterization of CD4+ T cells specific for glutamic acid decarboxylase (GAD65) and proinsulin in a patient with stiff-person syndrome but without type 1 diabetes. |
| 7266 | 20529823 | The aim of our study was to test the hypothesis that T regulatory cells express pro- and anti-inflammatory cytokines, elements of cytotoxicity and OX40/4-1BB molecules. |
| 7267 | 20529823 | Concurrently with the flow cytometric assessment of Tregs we separated CD4+CD25+CD127dim/- cells for further mRNA analysis. mRNA levels for transcription factor FoxP3, pro- and anti-inflammatory cytokines (interferon gamma, interleukin-2, interleukin-4, interleukin-10, transforming growth factor beta1 and tumor necrosis factor alpha), activatory molecules (OX40, 4-1BB) and elements of cytotoxicity (granzyme B, perforin 1) were determined by real-time PCR technique. |
| 7268 | 20529823 | Lower OX40 and higher 4-1BB mRNA but not protein levels in Treg cells in diabetic patients compared to the healthy children were noted. |
| 7269 | 20529823 | Our observations confirm the presence of mRNA for pro- and anti-inflammatory cytokines in CD4+CD25+CD127dim/- cells in the peripheral blood of children with T1DM. |
| 7270 | 20529823 | The aim of our study was to test the hypothesis that T regulatory cells express pro- and anti-inflammatory cytokines, elements of cytotoxicity and OX40/4-1BB molecules. |
| 7271 | 20529823 | Concurrently with the flow cytometric assessment of Tregs we separated CD4+CD25+CD127dim/- cells for further mRNA analysis. mRNA levels for transcription factor FoxP3, pro- and anti-inflammatory cytokines (interferon gamma, interleukin-2, interleukin-4, interleukin-10, transforming growth factor beta1 and tumor necrosis factor alpha), activatory molecules (OX40, 4-1BB) and elements of cytotoxicity (granzyme B, perforin 1) were determined by real-time PCR technique. |
| 7272 | 20529823 | Lower OX40 and higher 4-1BB mRNA but not protein levels in Treg cells in diabetic patients compared to the healthy children were noted. |
| 7273 | 20529823 | Our observations confirm the presence of mRNA for pro- and anti-inflammatory cytokines in CD4+CD25+CD127dim/- cells in the peripheral blood of children with T1DM. |
| 7274 | 20531289 | Furthermore, RSG treatment augmented the levels of the anti-inflammatory cytokine interleukin (IL)-10 and increased the recruitment of CD4+ CD25+ FoxP3+ cells, suggesting that regulatory T cells mediated the protection of the peritoneal membrane. |
| 7275 | 20540111 | Since most of the glutamic acid decarboxylase 65 (GAD65)-specific CD4(+) T cells in the NOD mouse are tolerogenic but unable to function in an autoimmune environment, we have activated a silent, monoclonal T-regulatory cell population (GAD65(217-230)-specific CD4(+) T cells) using a soluble I-A(αβ) (g7)/GAD65(217-230)/Fcγ2a dimer, and measured the effect on the ongoing polyclonal diabetogenic T-cell process. |
| 7276 | 20540111 | Activated GAD65(217-230)-specific T cells and a fraction of the diabetogenic (B(9-23)-specific) T cells were polarized toward the IL-10-secreting T-regulatory type 1-like function in the pancreas of diabetic NOD mice. |
| 7277 | 20544263 | IL-10/TGF-beta-treated dendritic cells, pulsed with insulin, specifically reduce the response to insulin of CD4+ effector/memory T cells from type 1 diabetic individuals. |
| 7278 | 20544729 | In this study, we provide evidence that the Icos and Icosl genes contribute to the diabetes process. |
| 7279 | 20544729 | Protection from diabetes in ICOS(-/-) and ICOSL(-/-) NOD mice was unexpectedly associated with the development of an autoimmune disorder of the neuro-muscular system, characterized by myositis, sensory ganglionitis and, to a reduced extent, inflammatory infiltrates in the CNS. |
| 7280 | 20544729 | This syndrome was reproduced upon adoptive transfer of CD4(+) and CD8(+) T cells from diseased donors to naïve NOD.scid recipients. |
| 7281 | 20544729 | Taken together, our findings indicate that costimulation signals play a key role in regulating immune tolerance in peripheral tissues and that the ICOS/ICOSL costimulatory pathway influences the balance between Treg and diabetogenic effector T cells. |
| 7282 | 20561438 | This study was aimed to detect the changes of peripheral CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells before and after T1D mice were treated with syn-BMT, and to investigate the effects of these cells in T1D and the effects of syn-BMT-inducing immunotolerance. |
| 7283 | 20561438 | On 30 day after syn-BMT, peripheral proportion of CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells were detected by flow cytometry. |
| 7284 | 20561438 | The proportion of peripheral CD4(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes, NK cells all increased in new-onset diabetic mice (p < 0.01), while the proportion of peripheral CD8(+) T lymphocytes decreased (p < 0.01). |
| 7285 | 20561438 | The ratio of CD4(+)/CD8(+) T lymphocytes and proportion of NK cells were both obviously lower than that in DC and NC mice (p < 0.01). |
| 7286 | 20561438 | On early period of diabetes onset, the proportions of CD4(+) T lymphocytes and NK cells, the ratio of CD4(+)/CD8(+) T lymphocytes increase, while proportion of CD8(+) T lymphocytes decreases in peripheral blood which mye be associated with onset of diabetes. |
| 7287 | 20561438 | This study was aimed to detect the changes of peripheral CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells before and after T1D mice were treated with syn-BMT, and to investigate the effects of these cells in T1D and the effects of syn-BMT-inducing immunotolerance. |
| 7288 | 20561438 | On 30 day after syn-BMT, peripheral proportion of CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells were detected by flow cytometry. |
| 7289 | 20561438 | The proportion of peripheral CD4(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes, NK cells all increased in new-onset diabetic mice (p < 0.01), while the proportion of peripheral CD8(+) T lymphocytes decreased (p < 0.01). |
| 7290 | 20561438 | The ratio of CD4(+)/CD8(+) T lymphocytes and proportion of NK cells were both obviously lower than that in DC and NC mice (p < 0.01). |
| 7291 | 20561438 | On early period of diabetes onset, the proportions of CD4(+) T lymphocytes and NK cells, the ratio of CD4(+)/CD8(+) T lymphocytes increase, while proportion of CD8(+) T lymphocytes decreases in peripheral blood which mye be associated with onset of diabetes. |
| 7292 | 20561438 | This study was aimed to detect the changes of peripheral CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells before and after T1D mice were treated with syn-BMT, and to investigate the effects of these cells in T1D and the effects of syn-BMT-inducing immunotolerance. |
| 7293 | 20561438 | On 30 day after syn-BMT, peripheral proportion of CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells were detected by flow cytometry. |
| 7294 | 20561438 | The proportion of peripheral CD4(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes, NK cells all increased in new-onset diabetic mice (p < 0.01), while the proportion of peripheral CD8(+) T lymphocytes decreased (p < 0.01). |
| 7295 | 20561438 | The ratio of CD4(+)/CD8(+) T lymphocytes and proportion of NK cells were both obviously lower than that in DC and NC mice (p < 0.01). |
| 7296 | 20561438 | On early period of diabetes onset, the proportions of CD4(+) T lymphocytes and NK cells, the ratio of CD4(+)/CD8(+) T lymphocytes increase, while proportion of CD8(+) T lymphocytes decreases in peripheral blood which mye be associated with onset of diabetes. |
| 7297 | 20561438 | This study was aimed to detect the changes of peripheral CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells before and after T1D mice were treated with syn-BMT, and to investigate the effects of these cells in T1D and the effects of syn-BMT-inducing immunotolerance. |
| 7298 | 20561438 | On 30 day after syn-BMT, peripheral proportion of CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells were detected by flow cytometry. |
| 7299 | 20561438 | The proportion of peripheral CD4(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes, NK cells all increased in new-onset diabetic mice (p < 0.01), while the proportion of peripheral CD8(+) T lymphocytes decreased (p < 0.01). |
| 7300 | 20561438 | The ratio of CD4(+)/CD8(+) T lymphocytes and proportion of NK cells were both obviously lower than that in DC and NC mice (p < 0.01). |
| 7301 | 20561438 | On early period of diabetes onset, the proportions of CD4(+) T lymphocytes and NK cells, the ratio of CD4(+)/CD8(+) T lymphocytes increase, while proportion of CD8(+) T lymphocytes decreases in peripheral blood which mye be associated with onset of diabetes. |
| 7302 | 20561438 | This study was aimed to detect the changes of peripheral CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells before and after T1D mice were treated with syn-BMT, and to investigate the effects of these cells in T1D and the effects of syn-BMT-inducing immunotolerance. |
| 7303 | 20561438 | On 30 day after syn-BMT, peripheral proportion of CD4(+) T lymphocytes, CD8(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes and NK cells were detected by flow cytometry. |
| 7304 | 20561438 | The proportion of peripheral CD4(+) T lymphocytes, CD4(+)/CD8(+) T lymphocytes, NK cells all increased in new-onset diabetic mice (p < 0.01), while the proportion of peripheral CD8(+) T lymphocytes decreased (p < 0.01). |
| 7305 | 20561438 | The ratio of CD4(+)/CD8(+) T lymphocytes and proportion of NK cells were both obviously lower than that in DC and NC mice (p < 0.01). |
| 7306 | 20561438 | On early period of diabetes onset, the proportions of CD4(+) T lymphocytes and NK cells, the ratio of CD4(+)/CD8(+) T lymphocytes increase, while proportion of CD8(+) T lymphocytes decreases in peripheral blood which mye be associated with onset of diabetes. |
| 7307 | 20565292 | Impaired antiviral CD8 and CD4 T-cell responses are often associated with chronic viral infections. |
| 7308 | 20565292 | Here we demonstrate that CD103, an alpha E integrin necessary for T-cell homing and retention in the gut and other epithelia expressed by the majority of naïve CD8(+), and CD4(+)CD25(+) T cells and some DC subsets, is unnecessary for controlling T-cell responses during chronic lymphocytic choriomeningitis virus clone 13 (LCMV cl13) infection. |
| 7309 | 20565292 | T-cell analysis following viral infection showed that the primary as well as the memory CD8(+) and CD4(+) T-cell responses among CD103-sufficient and CD103-deficient mice were identical. |
| 7310 | 20565292 | Interestingly, CD103 levels on the effector CD8(+) T cells became reduced soon after virus infection, with a small proportion of cells co-expressing PD-1 and CD103. |
| 7311 | 20565292 | In contrast, although no substantial differences in the frequency and number of the CD4(+)CD25(+) cell population were seen, CD103 expression increased significantly over time in this population, correlating with viral persistence. |
| 7312 | 20565292 | Impaired antiviral CD8 and CD4 T-cell responses are often associated with chronic viral infections. |
| 7313 | 20565292 | Here we demonstrate that CD103, an alpha E integrin necessary for T-cell homing and retention in the gut and other epithelia expressed by the majority of naïve CD8(+), and CD4(+)CD25(+) T cells and some DC subsets, is unnecessary for controlling T-cell responses during chronic lymphocytic choriomeningitis virus clone 13 (LCMV cl13) infection. |
| 7314 | 20565292 | T-cell analysis following viral infection showed that the primary as well as the memory CD8(+) and CD4(+) T-cell responses among CD103-sufficient and CD103-deficient mice were identical. |
| 7315 | 20565292 | Interestingly, CD103 levels on the effector CD8(+) T cells became reduced soon after virus infection, with a small proportion of cells co-expressing PD-1 and CD103. |
| 7316 | 20565292 | In contrast, although no substantial differences in the frequency and number of the CD4(+)CD25(+) cell population were seen, CD103 expression increased significantly over time in this population, correlating with viral persistence. |
| 7317 | 20565292 | Impaired antiviral CD8 and CD4 T-cell responses are often associated with chronic viral infections. |
| 7318 | 20565292 | Here we demonstrate that CD103, an alpha E integrin necessary for T-cell homing and retention in the gut and other epithelia expressed by the majority of naïve CD8(+), and CD4(+)CD25(+) T cells and some DC subsets, is unnecessary for controlling T-cell responses during chronic lymphocytic choriomeningitis virus clone 13 (LCMV cl13) infection. |
| 7319 | 20565292 | T-cell analysis following viral infection showed that the primary as well as the memory CD8(+) and CD4(+) T-cell responses among CD103-sufficient and CD103-deficient mice were identical. |
| 7320 | 20565292 | Interestingly, CD103 levels on the effector CD8(+) T cells became reduced soon after virus infection, with a small proportion of cells co-expressing PD-1 and CD103. |
| 7321 | 20565292 | In contrast, although no substantial differences in the frequency and number of the CD4(+)CD25(+) cell population were seen, CD103 expression increased significantly over time in this population, correlating with viral persistence. |
| 7322 | 20565292 | Impaired antiviral CD8 and CD4 T-cell responses are often associated with chronic viral infections. |
| 7323 | 20565292 | Here we demonstrate that CD103, an alpha E integrin necessary for T-cell homing and retention in the gut and other epithelia expressed by the majority of naïve CD8(+), and CD4(+)CD25(+) T cells and some DC subsets, is unnecessary for controlling T-cell responses during chronic lymphocytic choriomeningitis virus clone 13 (LCMV cl13) infection. |
| 7324 | 20565292 | T-cell analysis following viral infection showed that the primary as well as the memory CD8(+) and CD4(+) T-cell responses among CD103-sufficient and CD103-deficient mice were identical. |
| 7325 | 20565292 | Interestingly, CD103 levels on the effector CD8(+) T cells became reduced soon after virus infection, with a small proportion of cells co-expressing PD-1 and CD103. |
| 7326 | 20565292 | In contrast, although no substantial differences in the frequency and number of the CD4(+)CD25(+) cell population were seen, CD103 expression increased significantly over time in this population, correlating with viral persistence. |
| 7327 | 20599916 | Daily injections of F-FTS led to an increase in both the number and the migratory capacity of pancreatic Foxp3(+)CD4(+)CD25(+) Treg, while cleaved caspase 3 in the pancreas were significantly decreased, indicating reduced apoptosis. |
| 7328 | 20603635 | In particular, CD4(-)CD8(-) (double negative (DN)) T cells, which compose 1-3% of the total number of T lymphocytes, exhibit prominent antigen-specific immune tolerance properties and confer immune tolerance in models of allografts and xenografts. |
| 7329 | 20639483 | CD4+ CD25+ regulatory T cells prevent type 1 diabetes preceded by dendritic cell-dominant invasive insulitis by affecting chemotaxis and local invasiveness of dendritic cells. |
| 7330 | 20639483 | Although CD4(+)CD25(+) regulatory T cells (nTregs) induce tolerance that inhibits insulitis and T1D, the in vivo cellular mechanisms underlying this process remain largely unclear. |
| 7331 | 20639483 | However, ISL-DCs from nTreg-deficient recipient mice showed increased in vitro migration toward CCL19 and CCL21. |
| 7332 | 20639483 | CD4+ CD25+ regulatory T cells prevent type 1 diabetes preceded by dendritic cell-dominant invasive insulitis by affecting chemotaxis and local invasiveness of dendritic cells. |
| 7333 | 20639483 | Although CD4(+)CD25(+) regulatory T cells (nTregs) induce tolerance that inhibits insulitis and T1D, the in vivo cellular mechanisms underlying this process remain largely unclear. |
| 7334 | 20639483 | However, ISL-DCs from nTreg-deficient recipient mice showed increased in vitro migration toward CCL19 and CCL21. |
| 7335 | 20646763 | CD40 glycoforms and TNF-receptors 1 and 2 in the formation of CD40 receptor(s) in autoimmunity. |
| 7336 | 20646763 | We described a CD4(+)CD40(+) T cell (Th40) subset which is expanded in autoimmunity and is necessary and sufficient in transferring type 1 diabetes. |
| 7337 | 20646763 | Here we demonstrate that several CD40 receptor constellations exist on CD4 T cells. |
| 7338 | 20646763 | Interestingly, CD40 stimulation induces some CD40 receptor constellations that contain TNF-receptors 1 and 2 and targeting of those alters CD40 signaling outcomes in NOD Th40 cells. |
| 7339 | 20646763 | CD40 glycoforms and TNF-receptors 1 and 2 in the formation of CD40 receptor(s) in autoimmunity. |
| 7340 | 20646763 | We described a CD4(+)CD40(+) T cell (Th40) subset which is expanded in autoimmunity and is necessary and sufficient in transferring type 1 diabetes. |
| 7341 | 20646763 | Here we demonstrate that several CD40 receptor constellations exist on CD4 T cells. |
| 7342 | 20646763 | Interestingly, CD40 stimulation induces some CD40 receptor constellations that contain TNF-receptors 1 and 2 and targeting of those alters CD40 signaling outcomes in NOD Th40 cells. |
| 7343 | 20686126 | DC-induced Treg division required IL-2, which was provided by conventional CD4(+) T cells through an MHC class II (MHC II)-dependent interaction with DCs. |
| 7344 | 20686126 | Provision of exogenous IL-2 obviated the need for conventional CD4(+) T cells in the induction of Treg proliferation, but this process still required a contact-dependent but MHC II-independent interaction between DCs and Tregs. |
| 7345 | 20686126 | DC-induced Treg division required IL-2, which was provided by conventional CD4(+) T cells through an MHC class II (MHC II)-dependent interaction with DCs. |
| 7346 | 20686126 | Provision of exogenous IL-2 obviated the need for conventional CD4(+) T cells in the induction of Treg proliferation, but this process still required a contact-dependent but MHC II-independent interaction between DCs and Tregs. |
| 7347 | 20695767 | In healthy C57BL/6J (B6) mice, total CD4(+) and CD8(+) T-cell subsets were diminished by FTY720, but recently activated and memory subsets were spared and constituted significantly higher percentage of remaining T cells in blood. |
| 7348 | 20703438 | Studies employing T cell receptor transgenic T cells have convincingly shown that selective delivery of non-self model antigens to DEC-205(+) dendritic cells (DCs) in the steady-state can induce Foxp3-expressing CD4(+)CD25(+) regulatory T (Treg) cells from conventional CD4(+)CD25(-)Foxp3(-) T cells. |
| 7349 | 20703438 | Here, we show in proof-of-principle experiments that targeting a mimotope peptide to the endocytic receptor DEC-205 on DCs in NOD mice induces efficient conversion of pancreatic beta-cell-reactive BDC2.5 CD4(+) T cells into long-lived Foxp3(+) Treg cells. |
| 7350 | 20703438 | While de novo generation of BDC2.5 Treg cells did not interfere with disease progression, anti-DEC-205-mediated targeting of whole proinsulin in prediabetic NOD mice substantially reduced the incidence of diabetes. |
| 7351 | 20703438 | Studies employing T cell receptor transgenic T cells have convincingly shown that selective delivery of non-self model antigens to DEC-205(+) dendritic cells (DCs) in the steady-state can induce Foxp3-expressing CD4(+)CD25(+) regulatory T (Treg) cells from conventional CD4(+)CD25(-)Foxp3(-) T cells. |
| 7352 | 20703438 | Here, we show in proof-of-principle experiments that targeting a mimotope peptide to the endocytic receptor DEC-205 on DCs in NOD mice induces efficient conversion of pancreatic beta-cell-reactive BDC2.5 CD4(+) T cells into long-lived Foxp3(+) Treg cells. |
| 7353 | 20703438 | While de novo generation of BDC2.5 Treg cells did not interfere with disease progression, anti-DEC-205-mediated targeting of whole proinsulin in prediabetic NOD mice substantially reduced the incidence of diabetes. |
| 7354 | 20705519 | Increased spontaneous production of VEGF by CD4+ T cells in type 1 diabetes. |
| 7355 | 20705519 | Hence, these data indicate that there is a sustained spontaneous production of VEGF by CD4(+) T cells in type 1 diabetes, which is additionally exacerbated in DR. |
| 7356 | 20705519 | Increased spontaneous production of VEGF by CD4+ T cells in type 1 diabetes. |
| 7357 | 20705519 | Hence, these data indicate that there is a sustained spontaneous production of VEGF by CD4(+) T cells in type 1 diabetes, which is additionally exacerbated in DR. |
| 7358 | 20720201 | MEKK3 overexpression contributes to the hyperresponsiveness of IL-12-overproducing cells and CD4+ T conventional cells in nonobese diabetic mice. |
| 7359 | 20720201 | Aberrant p38 activation induced by various inflammatory stimuli in IL-12-overproducing cells is not due to defective MAPK phosphatase-1 induction in NOD mice. |
| 7360 | 20720201 | Deviated IKK and MAPKs activation also occurs in NOD CD4(+) Tconv cells, which is associated with higher rates of proliferation. |
| 7361 | 20720201 | All of the above evidence suggests that the signaling defects occur at the level of MAPK kinase kinase (MAK3K or MEKK). |
| 7362 | 20720201 | Further exploration shows that MEKK3, but not other MAP3Ks, is overexpressed in NOD IL-12-overproducing cells and CD4(+) Tconv cells independent of autoimmune inflammation. |
| 7363 | 20720201 | MEKK3 knockdown leads to reversal of the deviated IKK and MAPKs activation, resulting in reduced IL-12 production and decreased CD4(+) Tconv cell proliferation. |
| 7364 | 20720201 | MEKK3 overexpression contributes to the hyperresponsiveness of IL-12-overproducing cells and CD4+ T conventional cells in nonobese diabetic mice. |
| 7365 | 20720201 | Aberrant p38 activation induced by various inflammatory stimuli in IL-12-overproducing cells is not due to defective MAPK phosphatase-1 induction in NOD mice. |
| 7366 | 20720201 | Deviated IKK and MAPKs activation also occurs in NOD CD4(+) Tconv cells, which is associated with higher rates of proliferation. |
| 7367 | 20720201 | All of the above evidence suggests that the signaling defects occur at the level of MAPK kinase kinase (MAK3K or MEKK). |
| 7368 | 20720201 | Further exploration shows that MEKK3, but not other MAP3Ks, is overexpressed in NOD IL-12-overproducing cells and CD4(+) Tconv cells independent of autoimmune inflammation. |
| 7369 | 20720201 | MEKK3 knockdown leads to reversal of the deviated IKK and MAPKs activation, resulting in reduced IL-12 production and decreased CD4(+) Tconv cell proliferation. |
| 7370 | 20720201 | MEKK3 overexpression contributes to the hyperresponsiveness of IL-12-overproducing cells and CD4+ T conventional cells in nonobese diabetic mice. |
| 7371 | 20720201 | Aberrant p38 activation induced by various inflammatory stimuli in IL-12-overproducing cells is not due to defective MAPK phosphatase-1 induction in NOD mice. |
| 7372 | 20720201 | Deviated IKK and MAPKs activation also occurs in NOD CD4(+) Tconv cells, which is associated with higher rates of proliferation. |
| 7373 | 20720201 | All of the above evidence suggests that the signaling defects occur at the level of MAPK kinase kinase (MAK3K or MEKK). |
| 7374 | 20720201 | Further exploration shows that MEKK3, but not other MAP3Ks, is overexpressed in NOD IL-12-overproducing cells and CD4(+) Tconv cells independent of autoimmune inflammation. |
| 7375 | 20720201 | MEKK3 knockdown leads to reversal of the deviated IKK and MAPKs activation, resulting in reduced IL-12 production and decreased CD4(+) Tconv cell proliferation. |
| 7376 | 20720201 | MEKK3 overexpression contributes to the hyperresponsiveness of IL-12-overproducing cells and CD4+ T conventional cells in nonobese diabetic mice. |
| 7377 | 20720201 | Aberrant p38 activation induced by various inflammatory stimuli in IL-12-overproducing cells is not due to defective MAPK phosphatase-1 induction in NOD mice. |
| 7378 | 20720201 | Deviated IKK and MAPKs activation also occurs in NOD CD4(+) Tconv cells, which is associated with higher rates of proliferation. |
| 7379 | 20720201 | All of the above evidence suggests that the signaling defects occur at the level of MAPK kinase kinase (MAK3K or MEKK). |
| 7380 | 20720201 | Further exploration shows that MEKK3, but not other MAP3Ks, is overexpressed in NOD IL-12-overproducing cells and CD4(+) Tconv cells independent of autoimmune inflammation. |
| 7381 | 20720201 | MEKK3 knockdown leads to reversal of the deviated IKK and MAPKs activation, resulting in reduced IL-12 production and decreased CD4(+) Tconv cell proliferation. |
| 7382 | 20810982 | CD4(+)FOXP3(+) regulatory T cells are essential for immune tolerance, and murine studies suggest that their dysfunction can lead to type 1 diabetes (T1D). |
| 7383 | 20810982 | Recently, distinct subsets of CD4(+)FOXP3(+) T cells with differing function were identified. |
| 7384 | 20810982 | Therefore, we evaluated whether the relative fractions of CD4(+)FOXP3(+) subsets are altered in new-onset T1D subjects. |
| 7385 | 20810982 | Moreover, these T1D subjects had a higher proportion of both CD4(+) and CD8(+) T cells that secrete IL-17. |
| 7386 | 20810982 | CD4(+)FOXP3(+) regulatory T cells are essential for immune tolerance, and murine studies suggest that their dysfunction can lead to type 1 diabetes (T1D). |
| 7387 | 20810982 | Recently, distinct subsets of CD4(+)FOXP3(+) T cells with differing function were identified. |
| 7388 | 20810982 | Therefore, we evaluated whether the relative fractions of CD4(+)FOXP3(+) subsets are altered in new-onset T1D subjects. |
| 7389 | 20810982 | Moreover, these T1D subjects had a higher proportion of both CD4(+) and CD8(+) T cells that secrete IL-17. |
| 7390 | 20810982 | CD4(+)FOXP3(+) regulatory T cells are essential for immune tolerance, and murine studies suggest that their dysfunction can lead to type 1 diabetes (T1D). |
| 7391 | 20810982 | Recently, distinct subsets of CD4(+)FOXP3(+) T cells with differing function were identified. |
| 7392 | 20810982 | Therefore, we evaluated whether the relative fractions of CD4(+)FOXP3(+) subsets are altered in new-onset T1D subjects. |
| 7393 | 20810982 | Moreover, these T1D subjects had a higher proportion of both CD4(+) and CD8(+) T cells that secrete IL-17. |
| 7394 | 20810982 | CD4(+)FOXP3(+) regulatory T cells are essential for immune tolerance, and murine studies suggest that their dysfunction can lead to type 1 diabetes (T1D). |
| 7395 | 20810982 | Recently, distinct subsets of CD4(+)FOXP3(+) T cells with differing function were identified. |
| 7396 | 20810982 | Therefore, we evaluated whether the relative fractions of CD4(+)FOXP3(+) subsets are altered in new-onset T1D subjects. |
| 7397 | 20810982 | Moreover, these T1D subjects had a higher proportion of both CD4(+) and CD8(+) T cells that secrete IL-17. |
| 7398 | 20818148 | CD4(+)CD25(+) T cells which have also been described as regulatory T cells (Treg), have immune inhibitory functions in the immune system. |
| 7399 | 20818148 | The clinical features of IPEX syndrome include chronic dermatitis, enteropathy characterized by severe and refractory diarrhea, and autoimmune endocrinopathy, such as early-onset insulin-dependent diabetes mellitus, thyroiditis, or both. |
| 7400 | 20827324 | As an innovative strategy to circumvent these barriers, vaccine trials to stimulate antigen-specific T-cells polarized toward helper T-cells with a regulatory phenotype (Tregs, CD4+, CD25+, FoxP3+) have also been introduced. |
| 7401 | 20850948 | Immunotargeting of insulin reactive CD8 T cells to prevent diabetes. |
| 7402 | 20850948 | Insulin is one of the earliest targeted autoantigens in the immune destruction of insulin-producing beta cells by autoreactive CD4 and CD8 T cells in type 1 diabetes. |
| 7403 | 20850948 | In this study, we used Non-obese diabetic (NOD) transgenic T cells engineered to express MHC class I-insulin peptide complexes linked to a T cell activation component (InsCD3-ζ), to target insulin-reactive CD8 T cells. |
| 7404 | 20850948 | We showed that activated, but not naïve, InsCD3-ζ CD8 T cells killed diabetogenic insulin-reactive CD8 target cells in vitro, inducing antigen-specific cell death mediated via both the release of perforin and the Fas-Fas ligand pathway. |
| 7405 | 20850948 | Finally, in vivo, we showed that diabetes induced by adoptive transfer of insulin-reactive T cells was reduced following injection of activated InsCD3-ζ CD8 T cells. |
| 7406 | 20850948 | Thus, using this novel system we have demonstrated that InsCD3-ζ CD8 T cells can directly kill insulin-reactive CD8 T cells in vitro and by targeting insulin-specific CD8 T cells early in the course of disease alter the progression of spontaneous diabetes in vivo in NOD mice. |
| 7407 | 20855871 | In addition, transfer of CD8(+) T cells from diabetic animals into DORmO.RAG2(-/-) mice promoted insulitis by OVA-specific CD4(+) T cells. |
| 7408 | 20869956 | Compared with the untreated diabetic group, UA and metformin significantly improved blood glucose, glycosylated hemoglobin, glucose tolerance, insulin tolerance and plasma leptin levels as well as aminotransferase activity. |
| 7409 | 20869956 | Mice receiving UA or metformin supplementation had increased CD4(+)CD8(+) subpopulations in the thymus compared to the untreated diabetic mice. |
| 7410 | 20869956 | Concanavalin A-stimulated splenic T-lymphocyte proliferation and single-positive (CD4(+) and CD8(+)) subpopulations were significantly higher in the UA-supplemented diabetic groups than in the untreated diabetic group, but lipopolysaccharide-stimulated B-lymphocyte proliferation and the CD19(+) subpopulation were not significantly different among the groups. |
| 7411 | 20869956 | In the STZ/NA-induced diabetic mice, metformin increased the splenic T-lymphocyte CD4(+) and CD8(+) cell numbers without any change in T-lymphocyte proliferation. |
| 7412 | 20869956 | Compared with the untreated diabetic group, UA and metformin significantly improved blood glucose, glycosylated hemoglobin, glucose tolerance, insulin tolerance and plasma leptin levels as well as aminotransferase activity. |
| 7413 | 20869956 | Mice receiving UA or metformin supplementation had increased CD4(+)CD8(+) subpopulations in the thymus compared to the untreated diabetic mice. |
| 7414 | 20869956 | Concanavalin A-stimulated splenic T-lymphocyte proliferation and single-positive (CD4(+) and CD8(+)) subpopulations were significantly higher in the UA-supplemented diabetic groups than in the untreated diabetic group, but lipopolysaccharide-stimulated B-lymphocyte proliferation and the CD19(+) subpopulation were not significantly different among the groups. |
| 7415 | 20869956 | In the STZ/NA-induced diabetic mice, metformin increased the splenic T-lymphocyte CD4(+) and CD8(+) cell numbers without any change in T-lymphocyte proliferation. |
| 7416 | 20869956 | Compared with the untreated diabetic group, UA and metformin significantly improved blood glucose, glycosylated hemoglobin, glucose tolerance, insulin tolerance and plasma leptin levels as well as aminotransferase activity. |
| 7417 | 20869956 | Mice receiving UA or metformin supplementation had increased CD4(+)CD8(+) subpopulations in the thymus compared to the untreated diabetic mice. |
| 7418 | 20869956 | Concanavalin A-stimulated splenic T-lymphocyte proliferation and single-positive (CD4(+) and CD8(+)) subpopulations were significantly higher in the UA-supplemented diabetic groups than in the untreated diabetic group, but lipopolysaccharide-stimulated B-lymphocyte proliferation and the CD19(+) subpopulation were not significantly different among the groups. |
| 7419 | 20869956 | In the STZ/NA-induced diabetic mice, metformin increased the splenic T-lymphocyte CD4(+) and CD8(+) cell numbers without any change in T-lymphocyte proliferation. |
| 7420 | 20880188 | Our previous studies of the murine genetic locus Idd6 revealed the aryl hydrocarbon receptor nuclear translocator-like protein 2 (Arntl2) as a candidate gene for type 1 diabetes; and in Idd6 NOD.C3H congenic mice, Arntl2 upregulation is linked to decreased diabetes development. 2. |
| 7421 | 20880188 | Diabetes incidence was increased by Arntl2 mRNA interference in the congenic strain and this was associated with an increase in CD4(+) T cells and a decrease in regulatory T cells in the peripheral immune system. 4. |
| 7422 | 20884174 | Hence we addressed this issue by using such dual transplantation and demonstrate herein that seven weeks later, recipient db/db mice manifested improved body weight, reduced levels of blood glucose, and a reduction of plasma IL-6 and IL-1β. |
| 7423 | 20884174 | More importantly, this treatment regimen showed normal CD4/CD8 ratios, and increased plasma adiponectin levels, insulin sensitivity, and the number of insulin-producing cells. |
| 7424 | 20941602 | Naturally occurring regulatory T cells (nTregs; CD4(+)CD25(+)Foxp3(+)) are capable of suppressing the chronic inflammation observed in a variety of different animal models of autoimmune and chronic inflammatory diseases such as inflammatory bowel diseases, diabetes, and arthritis. |
| 7425 | 20941602 | Although several laboratories have described different methods to expand flow-purified nTregs or convert conventional/naïve T cells (CD4(+)Foxp3(-)) to Foxp3-expressing "induced" Tregs (iTregs; CD4(+)Foxp3(+)) ex vivo, we have found that many of these approaches are encumbered with their own limitations. |
| 7426 | 20941602 | We present a detailed protocol demonstrating that polyclonal activation of conventional CD4(+) T cells in the presence of IL-2, TGFβ, and all trans retinoic acid induces >90% conversion of these T cells to Foxp3-expressing iTregs as well as promotes a three- to fourfold increase in proliferation following a 4-day incubation period in vitro. |
| 7427 | 20941602 | Naturally occurring regulatory T cells (nTregs; CD4(+)CD25(+)Foxp3(+)) are capable of suppressing the chronic inflammation observed in a variety of different animal models of autoimmune and chronic inflammatory diseases such as inflammatory bowel diseases, diabetes, and arthritis. |
| 7428 | 20941602 | Although several laboratories have described different methods to expand flow-purified nTregs or convert conventional/naïve T cells (CD4(+)Foxp3(-)) to Foxp3-expressing "induced" Tregs (iTregs; CD4(+)Foxp3(+)) ex vivo, we have found that many of these approaches are encumbered with their own limitations. |
| 7429 | 20941602 | We present a detailed protocol demonstrating that polyclonal activation of conventional CD4(+) T cells in the presence of IL-2, TGFβ, and all trans retinoic acid induces >90% conversion of these T cells to Foxp3-expressing iTregs as well as promotes a three- to fourfold increase in proliferation following a 4-day incubation period in vitro. |
| 7430 | 20941602 | Naturally occurring regulatory T cells (nTregs; CD4(+)CD25(+)Foxp3(+)) are capable of suppressing the chronic inflammation observed in a variety of different animal models of autoimmune and chronic inflammatory diseases such as inflammatory bowel diseases, diabetes, and arthritis. |
| 7431 | 20941602 | Although several laboratories have described different methods to expand flow-purified nTregs or convert conventional/naïve T cells (CD4(+)Foxp3(-)) to Foxp3-expressing "induced" Tregs (iTregs; CD4(+)Foxp3(+)) ex vivo, we have found that many of these approaches are encumbered with their own limitations. |
| 7432 | 20941602 | We present a detailed protocol demonstrating that polyclonal activation of conventional CD4(+) T cells in the presence of IL-2, TGFβ, and all trans retinoic acid induces >90% conversion of these T cells to Foxp3-expressing iTregs as well as promotes a three- to fourfold increase in proliferation following a 4-day incubation period in vitro. |
| 7433 | 20956337 | The protective effects of MDSCs might be mediated by inducing anergy in autoreactive T cells and the development of CD4(+)CD25(+)Foxp3(+) Tregs. |
| 7434 | 21038470 | Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF. |
| 7435 | 21038470 | They inhibit CD4(+) T-cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL-2. |
| 7436 | 21038470 | The induction of CD8(+) Treg by anti-CD3 mAb requires TNF and signaling through the NF-κB cascade. |
| 7437 | 21038470 | The CD8(+) Treg express CD25, glucocorticoid-induced TNF receptor family, CTLA-4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8(+) Treg. |
| 7438 | 21050716 | To this end, we determined the feasibility of cloning and expanding human CD4(+) Treg specific for the type 1 diabetes autoantigens, GAD65 and proinsulin. |
| 7439 | 21050716 | Blood CD4(+) cells stimulated to divide in response to GAD65 (in three healthy individuals) or proinsulin (in one type 1 diabetic) were flow sorted into single cells and cultured on feeder cells in the presence of anti-CD3 monoclonal antibody, IL-2 and IL-4. |
| 7440 | 21050716 | Treg clones were not distinguished by markers of conventional CD4(+)CD25(+) Treg and suppressed independently of cell-cell contact but not via known soluble suppressor factors. |
| 7441 | 21050716 | To this end, we determined the feasibility of cloning and expanding human CD4(+) Treg specific for the type 1 diabetes autoantigens, GAD65 and proinsulin. |
| 7442 | 21050716 | Blood CD4(+) cells stimulated to divide in response to GAD65 (in three healthy individuals) or proinsulin (in one type 1 diabetic) were flow sorted into single cells and cultured on feeder cells in the presence of anti-CD3 monoclonal antibody, IL-2 and IL-4. |
| 7443 | 21050716 | Treg clones were not distinguished by markers of conventional CD4(+)CD25(+) Treg and suppressed independently of cell-cell contact but not via known soluble suppressor factors. |
| 7444 | 21050716 | To this end, we determined the feasibility of cloning and expanding human CD4(+) Treg specific for the type 1 diabetes autoantigens, GAD65 and proinsulin. |
| 7445 | 21050716 | Blood CD4(+) cells stimulated to divide in response to GAD65 (in three healthy individuals) or proinsulin (in one type 1 diabetic) were flow sorted into single cells and cultured on feeder cells in the presence of anti-CD3 monoclonal antibody, IL-2 and IL-4. |
| 7446 | 21050716 | Treg clones were not distinguished by markers of conventional CD4(+)CD25(+) Treg and suppressed independently of cell-cell contact but not via known soluble suppressor factors. |
| 7447 | 21099102 | Among these, protection mediated by CD4+Foxp3+ Tregs constitutes an essential pathway. |
| 7448 | 21099113 | CD4+CD25+Foxp3+ Tregs play a major role in prevention of autoimmune diseases. |
| 7449 | 21099113 | In vivo experiments showed that this Treg boost was partially dependent on TNF but not on IL-2. |
| 7450 | 21112637 | Increased GABA(A) channel subunits expression in CD8(+) but not in CD4(+) T cells in BB rats developing diabetes compared to their congenic littermates. |
| 7451 | 21112637 | We examined CD4(+) and CD8(+) T cells from diabetes prone (DR(lyp/lyp)) or resistant (DR(+/+)) congenic biobreeding (BB) rats for expression of GABA(A) channels. |
| 7452 | 21112637 | Our results show that BB rat CD4(+) and CD8(+) T cells express α1, α2, α3, α4, α6, β3, γ1, δ, ρ1 and ρ2 GABA(A) channel subunits. |
| 7453 | 21112637 | In CD8(+) T cells from DR(lyp/lyp) animals the subunits were significantly upregulated relative to expression levels in the CD8(+) T cells from DR(+/+) rats as well as from CD4(+) T cells from both DR(lyp/lyp) and DR(+/+) rats. |
| 7454 | 21112637 | Increased GABA(A) channel subunits expression in CD8(+) but not in CD4(+) T cells in BB rats developing diabetes compared to their congenic littermates. |
| 7455 | 21112637 | We examined CD4(+) and CD8(+) T cells from diabetes prone (DR(lyp/lyp)) or resistant (DR(+/+)) congenic biobreeding (BB) rats for expression of GABA(A) channels. |
| 7456 | 21112637 | Our results show that BB rat CD4(+) and CD8(+) T cells express α1, α2, α3, α4, α6, β3, γ1, δ, ρ1 and ρ2 GABA(A) channel subunits. |
| 7457 | 21112637 | In CD8(+) T cells from DR(lyp/lyp) animals the subunits were significantly upregulated relative to expression levels in the CD8(+) T cells from DR(+/+) rats as well as from CD4(+) T cells from both DR(lyp/lyp) and DR(+/+) rats. |
| 7458 | 21112637 | Increased GABA(A) channel subunits expression in CD8(+) but not in CD4(+) T cells in BB rats developing diabetes compared to their congenic littermates. |
| 7459 | 21112637 | We examined CD4(+) and CD8(+) T cells from diabetes prone (DR(lyp/lyp)) or resistant (DR(+/+)) congenic biobreeding (BB) rats for expression of GABA(A) channels. |
| 7460 | 21112637 | Our results show that BB rat CD4(+) and CD8(+) T cells express α1, α2, α3, α4, α6, β3, γ1, δ, ρ1 and ρ2 GABA(A) channel subunits. |
| 7461 | 21112637 | In CD8(+) T cells from DR(lyp/lyp) animals the subunits were significantly upregulated relative to expression levels in the CD8(+) T cells from DR(+/+) rats as well as from CD4(+) T cells from both DR(lyp/lyp) and DR(+/+) rats. |
| 7462 | 21112637 | Increased GABA(A) channel subunits expression in CD8(+) but not in CD4(+) T cells in BB rats developing diabetes compared to their congenic littermates. |
| 7463 | 21112637 | We examined CD4(+) and CD8(+) T cells from diabetes prone (DR(lyp/lyp)) or resistant (DR(+/+)) congenic biobreeding (BB) rats for expression of GABA(A) channels. |
| 7464 | 21112637 | Our results show that BB rat CD4(+) and CD8(+) T cells express α1, α2, α3, α4, α6, β3, γ1, δ, ρ1 and ρ2 GABA(A) channel subunits. |
| 7465 | 21112637 | In CD8(+) T cells from DR(lyp/lyp) animals the subunits were significantly upregulated relative to expression levels in the CD8(+) T cells from DR(+/+) rats as well as from CD4(+) T cells from both DR(lyp/lyp) and DR(+/+) rats. |
| 7466 | 21116786 | Programmed death-1 (PD-1) is a co-inhibitory receptor of the CD28/CTLA-4 family which is expressed on activated T cells and inhibits T cell activation after binding to PD-1 ligands. |
| 7467 | 21116786 | Although the expression of CTLA-4, PD-1 and FoxP3, which are inhibitory molecules of activated T cells, is reduced only on STZ injected wild type (WT) mice, CD4, CD8 and regulatory T cell populations were not changed in all experimental groups. |
| 7468 | 21116786 | When splenocytes were re-stimulated in ex vivo, the production of IL-2 and IFN-γ and the T cell proliferation were increased in all STZ injected mice, but the increment rate was less in PD-1 Tg groups. |
| 7469 | 21116786 | Although more experimental evidence needs to be provided, these results suggest that ligation of PD-1 and PD-L1/2 may have an effect on macrophages as well as does T cells. |
| 7470 | 21123117 | Serum levels of proinflammatory cytokines TNF-α, IFN-γ and IL17 were lower in IVIG treated animals when compared with controls, while IL10 level was higher. |
| 7471 | 21123117 | The number of CD4(+)Foxp3(+) cells was higher in pancreatic lymph nodes of heme-exposed IVIG treated mice. |
| 7472 | 21169553 | We previously described the NOD.c3c4 mouse, which is protected from type 1 diabetes (T1D) because of protective alleles at multiple insulin-dependent diabetes (Idd) genes, but develops autoimmune biliary disease (ABD) resembling primary biliary cirrhosis (PBC). |
| 7473 | 21169553 | The frequency of effector memory (CD44(+)CD62L(-)) and central memory (CD44(+)CD62L(+)) CD8 T cells is significantly increased in the intrahepatic lymphocyte fraction of NOD.ABD mice, and NOD.ABD CD8 T cells produce more IFN-γ and TNF-α, compared with controls. |
| 7474 | 21169553 | Unlike T1D where both CD4 and CD8 T cells are required for disease transfer, purified NOD.ABD CD8 T cells can transfer liver inflammation into NOD.c3c4 scid recipients, and disease transfer is ameliorated by cotransferring T regulatory cells. |
| 7475 | 21185938 | To explore a novel gene therapy strategy combining immunotherapy and β cell regeneration, we constructed a non-viral plasmid encoding proinsulin (PI) and pancreatic regenerating (Reg) III protein (pReg/PI). |
| 7476 | 21185938 | Treatment with pReg/PI also restored the balance of Th1/Th2 cytokines and expanded CD4(+)CD25(+)Foxp3(+) T regulatory cells, which may attribute to the establishment of self-immune tolerance. |
| 7477 | 21217831 | The first two axes in this study are related to the third and fourth axes of variation in the first study and also reflect variation in the abundance of CD4 and CD8 transcripts. |
| 7478 | 21235534 | The CD4:CD8 ratio was reduced drastically upon LCMV infection due to an expansion of CD8 effectors but ameliorated in ATG-treated mice. |
| 7479 | 21235534 | Although the percentage of CD4(+) CD25(+) regulatory T cells (T(regs) ) within the CD4(+) population was increased significantly after ATG therapy, their frequency in the periphery was reduced dramatically and never returned to normal baseline. |
| 7480 | 21235534 | The inability of ATG treatment to cure T1D in a stringent viral model (RIP-LCMV mice) is due at least partially to the inability to maintain or increase a sufficient CD4(+) CD25(+) T(regs) frequency, in striking contrast with what was reported in the NOD model. |
| 7481 | 21235534 | The CD4:CD8 ratio was reduced drastically upon LCMV infection due to an expansion of CD8 effectors but ameliorated in ATG-treated mice. |
| 7482 | 21235534 | Although the percentage of CD4(+) CD25(+) regulatory T cells (T(regs) ) within the CD4(+) population was increased significantly after ATG therapy, their frequency in the periphery was reduced dramatically and never returned to normal baseline. |
| 7483 | 21235534 | The inability of ATG treatment to cure T1D in a stringent viral model (RIP-LCMV mice) is due at least partially to the inability to maintain or increase a sufficient CD4(+) CD25(+) T(regs) frequency, in striking contrast with what was reported in the NOD model. |
| 7484 | 21235534 | The CD4:CD8 ratio was reduced drastically upon LCMV infection due to an expansion of CD8 effectors but ameliorated in ATG-treated mice. |
| 7485 | 21235534 | Although the percentage of CD4(+) CD25(+) regulatory T cells (T(regs) ) within the CD4(+) population was increased significantly after ATG therapy, their frequency in the periphery was reduced dramatically and never returned to normal baseline. |
| 7486 | 21235534 | The inability of ATG treatment to cure T1D in a stringent viral model (RIP-LCMV mice) is due at least partially to the inability to maintain or increase a sufficient CD4(+) CD25(+) T(regs) frequency, in striking contrast with what was reported in the NOD model. |
| 7487 | 21248249 | The E3 ubiquitin ligase Cbl-b regulates T cell activation thresholds and has been associated with protecting against type 1 diabetes, but its in vivo role in the process of self-tolerance has not been examined at the level of potentially autoaggressive CD4(+) T cells. |
| 7488 | 21248249 | By tracing the fate of pancreatic islet-reactive CD4(+) T cells in prediabetic 3A9-TCR × insHEL double-transgenic mice, we find that Cbl-b deficiency contrasts with AIRE or IL-2 deficiency, because it does not affect thymic negative selection of islet-reactive CD4(+) cells or the numbers of islet-specific CD4(+) or CD4(+)Foxp3(+) T cells in the periphery, although it decreased differentiation of inducible regulatory T cells from TGF-β-treated 3A9-TCR cells in vitro. |
| 7489 | 21248249 | The E3 ubiquitin ligase Cbl-b regulates T cell activation thresholds and has been associated with protecting against type 1 diabetes, but its in vivo role in the process of self-tolerance has not been examined at the level of potentially autoaggressive CD4(+) T cells. |
| 7490 | 21248249 | By tracing the fate of pancreatic islet-reactive CD4(+) T cells in prediabetic 3A9-TCR × insHEL double-transgenic mice, we find that Cbl-b deficiency contrasts with AIRE or IL-2 deficiency, because it does not affect thymic negative selection of islet-reactive CD4(+) cells or the numbers of islet-specific CD4(+) or CD4(+)Foxp3(+) T cells in the periphery, although it decreased differentiation of inducible regulatory T cells from TGF-β-treated 3A9-TCR cells in vitro. |
| 7491 | 21309048 | Type 1 diabetes is the result of a breakdown in immune regulation that leads to expansion of autoreactive CD4+ and CD8+ T cells, autoantibody-producing B lymphocytes and activation of the innate immune system. |
| 7492 | 21317396 | IL-2 and TGF-β1 play key roles in the immunobiology of Foxp3-expressing CD25(+)CD4(+) T cells (Foxp3(+)Treg). |
| 7493 | 21321581 | Protection against diabetes was accompanied by histone hyperacetylation in pancreas and spleen, enhanced frequency of CD4(+) CD62L(+) cells in the spleen, reduction in cellular infiltration of islets, restoration of normoglycemia and glucose-induced insulin release by beta cells. |
| 7494 | 21321581 | Activation of splenic T lymphocytes derived from protected mice in vitro with pharmacological agents that bypass the antigen receptor or immobilized anti-CD3 antibody resulted in enhanced expression of Ifng mRNA and protein without altering the expression of Il4, Il17, Il18, Inos and Tnfa genes nor the secretion of IL-2, IL-4, IL-17 and TNF-α proteins. |
| 7495 | 21321581 | Consistently, expression of the transcription factor involved in Ifng transcription, Tbet/Tbx21 but not Gata3 and Rorgt, respectively, required for the transcription of Il4 and Il17, was upregulated in activated splenocytes of protected mice. |
| 7496 | 21324454 | CD4+CD28 null T lymphocytes are expanded in young women with polycystic ovary syndrome. |
| 7497 | 21324454 | We demonstrated that women with PCOS showed an expansion of CD4(+)CD28(null) T cells, an aggressive population of T lymphocytes that has been recently associated with recurrent coronary instability and type 2 diabetes mellitus. |
| 7498 | 21324454 | CD4+CD28 null T lymphocytes are expanded in young women with polycystic ovary syndrome. |
| 7499 | 21324454 | We demonstrated that women with PCOS showed an expansion of CD4(+)CD28(null) T cells, an aggressive population of T lymphocytes that has been recently associated with recurrent coronary instability and type 2 diabetes mellitus. |
| 7500 | 21368230 | To understand better the plasticity of human Tregs in the context of type 1 diabetes, we characterized an IFN-γ-competent subset of human CD4(+)CD127(lo/-)CD25(+) Tregs. |
| 7501 | 21368230 | Purified IFN-γ(+) Tregs were assessed for suppressive function, degree of TSDR demethylation, and expression of Treg lineage markers FOXP3 and Helios. |
| 7502 | 21368230 | Naive Tregs were capable of upregulating expression of Th1-associated T-bet, CXCR3, and IFN-γ in response to IL-12. |
| 7503 | 21383770 | Therefore, the requirement for NK cells in β-cell destruction in the CD4-dependent T-cell antigen receptor transgenic NOD4.1 mice was examined. |
| 7504 | 21436590 | Here, we show that the α-isoform of myosin heavy chain (α-MyHC, which is encoded by the gene Myh6) is the pathogenic autoantigen for CD4+ T cells in a spontaneous mouse model of myocarditis. |
| 7505 | 21444661 | These tolerogenic pDCs convert naive anti-islet T cells into Foxp3(+) CD4(+) regulatory T cells (T reg cells) in pancreatic LNs. |
| 7506 | 21458378 | The suppression was likely to be mediated by T cells, as we found that regulatory CD4(+)CD25(+)Foxp3(+) cells were significantly increased in G/10-DC treated animals. |
| 7507 | 21458378 | In vivo, the G/10-DCs inhibited diabetogenic T cell proliferation; in vitro, they had reduced expression of costimulatory molecules and produced little IL-12/23 p40 or IL-6 but a large amount of IL-10 when compared with DCs matured in the presence of IL-4 (G/4-DC). |
| 7508 | 21464945 | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice. |
| 7509 | 21464945 | The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. |
| 7510 | 21464945 | In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. |
| 7511 | 21464945 | IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. |
| 7512 | 21464945 | These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. |
| 7513 | 21464945 | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice. |
| 7514 | 21464945 | The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. |
| 7515 | 21464945 | In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. |
| 7516 | 21464945 | IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. |
| 7517 | 21464945 | These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. |
| 7518 | 21464945 | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice. |
| 7519 | 21464945 | The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. |
| 7520 | 21464945 | In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. |
| 7521 | 21464945 | IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. |
| 7522 | 21464945 | These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. |
| 7523 | 21464945 | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice. |
| 7524 | 21464945 | The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. |
| 7525 | 21464945 | In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. |
| 7526 | 21464945 | IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. |
| 7527 | 21464945 | These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. |
| 7528 | 21469083 | Signaling through TLR2 promotes inflammation and modulates CD4(+) CD25(+) Tregs. |
| 7529 | 21469083 | Treatment of prediabetic mice with a synthetic TLR2 agonist diminished T1D and increased the number and function of CD4(+) CD25(+) Tregs, also conferring DCs with tolerogenic properties. |
| 7530 | 21469083 | LCMV increased the frequency of CD4(+) CD25(+) Tregs and their production of TGF-β more significantly in WT than TLR2-deficient mice. |
| 7531 | 21469083 | Furthermore, LCMV infection in vivo or LCMV-infected DCs in vitro rendered, via TLR2, CD4(+) CD25(+) Tregs capable of diminishing T1D. |
| 7532 | 21469083 | Signaling through TLR2 promotes inflammation and modulates CD4(+) CD25(+) Tregs. |
| 7533 | 21469083 | Treatment of prediabetic mice with a synthetic TLR2 agonist diminished T1D and increased the number and function of CD4(+) CD25(+) Tregs, also conferring DCs with tolerogenic properties. |
| 7534 | 21469083 | LCMV increased the frequency of CD4(+) CD25(+) Tregs and their production of TGF-β more significantly in WT than TLR2-deficient mice. |
| 7535 | 21469083 | Furthermore, LCMV infection in vivo or LCMV-infected DCs in vitro rendered, via TLR2, CD4(+) CD25(+) Tregs capable of diminishing T1D. |
| 7536 | 21469083 | Signaling through TLR2 promotes inflammation and modulates CD4(+) CD25(+) Tregs. |
| 7537 | 21469083 | Treatment of prediabetic mice with a synthetic TLR2 agonist diminished T1D and increased the number and function of CD4(+) CD25(+) Tregs, also conferring DCs with tolerogenic properties. |
| 7538 | 21469083 | LCMV increased the frequency of CD4(+) CD25(+) Tregs and their production of TGF-β more significantly in WT than TLR2-deficient mice. |
| 7539 | 21469083 | Furthermore, LCMV infection in vivo or LCMV-infected DCs in vitro rendered, via TLR2, CD4(+) CD25(+) Tregs capable of diminishing T1D. |
| 7540 | 21469083 | Signaling through TLR2 promotes inflammation and modulates CD4(+) CD25(+) Tregs. |
| 7541 | 21469083 | Treatment of prediabetic mice with a synthetic TLR2 agonist diminished T1D and increased the number and function of CD4(+) CD25(+) Tregs, also conferring DCs with tolerogenic properties. |
| 7542 | 21469083 | LCMV increased the frequency of CD4(+) CD25(+) Tregs and their production of TGF-β more significantly in WT than TLR2-deficient mice. |
| 7543 | 21469083 | Furthermore, LCMV infection in vivo or LCMV-infected DCs in vitro rendered, via TLR2, CD4(+) CD25(+) Tregs capable of diminishing T1D. |
| 7544 | 21469091 | Reduced IL-2 expression in NOD mice leads to a temporal increase in CD62Llo FoxP3+ CD4+ T cells with limited suppressor activity. |
| 7545 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7546 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7547 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7548 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7549 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7550 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7551 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7552 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7553 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7554 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7555 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7556 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7557 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7558 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7559 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7560 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7561 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7562 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7563 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7564 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7565 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7566 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7567 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7568 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7569 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7570 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7571 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7572 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7573 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7574 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7575 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7576 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7577 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7578 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7579 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7580 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7581 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7582 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7583 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7584 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7585 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7586 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7587 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7588 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7589 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7590 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7591 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7592 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7593 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7594 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7595 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7596 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7597 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7598 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7599 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7600 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7601 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7602 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7603 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7604 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7605 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7606 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7607 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7608 | 21469125 | In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. |
| 7609 | 21469125 | Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. |
| 7610 | 21469125 | We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. |
| 7611 | 21469125 | We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. |
| 7612 | 21469125 | IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. |
| 7613 | 21469125 | We addressed whether CD4(+) T cells require IL-1β to induce diabetes. |
| 7614 | 21469125 | We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. |
| 7615 | 21469125 | Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. |
| 7616 | 21469125 | We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo. |
| 7617 | 21469129 | Antigen-presenting cell-associated four-domain MHC class II (MHC-II) molecules play a central role in activating autoreactive CD4(+) T cells involved in multiple sclerosis (MS) and type 1 diabetes (T1D). |
| 7618 | 21478402 | The inhibitory effect of AGEs on infection was associated with a RAGE-independent downregulation of CD4 at the cell membrane and by a RAGE-dependent repression of the CXCR4 and CCR5 HIV-1 receptors. |
| 7619 | 21478402 | AGEs induce the secretion of proinflammatory cytokines IL-6, TNF-α, and IL-12, but not RANTES or MIP-1α, and did not lead to MDDC maturation as demonstrated by the lack of expression of the CD83 molecule. |
| 7620 | 21505262 | Hence, in the NOD mouse, Tssp is a critical regulator of diabetes development through the selection of the autoreactive CD4 T cell repertoire. |
| 7621 | 21543717 | Foxp3(+) regulatory T cells (Tregs) originate in the thymus, but the Treg phenotype can also be induced in peripheral lymphoid organs or in vitro by stimulation of conventional CD4(+) T cells with IL-2 and TGF-β. |
| 7622 | 21543717 | Most Treg-typical transcripts were shared by NOD or B6g7 TGF-Tregs, except for a small group of differentially expressed genes, including genes relevant for suppressive activity (Lrrc32, Ctla4, and Cd73). |
| 7623 | 21573001 | The discrepancy between these two groups is thought to be associated with T-cell avidity, including CD8 and/or CD4 T cells. |
| 7624 | 21573001 | For this purpose, we build a series of mathematical models incorporating first one clone then multiple clones of islet-specific and pathogenic CD8 and/or CD4 T cells, together with B lymphocytes, to investigate the interaction of T-cell avidity with autoantibodies in predicting disease onset. |
| 7625 | 21573001 | The discrepancy between these two groups is thought to be associated with T-cell avidity, including CD8 and/or CD4 T cells. |
| 7626 | 21573001 | For this purpose, we build a series of mathematical models incorporating first one clone then multiple clones of islet-specific and pathogenic CD8 and/or CD4 T cells, together with B lymphocytes, to investigate the interaction of T-cell avidity with autoantibodies in predicting disease onset. |
| 7627 | 21613616 | We have previously proposed that sequence variation of the CD101 gene between NOD and C57BL/6 mice accounts for the protection from type 1 diabetes (T1D) provided by the insulin-dependent diabetes susceptibility region 10 (Idd10), a <1 Mb region on mouse chromosome 3. |
| 7628 | 21613616 | Susceptibility to T1D was correlated with genotype-dependent CD101 expression on multiple cell subsets, including Foxp3(+) regulatory CD4(+) T cells, CD11c(+) dendritic cells, and Gr1(+) myeloid cells. |
| 7629 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7630 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7631 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7632 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7633 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7634 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7635 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7636 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7637 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7638 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7639 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7640 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7641 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7642 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7643 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7644 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7645 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7646 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7647 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7648 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7649 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7650 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7651 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7652 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7653 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7654 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7655 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7656 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7657 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7658 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7659 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7660 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7661 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7662 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7663 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7664 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7665 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7666 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7667 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7668 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7669 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7670 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7671 | 21620894 | Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes. |
| 7672 | 21620894 | We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. |
| 7673 | 21620894 | There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. |
| 7674 | 21620894 | Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. |
| 7675 | 21620894 | There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. |
| 7676 | 21620894 | Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. |
| 7677 | 21620894 | In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes. |
| 7678 | 21626409 | Herein, we discuss the critical sub-population of dendritic cells responsible for mediating both the cross-presentation of islet antigen to CD8(+) T cells and the direct presentation of beta cell antigen to CD4(+) T cells. |
| 7679 | 21626409 | These cells, termed merocytic dendritic cells (mcDC), are more numerous in non-obese diabetic (NOD), and antigen-loaded mcDC rescue CD8(+) T cells from peripheral anergy and deletion, and stimulate islet-reactive CD4(+) T cells. |
| 7680 | 21626409 | Herein, we discuss the critical sub-population of dendritic cells responsible for mediating both the cross-presentation of islet antigen to CD8(+) T cells and the direct presentation of beta cell antigen to CD4(+) T cells. |
| 7681 | 21626409 | These cells, termed merocytic dendritic cells (mcDC), are more numerous in non-obese diabetic (NOD), and antigen-loaded mcDC rescue CD8(+) T cells from peripheral anergy and deletion, and stimulate islet-reactive CD4(+) T cells. |
| 7682 | 21641234 | Anti-TNF rescue CD4+Foxp3+ regulatory T cells in patients with type 1 diabetes from effects mediated by TNF. |
| 7683 | 21641234 | It indicates that TNF reduces the number and frequency of regulatory CD4(+)Foxp3(+) T cells in children with diabetes type 1 and that in vitro treatment with anti-TNF antibody seems to rescue this cell subset from its defective effects. |
| 7684 | 21641234 | Anti-TNF rescue CD4+Foxp3+ regulatory T cells in patients with type 1 diabetes from effects mediated by TNF. |
| 7685 | 21641234 | It indicates that TNF reduces the number and frequency of regulatory CD4(+)Foxp3(+) T cells in children with diabetes type 1 and that in vitro treatment with anti-TNF antibody seems to rescue this cell subset from its defective effects. |
| 7686 | 21647406 | DCs play a crucial role in the presentation of autoantigen and activation of diabetogenic T cells, and IRF4 and IRF8 are crucial genes involved in the development of DCs. |
| 7687 | 21647406 | Importantly, levels of IRF4 and IRF8 expression were lower in tolerogenic bone marrow derived DCs (BMDCs) generated with GM-CSF as compared to immunogenic BMDCs generated with GM-CSF and IL-4. |
| 7688 | 21647406 | Analysis of splenic DCs subsets indicated that high expression of IRF4 was associated with increased levels of CD4(+)CD8α(-)IRF4(+)CD11c(+) DCs but not CD4(-)CD8α(+)IRF8(+)CD11c(+) DCs in NOD mice. |
| 7689 | 21647406 | Our results showed that IRF4 expression was up-regulated in NOD mice and correlated with the increased levels of CD4(+)CD8α(-) DCs, suggesting that IRF4 may be involved in abnormal DC functions in type 1 diabetes in NOD mice. |
| 7690 | 21647406 | DCs play a crucial role in the presentation of autoantigen and activation of diabetogenic T cells, and IRF4 and IRF8 are crucial genes involved in the development of DCs. |
| 7691 | 21647406 | Importantly, levels of IRF4 and IRF8 expression were lower in tolerogenic bone marrow derived DCs (BMDCs) generated with GM-CSF as compared to immunogenic BMDCs generated with GM-CSF and IL-4. |
| 7692 | 21647406 | Analysis of splenic DCs subsets indicated that high expression of IRF4 was associated with increased levels of CD4(+)CD8α(-)IRF4(+)CD11c(+) DCs but not CD4(-)CD8α(+)IRF8(+)CD11c(+) DCs in NOD mice. |
| 7693 | 21647406 | Our results showed that IRF4 expression was up-regulated in NOD mice and correlated with the increased levels of CD4(+)CD8α(-) DCs, suggesting that IRF4 may be involved in abnormal DC functions in type 1 diabetes in NOD mice. |
| 7694 | 21670318 | Furthermore, these cells were activated by Ag, leading to cytokine production (CD4) and efficient cytolytic killing of targets (CD8). |
| 7695 | 21674137 | A distinct role of CD4+ Th17- and Th17-stimulated CD8+ CTL in the pathogenesis of type 1 diabetes and experimental autoimmune encephalomyelitis. |
| 7696 | 21674137 | Both CD4(+) Th17-cells and CD8(+) cytotoxic T lymphocytes (CTLs) are involved in type 1 diabetes and experimental autoimmune encephalomyelitis (EAE). |
| 7697 | 21674137 | We generated ovalbumin (OVA)- or myelin oligodendrocyte glycoprotein (MOG)-specific Th17 cells expressing RORγt and IL-17 by in vitro co-culturing OVA-pulsed and MOG(35-55) peptide-pulsed dendritic cells (DC(OVA) and DC(MOG)) with CD4(+) T cells derived from transgenic OTII and MOG-T cell receptor mice, respectively. |
| 7698 | 21674137 | To assess the above question, we adoptively transferred OVA-specific Th17 cells into transgenic rat insulin promoter (RIP)-mOVA mice or RIP-mOVA mice treated with anti-CD8 antibody to deplete Th17-stimulated CD8(+) T cells. |
| 7699 | 21674137 | A distinct role of CD4+ Th17- and Th17-stimulated CD8+ CTL in the pathogenesis of type 1 diabetes and experimental autoimmune encephalomyelitis. |
| 7700 | 21674137 | Both CD4(+) Th17-cells and CD8(+) cytotoxic T lymphocytes (CTLs) are involved in type 1 diabetes and experimental autoimmune encephalomyelitis (EAE). |
| 7701 | 21674137 | We generated ovalbumin (OVA)- or myelin oligodendrocyte glycoprotein (MOG)-specific Th17 cells expressing RORγt and IL-17 by in vitro co-culturing OVA-pulsed and MOG(35-55) peptide-pulsed dendritic cells (DC(OVA) and DC(MOG)) with CD4(+) T cells derived from transgenic OTII and MOG-T cell receptor mice, respectively. |
| 7702 | 21674137 | To assess the above question, we adoptively transferred OVA-specific Th17 cells into transgenic rat insulin promoter (RIP)-mOVA mice or RIP-mOVA mice treated with anti-CD8 antibody to deplete Th17-stimulated CD8(+) T cells. |
| 7703 | 21674137 | A distinct role of CD4+ Th17- and Th17-stimulated CD8+ CTL in the pathogenesis of type 1 diabetes and experimental autoimmune encephalomyelitis. |
| 7704 | 21674137 | Both CD4(+) Th17-cells and CD8(+) cytotoxic T lymphocytes (CTLs) are involved in type 1 diabetes and experimental autoimmune encephalomyelitis (EAE). |
| 7705 | 21674137 | We generated ovalbumin (OVA)- or myelin oligodendrocyte glycoprotein (MOG)-specific Th17 cells expressing RORγt and IL-17 by in vitro co-culturing OVA-pulsed and MOG(35-55) peptide-pulsed dendritic cells (DC(OVA) and DC(MOG)) with CD4(+) T cells derived from transgenic OTII and MOG-T cell receptor mice, respectively. |
| 7706 | 21674137 | To assess the above question, we adoptively transferred OVA-specific Th17 cells into transgenic rat insulin promoter (RIP)-mOVA mice or RIP-mOVA mice treated with anti-CD8 antibody to deplete Th17-stimulated CD8(+) T cells. |
| 7707 | 21697456 | Both anti-PD-L1 mAbs precipitated diabetes in adoptive transfer models of CD4(+) and CD8(+) T cell-driven diabetes. |
| 7708 | 21697456 | Taken together, these data demonstrate that the PD-L1:B7-1 pathway inhibits potentially pathogenic self-reactive effector CD4(+) and CD8(+) T cell responses in vivo, and suggest that the immunoinhibitory functions of this pathway may be particularly important during the later phases of diabetogenesis. |
| 7709 | 21697456 | Both anti-PD-L1 mAbs precipitated diabetes in adoptive transfer models of CD4(+) and CD8(+) T cell-driven diabetes. |
| 7710 | 21697456 | Taken together, these data demonstrate that the PD-L1:B7-1 pathway inhibits potentially pathogenic self-reactive effector CD4(+) and CD8(+) T cell responses in vivo, and suggest that the immunoinhibitory functions of this pathway may be particularly important during the later phases of diabetogenesis. |
| 7711 | 21708895 | Recently described forkhead box protein 3 (FoxP3) transcription factor is a key molecule in CD4+ CD25hi+ T-cell characterization. |
| 7712 | 21708895 | Randomly selected iNKT cell clones (CD4+, double negative, CD8+) expressed FoxP3 mRNA and protein at different levels upon stimulation as supported by various approaches. |
| 7713 | 21708895 | Recently described forkhead box protein 3 (FoxP3) transcription factor is a key molecule in CD4+ CD25hi+ T-cell characterization. |
| 7714 | 21708895 | Randomly selected iNKT cell clones (CD4+, double negative, CD8+) expressed FoxP3 mRNA and protein at different levels upon stimulation as supported by various approaches. |
| 7715 | 21715555 | Uncoupling of proliferation and cytokines from suppression within the CD4+CD25+Foxp3+ T-cell compartment in the 1st year of human type 1 diabetes. |
| 7716 | 21724410 | Tissular T(regs): a unique population of adipose-tissue-resident Foxp3+CD4+ T cells that impacts organismal metabolism. |
| 7717 | 21724410 | Foxp3+CD4+ regulatory T (T(reg)) cells are a key population in controlling the immune response. |
| 7718 | 21724410 | Tissular T(regs): a unique population of adipose-tissue-resident Foxp3+CD4+ T cells that impacts organismal metabolism. |
| 7719 | 21724410 | Foxp3+CD4+ regulatory T (T(reg)) cells are a key population in controlling the immune response. |
| 7720 | 21727190 | Tissue-specific expression of B7x protects from CD4 T cell-mediated autoimmunity. |
| 7721 | 21727190 | B7x, an inhibitory member of the B7/CD28 superfamily, is highly expressed in a broad range of nonhematopoietic organs, suggesting a role in maintaining peripheral tolerance. |
| 7722 | 21734016 | Islet amyloid polypeptide is a target antigen for diabetogenic CD4+ T cells. |
| 7723 | 21734073 | Flow cytometric analysis showed a significant increase in the number of CD4(+)CD25(+)Foxp3(+) T regulatory cells in TNFR1-deficient mice. |
| 7724 | 21737880 | Tregs, defined by the markers CD4 and FoxP3, regulate immune responses by suppressing effector T cells and are recruited to sites of action by the chemokine CCL22. |
| 7725 | 21737880 | CCL22 expression increased the frequency of Tregs, produced higher levels of TGF-β in the CD4+ T cell population near islets, and decreased the frequency of circulating autoreactive CD8+ T cells and CD8+ IFN-γ–producing T cells. |
| 7726 | 21737880 | Tregs, defined by the markers CD4 and FoxP3, regulate immune responses by suppressing effector T cells and are recruited to sites of action by the chemokine CCL22. |
| 7727 | 21737880 | CCL22 expression increased the frequency of Tregs, produced higher levels of TGF-β in the CD4+ T cell population near islets, and decreased the frequency of circulating autoreactive CD8+ T cells and CD8+ IFN-γ–producing T cells. |
| 7728 | 21742976 | Anti-CD3 treatment induced a transient systemic rise in the percentage but not absolute number of CD4(+)Foxp3(+) Tregs due to selective depletion of CD4(+)Foxp3(-) conventional T cells. |
| 7729 | 21742976 | T cell depletion induced by FNB anti-CD3 mAb was independent of the proapoptotic proteins Fas, caspase-3, and Bim and was not inhibited by overexpression of the anti-apoptotic protein, Bcl-2. |
| 7730 | 21785903 | Fasting serum DPP-4 enzymatic activity, plasma glucose (FPG), CD26 expression on CD3+, CD4+ and CD8+ lymphocytes, HbA1c and body mass index (BMI) were assessed. |
| 7731 | 21785903 | DPP-4 enzymatic activity was determined by kinetic enzyme assay, ICA and GAD were assessed by ELISA. |
| 7732 | 21785903 | Determination of the CD26 expression on CD3+, CD4+ and CD8+ lymphocytes was performed by flow-cytometric analysis. |
| 7733 | 21785903 | Fasting serum DPP-4 activity was independent from the ICA or GAD status of patients with T1DM. |
| 7734 | 21785903 | Fasting serum DPP-4 enzymatic activity, plasma glucose (FPG), CD26 expression on CD3+, CD4+ and CD8+ lymphocytes, HbA1c and body mass index (BMI) were assessed. |
| 7735 | 21785903 | DPP-4 enzymatic activity was determined by kinetic enzyme assay, ICA and GAD were assessed by ELISA. |
| 7736 | 21785903 | Determination of the CD26 expression on CD3+, CD4+ and CD8+ lymphocytes was performed by flow-cytometric analysis. |
| 7737 | 21785903 | Fasting serum DPP-4 activity was independent from the ICA or GAD status of patients with T1DM. |
| 7738 | 21807362 | Surprisingly, CD4(+) T helper cells from these patients secreted similar levels of galectin-1 compared to healthy donors, probably mediated by Th17 cytokines. |
| 7739 | 21807362 | In conclusion, CD4(+) T helper lymphocytes from T1D patients produce normal levels of the immunoregulator galectin-1 but its reduced synthesis by monocytes helps to maintain a skewed pro-inflammatory response. |
| 7740 | 21807362 | Surprisingly, CD4(+) T helper cells from these patients secreted similar levels of galectin-1 compared to healthy donors, probably mediated by Th17 cytokines. |
| 7741 | 21807362 | In conclusion, CD4(+) T helper lymphocytes from T1D patients produce normal levels of the immunoregulator galectin-1 but its reduced synthesis by monocytes helps to maintain a skewed pro-inflammatory response. |
| 7742 | 21820917 | Three main types of CD4+ regulatory T cells can be distinguished based upon whether they express Foxp3 and differentiate naturally in the thymus (natural Tregs) or are induced in the periphery (inducible Tregs); or whether they are FoxP3 negative but secrete IL-10 in response to antigen (Tregulatory type 1, Tr1 cells). |
| 7743 | 21850236 | Regulation of cathepsin G reduces the activation of proinsulin-reactive T cells from type 1 diabetes patients. |
| 7744 | 21850236 | Self-proteins can be processed by cathepsins (Cats) within endocytic compartments and loaded to major histocompatibility complex (MHC) class II molecules for CD4(+) T cell inspection. |
| 7745 | 21873518 | Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 homolog that is required for maximal regulatory T cell function and for the control of CD4(+) and CD8(+) T cell homeostasis. |
| 7746 | 21873518 | Adoptive transfer experiments revealed that LAG-3 was primarily responsible for limiting the pathogenic potential of CD4(+) T cells and, to a lesser extent, CD8(+) T cells. |
| 7747 | 21873518 | Lag3(-)(/)(-) mice exhibited accelerated, invasive insulitis, corresponding to increased CD4(+) and CD8(+) T cell islet infiltration and intraislet proliferation. |
| 7748 | 21873518 | The frequencies of islet Ag-reactive chromogranin A-specific CD4(+) T cells and islet specific glucose-6-phosphatase-specific CD8(+) T cells were significantly increased in the islets of Lag3(-)(/)(-) mice, suggesting an early expansion of pathogenic clones that is normally restrained by LAG-3. |
| 7749 | 21873518 | We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting autoimmunity in disease-prone environments. |
| 7750 | 21873518 | Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 homolog that is required for maximal regulatory T cell function and for the control of CD4(+) and CD8(+) T cell homeostasis. |
| 7751 | 21873518 | Adoptive transfer experiments revealed that LAG-3 was primarily responsible for limiting the pathogenic potential of CD4(+) T cells and, to a lesser extent, CD8(+) T cells. |
| 7752 | 21873518 | Lag3(-)(/)(-) mice exhibited accelerated, invasive insulitis, corresponding to increased CD4(+) and CD8(+) T cell islet infiltration and intraislet proliferation. |
| 7753 | 21873518 | The frequencies of islet Ag-reactive chromogranin A-specific CD4(+) T cells and islet specific glucose-6-phosphatase-specific CD8(+) T cells were significantly increased in the islets of Lag3(-)(/)(-) mice, suggesting an early expansion of pathogenic clones that is normally restrained by LAG-3. |
| 7754 | 21873518 | We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting autoimmunity in disease-prone environments. |
| 7755 | 21873518 | Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 homolog that is required for maximal regulatory T cell function and for the control of CD4(+) and CD8(+) T cell homeostasis. |
| 7756 | 21873518 | Adoptive transfer experiments revealed that LAG-3 was primarily responsible for limiting the pathogenic potential of CD4(+) T cells and, to a lesser extent, CD8(+) T cells. |
| 7757 | 21873518 | Lag3(-)(/)(-) mice exhibited accelerated, invasive insulitis, corresponding to increased CD4(+) and CD8(+) T cell islet infiltration and intraislet proliferation. |
| 7758 | 21873518 | The frequencies of islet Ag-reactive chromogranin A-specific CD4(+) T cells and islet specific glucose-6-phosphatase-specific CD8(+) T cells were significantly increased in the islets of Lag3(-)(/)(-) mice, suggesting an early expansion of pathogenic clones that is normally restrained by LAG-3. |
| 7759 | 21873518 | We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting autoimmunity in disease-prone environments. |
| 7760 | 21873518 | Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 homolog that is required for maximal regulatory T cell function and for the control of CD4(+) and CD8(+) T cell homeostasis. |
| 7761 | 21873518 | Adoptive transfer experiments revealed that LAG-3 was primarily responsible for limiting the pathogenic potential of CD4(+) T cells and, to a lesser extent, CD8(+) T cells. |
| 7762 | 21873518 | Lag3(-)(/)(-) mice exhibited accelerated, invasive insulitis, corresponding to increased CD4(+) and CD8(+) T cell islet infiltration and intraislet proliferation. |
| 7763 | 21873518 | The frequencies of islet Ag-reactive chromogranin A-specific CD4(+) T cells and islet specific glucose-6-phosphatase-specific CD8(+) T cells were significantly increased in the islets of Lag3(-)(/)(-) mice, suggesting an early expansion of pathogenic clones that is normally restrained by LAG-3. |
| 7764 | 21873518 | We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting autoimmunity in disease-prone environments. |
| 7765 | 21873518 | Lymphocyte activation gene-3 (LAG-3; CD223) is a CD4 homolog that is required for maximal regulatory T cell function and for the control of CD4(+) and CD8(+) T cell homeostasis. |
| 7766 | 21873518 | Adoptive transfer experiments revealed that LAG-3 was primarily responsible for limiting the pathogenic potential of CD4(+) T cells and, to a lesser extent, CD8(+) T cells. |
| 7767 | 21873518 | Lag3(-)(/)(-) mice exhibited accelerated, invasive insulitis, corresponding to increased CD4(+) and CD8(+) T cell islet infiltration and intraislet proliferation. |
| 7768 | 21873518 | The frequencies of islet Ag-reactive chromogranin A-specific CD4(+) T cells and islet specific glucose-6-phosphatase-specific CD8(+) T cells were significantly increased in the islets of Lag3(-)(/)(-) mice, suggesting an early expansion of pathogenic clones that is normally restrained by LAG-3. |
| 7769 | 21873518 | We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting autoimmunity in disease-prone environments. |
| 7770 | 21873805 | Association of circulating fractalkine (CX3CL1) and CX3CR1(+)CD4(+) T cells with common carotid artery intima-media thickness in patients with chronic kidney disease. |
| 7771 | 21887518 | Altered proportions of naïve, central memory and terminally differentiated central memory subsets among CD4+ and CD8 + T cells expressing CD26 in patients with type 1 diabetes. |
| 7772 | 21887518 | In peripheral blood from 55 patients with type 1 diabetes and 20 healthy controls, CD4(+) and CD8(+) T cells expressing CD26 were differentiated into naïve (N, CD45RA(+)CCR7(+)), central memory (CM, CD45RA(-)CCR7(+)), effector memory (EM, CD45RA(-)CCR7(-)), and terminally differentiated effector memory (TEMRA, CD45RA(+)CCR7(-)). |
| 7773 | 21887518 | In type 1 diabetes, CD4(+) and CD8(+) T cells expressing CD26 showed a distinctive differentiation profile: percentages and absolute numbers of CM and N cells were reduced, whereas those of TEMRA cells were markedly increased. |
| 7774 | 21887518 | Altered proportions of naïve, central memory and terminally differentiated central memory subsets among CD4+ and CD8 + T cells expressing CD26 in patients with type 1 diabetes. |
| 7775 | 21887518 | In peripheral blood from 55 patients with type 1 diabetes and 20 healthy controls, CD4(+) and CD8(+) T cells expressing CD26 were differentiated into naïve (N, CD45RA(+)CCR7(+)), central memory (CM, CD45RA(-)CCR7(+)), effector memory (EM, CD45RA(-)CCR7(-)), and terminally differentiated effector memory (TEMRA, CD45RA(+)CCR7(-)). |
| 7776 | 21887518 | In type 1 diabetes, CD4(+) and CD8(+) T cells expressing CD26 showed a distinctive differentiation profile: percentages and absolute numbers of CM and N cells were reduced, whereas those of TEMRA cells were markedly increased. |
| 7777 | 21887518 | Altered proportions of naïve, central memory and terminally differentiated central memory subsets among CD4+ and CD8 + T cells expressing CD26 in patients with type 1 diabetes. |
| 7778 | 21887518 | In peripheral blood from 55 patients with type 1 diabetes and 20 healthy controls, CD4(+) and CD8(+) T cells expressing CD26 were differentiated into naïve (N, CD45RA(+)CCR7(+)), central memory (CM, CD45RA(-)CCR7(+)), effector memory (EM, CD45RA(-)CCR7(-)), and terminally differentiated effector memory (TEMRA, CD45RA(+)CCR7(-)). |
| 7779 | 21887518 | In type 1 diabetes, CD4(+) and CD8(+) T cells expressing CD26 showed a distinctive differentiation profile: percentages and absolute numbers of CM and N cells were reduced, whereas those of TEMRA cells were markedly increased. |
| 7780 | 21925473 | IL-27, a cytokine consisting of IL-27p28 and Epstein-Barr virus-induced gene 3 (EBI3), binds a membrane-bound heterodimeric receptor consisting of the IL-27 receptor α chain (WSX-1) and gp130. |
| 7781 | 21925473 | We evaluated blood glucose and islet proinsulin concentrations, inflammatory cell infiltration in islets, and expression of IL-1β mRNA in pancreas in wild-type (WT), EBI3(-/-), and WSX-1(-/-) mice treated with streptozotocin (STZ). |
| 7782 | 21925473 | Hyperglycemia was augmented in EBI3(-/-) and WSX-1(-/-) mice compared with WT mice. |
| 7783 | 21925473 | Islet proinsulin levels after STZ treatment were lower in EBI3(-/-) and WSX-1(-/-) mice than in WT mice. |
| 7784 | 21925473 | The infiltration of islets by F4/80(+)CD11c(-)7/4(-) macrophages, CD4(+) T cells, and CD8(+) T cells was increased in EBI3(-/-) and WSX-1(-/-) mice compared with WT mice. |
| 7785 | 21925473 | The administration of recombinant IL-27, compared with control, decreased the blood glucose level, immune cell infiltration into islets, and IL-1β mRNA expression in the pancreas and increased islet proinsulin levels in WT and EBI3(-/-) mice. |
| 7786 | 21949373 | Specificity and detection of insulin-reactive CD4+ T cells in type 1 diabetes in the nonobese diabetic (NOD) mouse. |
| 7787 | 21949373 | In the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D), an insulin peptide (B:9-23) is a major target for pathogenic CD4(+) T cells. |
| 7788 | 21949373 | In the thymus, the absence of this type of processing combined with the low affinity of B:9-23 binding to IA(g7) in register 3 may explain the escape of insulin-specific CD4(+) T cells from the mechanisms that usually eliminate self-reactive T cells. |
| 7789 | 21949373 | Specificity and detection of insulin-reactive CD4+ T cells in type 1 diabetes in the nonobese diabetic (NOD) mouse. |
| 7790 | 21949373 | In the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D), an insulin peptide (B:9-23) is a major target for pathogenic CD4(+) T cells. |
| 7791 | 21949373 | In the thymus, the absence of this type of processing combined with the low affinity of B:9-23 binding to IA(g7) in register 3 may explain the escape of insulin-specific CD4(+) T cells from the mechanisms that usually eliminate self-reactive T cells. |
| 7792 | 21949373 | Specificity and detection of insulin-reactive CD4+ T cells in type 1 diabetes in the nonobese diabetic (NOD) mouse. |
| 7793 | 21949373 | In the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D), an insulin peptide (B:9-23) is a major target for pathogenic CD4(+) T cells. |
| 7794 | 21949373 | In the thymus, the absence of this type of processing combined with the low affinity of B:9-23 binding to IA(g7) in register 3 may explain the escape of insulin-specific CD4(+) T cells from the mechanisms that usually eliminate self-reactive T cells. |
| 7795 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 7796 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 7797 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 7798 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 7799 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 7800 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 7801 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 7802 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 7803 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 7804 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 7805 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 7806 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 7807 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 7808 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 7809 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 7810 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 7811 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 7812 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 7813 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 7814 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 7815 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 7816 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 7817 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 7818 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 7819 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 7820 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 7821 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 7822 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 7823 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 7824 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 7825 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 7826 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 7827 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 7828 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 7829 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 7830 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 7831 | 21966503 | Notably, oral treatment with GABA significantly increased the frequency of CD4(+)Foxp3(+) Tregs in mice. |
| 7832 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7833 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7834 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7835 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7836 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7837 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7838 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7839 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7840 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7841 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7842 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7843 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7844 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7845 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7846 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7847 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7848 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7849 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7850 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7851 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7852 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7853 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7854 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7855 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7856 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7857 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7858 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7859 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7860 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7861 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7862 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7863 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7864 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7865 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7866 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7867 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7868 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7869 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7870 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7871 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7872 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7873 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7874 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7875 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7876 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7877 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7878 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7879 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7880 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7881 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7882 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7883 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7884 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7885 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7886 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7887 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7888 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7889 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7890 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7891 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7892 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7893 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7894 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7895 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7896 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7897 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7898 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7899 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7900 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7901 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7902 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7903 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7904 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7905 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7906 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7907 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7908 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7909 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7910 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7911 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7912 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7913 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7914 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7915 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7916 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7917 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7918 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7919 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7920 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7921 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7922 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7923 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7924 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7925 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7926 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7927 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7928 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7929 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7930 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7931 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7932 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7933 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7934 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7935 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7936 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7937 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7938 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7939 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7940 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7941 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7942 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7943 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7944 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7945 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7946 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7947 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7948 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7949 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7950 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7951 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7952 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7953 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7954 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7955 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7956 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7957 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7958 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7959 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7960 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7961 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7962 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7963 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7964 | 21983870 | Alterations of peripheral CD4+CD25+Foxp3+ T regulatory cells in mice with STZ-induced diabetes. |
| 7965 | 21983870 | CD4+CD25+T regulatory cells (Tregs) play pivotal roles in controlling immune homeostasis, immunity and tolerance. |
| 7966 | 21983870 | The effect of hyperglycemia on CD4+CD25+Tregs has not yet been addressed. |
| 7967 | 21983870 | Here we used streptozotocin (STZ)-induced diabetic mice to study the effects of long-term hyperglycemia on CD4+CD25+Tregs in vivo. |
| 7968 | 21983870 | Four months after the onset of diabetes, the frequency of CD4+CD25+Foxp3+ T regulatory cells was significantly elevated in the spleen, peripheral blood lymphocytes (PBLs), peripheral lymph nodes (pLNs) and mesenteric LNs (mLNs). |
| 7969 | 21983870 | CD4+CD25+Tregs obtained from mice with diabetes displayed defective immunosuppressive functions and an activated/memory phenotype. |
| 7970 | 21983870 | Insulin administration rescued these changes in the CD4+CD25+ Tregs of diabetic mice. |
| 7971 | 21983870 | The percentage of thymic CD4+CD25+ naturally occurring Tregs (nTregs) and peripheral CD4+Helios+Foxp3+ nTregs were markedly enhanced in diabetic mice, indicating that thymic output contributed to the increased frequency of peripheral CD4+CD25+Tregs in diabetic mice. |
| 7972 | 21983870 | In an in vitro assay in which Tregs were induced from CD4+CD25- T cells by transforming growth factor (TGF)-β, high glucose enhanced the efficiency of CD4+CD25+Foxp3+ inducible Tregs (iTregs) induction. |
| 7973 | 21983870 | In addition, CD4+CD25- T cells from diabetic mice were more susceptible to CD4+CD25+Foxp3+ iTreg differentiation than those cells from control mice. |
| 7974 | 21983870 | These data, together with the enhanced frequency of CD4+Helios-Foxp3+ iTregs in the periphery of mice with diabetes, indicate that enhanced CD4+CD25+Foxp3+ iTreg induction also contributes to a peripheral increase iCD4+CD25+Tregs in diabetic mice. |
| 7975 | 21983870 | Our data show that hyperglycemia may alter the frequency of CD4+CD25+Foxp3+ Tregs in mice, which may result in late-state immune dysfunction in patients with diabetes. |
| 7976 | 22063316 | We show that treatment of non-obese diabetic (NOD) mice with an OX40 agonistic antibody (OX86) reduced type 1 diabetes (T1D) incidence by inducing both CD4(+)CD25(+)Foxp3(+) Tregs and CD4(+)Foxp3(-) T cells expressing the latency-associated peptide (LAP). |
| 7977 | 22063316 | These OX86-induced CD4(+)Foxp3(-)LAP(+) T cells also demonstrated suppressive activity in vitro. |
| 7978 | 22063316 | Synergy resulted from an expansion of IL-10-expressing insB9:23-reactive Tregs which augmented the proportion of CD4(+) T cells with in vivo suppressive activity. |
| 7979 | 22063316 | We show that treatment of non-obese diabetic (NOD) mice with an OX40 agonistic antibody (OX86) reduced type 1 diabetes (T1D) incidence by inducing both CD4(+)CD25(+)Foxp3(+) Tregs and CD4(+)Foxp3(-) T cells expressing the latency-associated peptide (LAP). |
| 7980 | 22063316 | These OX86-induced CD4(+)Foxp3(-)LAP(+) T cells also demonstrated suppressive activity in vitro. |
| 7981 | 22063316 | Synergy resulted from an expansion of IL-10-expressing insB9:23-reactive Tregs which augmented the proportion of CD4(+) T cells with in vivo suppressive activity. |
| 7982 | 22063316 | We show that treatment of non-obese diabetic (NOD) mice with an OX40 agonistic antibody (OX86) reduced type 1 diabetes (T1D) incidence by inducing both CD4(+)CD25(+)Foxp3(+) Tregs and CD4(+)Foxp3(-) T cells expressing the latency-associated peptide (LAP). |
| 7983 | 22063316 | These OX86-induced CD4(+)Foxp3(-)LAP(+) T cells also demonstrated suppressive activity in vitro. |
| 7984 | 22063316 | Synergy resulted from an expansion of IL-10-expressing insB9:23-reactive Tregs which augmented the proportion of CD4(+) T cells with in vivo suppressive activity. |
| 7985 | 22065673 | In nonobese diabetic (NOD) mice, two sets of autoreactive CD4(+) T cells recognize the B:9-23 segment of the insulin B chain. |
| 7986 | 22068235 | Given the role of Fas-mediated signaling in regulating effector T cell responses, we tested if pancreatic islets can be engineered ex vivo to display on their surface an apoptotic form of Fas ligand protein chimeric with streptavidin (SA-FasL) and whether such engineered islets induce tolerance in allogeneic hosts. |
| 7987 | 22068235 | Tolerance was initiated and maintained by CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells, as their depletion early during tolerance induction or late after established tolerance resulted in prompt graft rejection. |
| 7988 | 22116888 | FoxP3-expressing CD4(+) regulatory T cells (Tregs) are potential candidates to control autoimmunity because they play a central role in maintaining self-tolerance. |
| 7989 | 22140261 | Furthermore, we found that Gr1(+)CD11b(+) cells could suppress diabetogenic CD4 and CD8 T cell function in an IL-10-, NO-, and cell contact-dependent manner. |
| 7990 | 22156513 | Here, we have reevaluated the contribution of CD28-CD80/86 costimulation in the LCMV system by use of CD80/86-deficient mice, and our results demonstrate that a disruption of CD28-CD80/86 signaling compromises the magnitude, phenotype, and/or functionality of LCMV-specific CD8(+) and/or CD4(+) T cell populations in all stages of the T cell response. |
| 7991 | 22156513 | Notably, a profound inhibition of secondary T cell immunity in LCMV-immune CD80/86-deficient mice emerged as a composite of both defective memory T cell development and a specific requirement for CD80 but not CD86 in the recall response, while a related experimental scenario of CD28-dependent yet CD80/86-independent secondary CD8(+) T cell immunity suggests the existence of a CD28 ligand other than CD80/86. |
| 7992 | 22156513 | Furthermore, we provide evidence that regulatory T cells (T(REG)s), the homeostasis of which is altered in CD80/86(-/-) mice, contribute to restrained LCMV-specific CD8(+) T cell responses in the presence of CD80/86. |
| 7993 | 22174447 | We tested these hypotheses by investigating whether infection with the filarial nematode Litomosoides sigmodontis prevents diabetes onset in IL-4-deficient NOD mice and whether depletion or absence of regulatory T cells, IL-10, or TGF-β alters helminth-mediated protection. |
| 7994 | 22174447 | Infections in immunocompetent and IL-4-deficient NOD mice were accompanied by increases in CD4(+)CD25(+)Foxp3(+) regulatory T cell frequencies and numbers, respectively, and helminth infection increased the proliferation of CD4(+)Foxp3(+) cells. |
| 7995 | 22174945 | A phase II clinical trial with glutamic acid decarboxylase (GAD) 65 formulated with aluminium hydroxide (GAD-alum) has shown efficacy in preserving residual insulin secretion in children and adolescents with recent-onset type 1 diabetes (T1D). |
| 7996 | 22174945 | Peripheral blood mononuclear cells (PBMC) were stimulated in vitro with GAD(65). |
| 7997 | 22174945 | Frequencies of naïve, central and effector memory CD4+ and CD8+ T cells were measured, together with cytokine secretion, proliferation, gene expression and serum GAD(65) autoantibody (GADA) levels. |
| 7998 | 22174945 | Moreover, post-treatment serum GADA titres remained persistently increased in the GAD-alum arm, but did not inhibit GAD(65) enzymatic activity. |
| 7999 | 22174945 | In parallel to a GAD(65)-induced T-cell activation, our results show induction of T-cell inhibitory pathways important for regulating the GAD(65) immunity. |
| 8000 | 22178917 | The combined action of these proteases generates antigenic peptides from antigens, which are loaded to MHC II molecules for CD4+ T cell presentation. |
| 8001 | 22186414 | Galectin-9 and T cell immunoglobulin mucin-3 pathway is a therapeutic target for type 1 diabetes. |
| 8002 | 22186414 | Galectin-9 (Gal-9), a ligand for T cell Ig mucin-3 (Tim-3), induces apoptosis in cluster of differentiation 4 (CD4)(+) Tim-3(+) T helper 1 (T(H)1) cells via the Gal-9-Tim-3 pathway and negatively regulates T(H)1 immunity. |
| 8003 | 22186414 | Gal-9 induced apoptosis of CD4(+)Tim-3(+) T(H)1 cells at the concentration of 0.2 μM, whereas RMT3-23 failed to enhance the apoptosis of CD4(+)Tim-3(+) T(H)1 cells. |
| 8004 | 22186414 | Although Gal-9 exhibited certain therapeutic potential against autoimmune diabetes by enhancing apoptosis of CD4(+)Tim-3(+) T(H)1 cells, RMT3-23 exhibited prominent therapeutic efficacy by suppressing the TNF-α production and activation of DC. |
| 8005 | 22186414 | Galectin-9 and T cell immunoglobulin mucin-3 pathway is a therapeutic target for type 1 diabetes. |
| 8006 | 22186414 | Galectin-9 (Gal-9), a ligand for T cell Ig mucin-3 (Tim-3), induces apoptosis in cluster of differentiation 4 (CD4)(+) Tim-3(+) T helper 1 (T(H)1) cells via the Gal-9-Tim-3 pathway and negatively regulates T(H)1 immunity. |
| 8007 | 22186414 | Gal-9 induced apoptosis of CD4(+)Tim-3(+) T(H)1 cells at the concentration of 0.2 μM, whereas RMT3-23 failed to enhance the apoptosis of CD4(+)Tim-3(+) T(H)1 cells. |
| 8008 | 22186414 | Although Gal-9 exhibited certain therapeutic potential against autoimmune diabetes by enhancing apoptosis of CD4(+)Tim-3(+) T(H)1 cells, RMT3-23 exhibited prominent therapeutic efficacy by suppressing the TNF-α production and activation of DC. |
| 8009 | 22186414 | Galectin-9 and T cell immunoglobulin mucin-3 pathway is a therapeutic target for type 1 diabetes. |
| 8010 | 22186414 | Galectin-9 (Gal-9), a ligand for T cell Ig mucin-3 (Tim-3), induces apoptosis in cluster of differentiation 4 (CD4)(+) Tim-3(+) T helper 1 (T(H)1) cells via the Gal-9-Tim-3 pathway and negatively regulates T(H)1 immunity. |
| 8011 | 22186414 | Gal-9 induced apoptosis of CD4(+)Tim-3(+) T(H)1 cells at the concentration of 0.2 μM, whereas RMT3-23 failed to enhance the apoptosis of CD4(+)Tim-3(+) T(H)1 cells. |
| 8012 | 22186414 | Although Gal-9 exhibited certain therapeutic potential against autoimmune diabetes by enhancing apoptosis of CD4(+)Tim-3(+) T(H)1 cells, RMT3-23 exhibited prominent therapeutic efficacy by suppressing the TNF-α production and activation of DC. |
| 8013 | 22228716 | We determined all major T-cell subpopulations via six-color flow cytometry, including CD8+ and CD4+ T cells, CD4+ T-helper (Th) subpopulations, and natural CD4+CD25+FoxP3+ T-regulatory (Treg) cells. |
| 8014 | 22228716 | Morbidly obese subjects had a selective increase in peripheral blood CD4+ naive, memory, natural CD4+CD25+FoxP3+ Treg, and Th2 T cells, whereas CD8+ T cells were normal. |
| 8015 | 22228716 | CD4+ and CD8+ T-cell proliferation was increased, whereas the TCRB repertoire was not significantly altered. |
| 8016 | 22228716 | Plasma levels of cytokines CCL5 and IL-7 were elevated. |
| 8017 | 22228716 | CD4+ T-cell numbers correlated positively with fasting insulin levels. |
| 8018 | 22228716 | The peripheral blood T-cell compartment of morbidly obese subjects is characterized by increased homeostatic T-cell proliferation to which cytokines IL-7 and CCL5, among others, might contribute. |
| 8019 | 22228716 | We determined all major T-cell subpopulations via six-color flow cytometry, including CD8+ and CD4+ T cells, CD4+ T-helper (Th) subpopulations, and natural CD4+CD25+FoxP3+ T-regulatory (Treg) cells. |
| 8020 | 22228716 | Morbidly obese subjects had a selective increase in peripheral blood CD4+ naive, memory, natural CD4+CD25+FoxP3+ Treg, and Th2 T cells, whereas CD8+ T cells were normal. |
| 8021 | 22228716 | CD4+ and CD8+ T-cell proliferation was increased, whereas the TCRB repertoire was not significantly altered. |
| 8022 | 22228716 | Plasma levels of cytokines CCL5 and IL-7 were elevated. |
| 8023 | 22228716 | CD4+ T-cell numbers correlated positively with fasting insulin levels. |
| 8024 | 22228716 | The peripheral blood T-cell compartment of morbidly obese subjects is characterized by increased homeostatic T-cell proliferation to which cytokines IL-7 and CCL5, among others, might contribute. |
| 8025 | 22228716 | We determined all major T-cell subpopulations via six-color flow cytometry, including CD8+ and CD4+ T cells, CD4+ T-helper (Th) subpopulations, and natural CD4+CD25+FoxP3+ T-regulatory (Treg) cells. |
| 8026 | 22228716 | Morbidly obese subjects had a selective increase in peripheral blood CD4+ naive, memory, natural CD4+CD25+FoxP3+ Treg, and Th2 T cells, whereas CD8+ T cells were normal. |
| 8027 | 22228716 | CD4+ and CD8+ T-cell proliferation was increased, whereas the TCRB repertoire was not significantly altered. |
| 8028 | 22228716 | Plasma levels of cytokines CCL5 and IL-7 were elevated. |
| 8029 | 22228716 | CD4+ T-cell numbers correlated positively with fasting insulin levels. |
| 8030 | 22228716 | The peripheral blood T-cell compartment of morbidly obese subjects is characterized by increased homeostatic T-cell proliferation to which cytokines IL-7 and CCL5, among others, might contribute. |
| 8031 | 22228716 | We determined all major T-cell subpopulations via six-color flow cytometry, including CD8+ and CD4+ T cells, CD4+ T-helper (Th) subpopulations, and natural CD4+CD25+FoxP3+ T-regulatory (Treg) cells. |
| 8032 | 22228716 | Morbidly obese subjects had a selective increase in peripheral blood CD4+ naive, memory, natural CD4+CD25+FoxP3+ Treg, and Th2 T cells, whereas CD8+ T cells were normal. |
| 8033 | 22228716 | CD4+ and CD8+ T-cell proliferation was increased, whereas the TCRB repertoire was not significantly altered. |
| 8034 | 22228716 | Plasma levels of cytokines CCL5 and IL-7 were elevated. |
| 8035 | 22228716 | CD4+ T-cell numbers correlated positively with fasting insulin levels. |
| 8036 | 22228716 | The peripheral blood T-cell compartment of morbidly obese subjects is characterized by increased homeostatic T-cell proliferation to which cytokines IL-7 and CCL5, among others, might contribute. |
| 8037 | 22238605 | Depletion of B2 but not B1a B cells in BAFF receptor-deficient ApoE mice attenuates atherosclerosis by potently ameliorating arterial inflammation. |
| 8038 | 22238605 | Here, we examined the development of atherosclerosis in BAFF-R deficient ApoE(-/-) mice because B2 cells but not B1a cells are selectively depleted in BAFF-R deficient mice. |
| 8039 | 22238605 | We fed BAFF-R(-/-) ApoE(-/-) (BaffR.ApoE DKO) and BAFF-R(+/+)ApoE(-/-) (ApoE KO) mice a high fat diet (HFD) for 8-weeks. |
| 8040 | 22238605 | BAFF-R deficiency in ApoE(-/-) mice was also associated with a reduced expression of VCAM-1 and fewer macrophages, dendritic cells, CD4+ and CD8+ T cell infiltrates and PCNA+ cells in lesions. |
| 8041 | 22270834 | Dendritic cells with TGF-β1 and IL-2 differentiate naive CD4+ T cells into alloantigen-specific and allograft protective Foxp3+ regulatory T cells. |
| 8042 | 22277969 | Moreover, IL-10 expression by CD4(+)CD25(high)CCR6(+)FoxP3 cells returning to the peripheral circulation was increased in patients with type 1 diabetes treated with teplizumab. |
| 8043 | 22287719 | Adjuvant immunotherapy of experimental autoimmune encephalomyelitis: immature myeloid cells expressing CXCL10 and CXCL16 attract CXCR3+CXCR6+ and myelin-specific T cells to the draining lymph nodes rather than the central nervous system. |
| 8044 | 22287719 | Immature myeloid cells in dLNs expressed the chemokines CXCL10 and CXCL16 in an IFN-γ-dependent manner. |
| 8045 | 22287719 | Subsequently, CD4(+) T cells coexpressing the cognate chemokine receptors CXCR3 and CXCR6 and myelin oligodendrocyte glycoprotein (MOG)-specific CD4(+) T cells accumulated within the chemokine-expressing dLNs, rather than within the CNS. |
| 8046 | 22287719 | In addition to altering the distribution of MOG-specific T cells, adjuvant treatment suppressed development of MOG-specific IL-17. |
| 8047 | 22287719 | Thus, adjuvant immunotherapy of EAE requires IFN-γ, which suppresses development of the Th17 response, and diverts autoreactive T cells away from the CNS toward immature myeloid cells expressing CXCL10 and CXCL16 in the lymph nodes. |
| 8048 | 22291182 | The interplay of CD4(+) and CD8(+) T cells targeting autoantigens is responsible for the progression of a number of autoimmune diseases, including type 1 diabetes mellitus (T1D). |
| 8049 | 22291182 | The anti-CD98hc mAb also inhibited Ag-specific proliferation and the acquisition of effector function by CD4(+) and CD8(+) T cells in vitro and in vivo. |
| 8050 | 22291182 | The interplay of CD4(+) and CD8(+) T cells targeting autoantigens is responsible for the progression of a number of autoimmune diseases, including type 1 diabetes mellitus (T1D). |
| 8051 | 22291182 | The anti-CD98hc mAb also inhibited Ag-specific proliferation and the acquisition of effector function by CD4(+) and CD8(+) T cells in vitro and in vivo. |
| 8052 | 22294241 | T lymphocytes bearing the αβ T cell receptor (TCR) but lacking CD4, CD8, and markers of natural killer (NK) cell differentiation are known as 'double-negative' (DN) T cells and have been described in both humans and rodent models. |
| 8053 | 22323564 | Insulin sensitive and resistant obesity in humans: AMPK activity, oxidative stress, and depot-specific changes in gene expression in adipose tissue. |
| 8054 | 22323564 | We previously reported that adenosine monophosphate-activated protein kinase (AMPK) activity is lower in adipose tissue of morbidly obese individuals who are insulin resistant than in comparably obese people who are insulin sensitive. |
| 8055 | 22323564 | We confirmed that AMPK activity is diminished in the insulin resistant group. |
| 8056 | 22323564 | A custom PCR array revealed increases in mRNA levels of a wide variety of genes associated with inflammation and decreases in PGC-1α and Nampt in omental fat of the insulin resistant group. |
| 8057 | 22323564 | In contrast, subcutaneous abdominal fat of the same patients showed increases in PTP-1b, VEGFa, IFNγ, PAI-1, and NOS-2 not observed in omental fat. |
| 8058 | 22323564 | Only angiotensinogen and CD4(+) mRNA levels were increased in both depots. |
| 8059 | 22323564 | Thus, adipose tissues of markedly obese insulin resistant individuals uniformly show decreased AMPK activity and increased oxidative stress compared with insulin sensitive patients. |
| 8060 | 22341303 | We performed our analysis in 5 pairs of monozygotic twins, 3 of which were concordant and 2 discordant for T1D, by combining flow cytometry and CDR3 spectratyping on both CD4+ and CD8+ T-cells. |
| 8061 | 22371394 | CD4(+) type II NKT cells mediate ICOS and programmed death-1-dependent regulation of type 1 diabetes. |
| 8062 | 22371394 | In this study, we show that CD4(+) 24αβ type II NKT cells, but not CD4/CD8 double-negative NKT cells, were sufficient to downregulate diabetogenic CD4(+) BDC2.5 NOD T cells in adoptive transfer experiments. |
| 8063 | 22371394 | CD4(+) 24αβ NKT cells exhibited a memory phenotype including high ICOS expression, increased cytokine production, and limited display of NK cell markers, compared with double-negative 24αβ NKT cells. |
| 8064 | 22371394 | CD4(+) type II NKT cells mediate ICOS and programmed death-1-dependent regulation of type 1 diabetes. |
| 8065 | 22371394 | In this study, we show that CD4(+) 24αβ type II NKT cells, but not CD4/CD8 double-negative NKT cells, were sufficient to downregulate diabetogenic CD4(+) BDC2.5 NOD T cells in adoptive transfer experiments. |
| 8066 | 22371394 | CD4(+) 24αβ NKT cells exhibited a memory phenotype including high ICOS expression, increased cytokine production, and limited display of NK cell markers, compared with double-negative 24αβ NKT cells. |
| 8067 | 22371394 | CD4(+) type II NKT cells mediate ICOS and programmed death-1-dependent regulation of type 1 diabetes. |
| 8068 | 22371394 | In this study, we show that CD4(+) 24αβ type II NKT cells, but not CD4/CD8 double-negative NKT cells, were sufficient to downregulate diabetogenic CD4(+) BDC2.5 NOD T cells in adoptive transfer experiments. |
| 8069 | 22371394 | CD4(+) 24αβ NKT cells exhibited a memory phenotype including high ICOS expression, increased cytokine production, and limited display of NK cell markers, compared with double-negative 24αβ NKT cells. |
| 8070 | 22403296 | Following the fate of one insulin-reactive CD4 T cell: conversion into Teffs and Tregs in the periphery controls diabetes in NOD mice. |
| 8071 | 22403296 | Insulin B chain 9-23 (B:9-23) autoreactive CD4 T cells are key for initiating autoimmune diabetes in NOD mice; however, little is known regarding their origin and function. |
| 8072 | 22403296 | Following the fate of one insulin-reactive CD4 T cell: conversion into Teffs and Tregs in the periphery controls diabetes in NOD mice. |
| 8073 | 22403296 | Insulin B chain 9-23 (B:9-23) autoreactive CD4 T cells are key for initiating autoimmune diabetes in NOD mice; however, little is known regarding their origin and function. |
| 8074 | 22427377 | Nonobese diabetic RIP-IL35 transgenic mice exhibited decreased islet infiltration with substantial reductions in the number of CD4(+) and CD8(+) T cells, and frequency of glucose-6-phosphatase catalytic subunit-related protein-specific CD8(+) T cells. |
| 8075 | 22428018 | The gluten-containing STD diet led to a significantly decreased proportion of γδ T cells in all lymphoid compartments studied, although an increase was detected in some γδ T cell subsets (CD8(+), CD103(+)). |
| 8076 | 22428018 | Further, it decreased the proportion of CD4(+)CD62L(+) T cells in Peyer's patches. |
| 8077 | 22428018 | Interestingly, no diet-induced changes were found among CD4(+)Foxp3(+) T cells or CD3(+)CD49b(+)cells (NKT cells) and CD3(-)CD49b(+) (NK) cells. |
| 8078 | 22428018 | Mice fed the STD diet showed increased proportions of CD4(+)CD45RB(high+) and CD103(+) T cells and a lower proportion of CD4(+)CD45RB(low+) T cells in both mucosal and non-mucosal compartments. |
| 8079 | 22428018 | The gluten-containing STD diet led to a significantly decreased proportion of γδ T cells in all lymphoid compartments studied, although an increase was detected in some γδ T cell subsets (CD8(+), CD103(+)). |
| 8080 | 22428018 | Further, it decreased the proportion of CD4(+)CD62L(+) T cells in Peyer's patches. |
| 8081 | 22428018 | Interestingly, no diet-induced changes were found among CD4(+)Foxp3(+) T cells or CD3(+)CD49b(+)cells (NKT cells) and CD3(-)CD49b(+) (NK) cells. |
| 8082 | 22428018 | Mice fed the STD diet showed increased proportions of CD4(+)CD45RB(high+) and CD103(+) T cells and a lower proportion of CD4(+)CD45RB(low+) T cells in both mucosal and non-mucosal compartments. |
| 8083 | 22428018 | The gluten-containing STD diet led to a significantly decreased proportion of γδ T cells in all lymphoid compartments studied, although an increase was detected in some γδ T cell subsets (CD8(+), CD103(+)). |
| 8084 | 22428018 | Further, it decreased the proportion of CD4(+)CD62L(+) T cells in Peyer's patches. |
| 8085 | 22428018 | Interestingly, no diet-induced changes were found among CD4(+)Foxp3(+) T cells or CD3(+)CD49b(+)cells (NKT cells) and CD3(-)CD49b(+) (NK) cells. |
| 8086 | 22428018 | Mice fed the STD diet showed increased proportions of CD4(+)CD45RB(high+) and CD103(+) T cells and a lower proportion of CD4(+)CD45RB(low+) T cells in both mucosal and non-mucosal compartments. |
| 8087 | 22461703 | Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. |
| 8088 | 22461703 | Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. |
| 8089 | 22461703 | We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. |
| 8090 | 22461703 | Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. |
| 8091 | 22461703 | Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. |
| 8092 | 22461703 | We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. |
| 8093 | 22461703 | Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. |
| 8094 | 22461703 | Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. |
| 8095 | 22461703 | We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. |
| 8096 | 22488364 | We have investigated the role of CD40 signaling in islet-reactive, diabetogenic CD4(+) Th1 T-cell clones. |
| 8097 | 22488364 | Using multispectral flow cytometry, we showed that CD40 and CD154 are co-expressed and form complexes on the surface of activated T cells. |
| 8098 | 22488364 | We also demonstrate that activated Tcells can transactivate CD4(+) CD40(+) T cells through the CD40-CD154 pathway. |
| 8099 | 22488364 | These data indicate that CD40 is an important signaling molecule on autoreactive CD4(+) T cells and contributes to their pathogenic effector function. |
| 8100 | 22488364 | We have investigated the role of CD40 signaling in islet-reactive, diabetogenic CD4(+) Th1 T-cell clones. |
| 8101 | 22488364 | Using multispectral flow cytometry, we showed that CD40 and CD154 are co-expressed and form complexes on the surface of activated T cells. |
| 8102 | 22488364 | We also demonstrate that activated Tcells can transactivate CD4(+) CD40(+) T cells through the CD40-CD154 pathway. |
| 8103 | 22488364 | These data indicate that CD40 is an important signaling molecule on autoreactive CD4(+) T cells and contributes to their pathogenic effector function. |
| 8104 | 22488364 | We have investigated the role of CD40 signaling in islet-reactive, diabetogenic CD4(+) Th1 T-cell clones. |
| 8105 | 22488364 | Using multispectral flow cytometry, we showed that CD40 and CD154 are co-expressed and form complexes on the surface of activated T cells. |
| 8106 | 22488364 | We also demonstrate that activated Tcells can transactivate CD4(+) CD40(+) T cells through the CD40-CD154 pathway. |
| 8107 | 22488364 | These data indicate that CD40 is an important signaling molecule on autoreactive CD4(+) T cells and contributes to their pathogenic effector function. |
| 8108 | 22547652 | We found that Dll4 pharmacological blockade induces accumulation of tDCs and CD4(+)CD25(+)FoxP3(+) regulatory T cells (T(reg) cells) in the thymic cortex. |
| 8109 | 22547652 | Anti-Dll4 treatment converts CD4(-)CD8(-)c-kit(+)CD44(+)CD25(-) (DN1) T cell progenitors to immature DCs that induce ex vivo differentiation of naive CD4(+) T cells into T(reg) cells. |
| 8110 | 22547652 | Induction of these tolerogenic DN1-derived tDCs and the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in the context of transcriptional up-regulation of PU.1, Irf-4, Irf-8, and CSF-1, genes critical for DC differentiation, and are abrogated in thymectomized mice. |
| 8111 | 22547652 | We found that Dll4 pharmacological blockade induces accumulation of tDCs and CD4(+)CD25(+)FoxP3(+) regulatory T cells (T(reg) cells) in the thymic cortex. |
| 8112 | 22547652 | Anti-Dll4 treatment converts CD4(-)CD8(-)c-kit(+)CD44(+)CD25(-) (DN1) T cell progenitors to immature DCs that induce ex vivo differentiation of naive CD4(+) T cells into T(reg) cells. |
| 8113 | 22547652 | Induction of these tolerogenic DN1-derived tDCs and the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in the context of transcriptional up-regulation of PU.1, Irf-4, Irf-8, and CSF-1, genes critical for DC differentiation, and are abrogated in thymectomized mice. |
| 8114 | 22560862 | Significantly higher Dectin-1 expression was also detected in CD4(+) T, CD8(+) T, B cells and NK cells from T2D patients compared to controls. |
| 8115 | 22560862 | In contrast, monocytes from T2D patients with poor glycemic control (HbA1c>8%) showed a diminished percentage of Dectin-1(+)/TLR2(+) cells. |
| 8116 | 22560862 | Negative correlations between the percent of Dectin-1(+)/TLR2(+) cells and fasting plasma glucose levels (FPG) and HbA1c levels were found. |
| 8117 | 22579473 | Interleukin-21 receptor-mediated signals control autoreactive T cell infiltration in pancreatic islets. |
| 8118 | 22579473 | It remains unclear how interleukin-21 receptor (IL-21R) contributes to type 1 diabetes. |
| 8119 | 22579473 | Here we have shown that dendritic cells (DCs) in the pancreas required IL-21R not for antigen uptake, but to acquire the chemokine receptor CCR7 and migrate into the draining lymph node. |
| 8120 | 22579473 | Consequently, less antigen, major histocompatibility complex (MHC) class II, and CD86 was provided to autoreactive effector cells in Il21r(-/-) mice, impairing CD4(+) T cell activation, CD40:CD40L interactions, and pancreatic infiltration by autoreactive T cells. |
| 8121 | 22579473 | CD40 crosslinking restored defective CD4(+) cell expansion and CD4 independently expanded autoreactive CD8(+) cells, but CD8(+) cells still required CD4(+) cells to reach the pancreas and induce diabetes. |
| 8122 | 22579473 | We conclude that IL-21R controls both antigen transport by DCs and the crucial beacon function of CD4(+) cells for autoreactive CD8(+) cells to reach the islets. |
| 8123 | 22579473 | Interleukin-21 receptor-mediated signals control autoreactive T cell infiltration in pancreatic islets. |
| 8124 | 22579473 | It remains unclear how interleukin-21 receptor (IL-21R) contributes to type 1 diabetes. |
| 8125 | 22579473 | Here we have shown that dendritic cells (DCs) in the pancreas required IL-21R not for antigen uptake, but to acquire the chemokine receptor CCR7 and migrate into the draining lymph node. |
| 8126 | 22579473 | Consequently, less antigen, major histocompatibility complex (MHC) class II, and CD86 was provided to autoreactive effector cells in Il21r(-/-) mice, impairing CD4(+) T cell activation, CD40:CD40L interactions, and pancreatic infiltration by autoreactive T cells. |
| 8127 | 22579473 | CD40 crosslinking restored defective CD4(+) cell expansion and CD4 independently expanded autoreactive CD8(+) cells, but CD8(+) cells still required CD4(+) cells to reach the pancreas and induce diabetes. |
| 8128 | 22579473 | We conclude that IL-21R controls both antigen transport by DCs and the crucial beacon function of CD4(+) cells for autoreactive CD8(+) cells to reach the islets. |
| 8129 | 22579473 | Interleukin-21 receptor-mediated signals control autoreactive T cell infiltration in pancreatic islets. |
| 8130 | 22579473 | It remains unclear how interleukin-21 receptor (IL-21R) contributes to type 1 diabetes. |
| 8131 | 22579473 | Here we have shown that dendritic cells (DCs) in the pancreas required IL-21R not for antigen uptake, but to acquire the chemokine receptor CCR7 and migrate into the draining lymph node. |
| 8132 | 22579473 | Consequently, less antigen, major histocompatibility complex (MHC) class II, and CD86 was provided to autoreactive effector cells in Il21r(-/-) mice, impairing CD4(+) T cell activation, CD40:CD40L interactions, and pancreatic infiltration by autoreactive T cells. |
| 8133 | 22579473 | CD40 crosslinking restored defective CD4(+) cell expansion and CD4 independently expanded autoreactive CD8(+) cells, but CD8(+) cells still required CD4(+) cells to reach the pancreas and induce diabetes. |
| 8134 | 22579473 | We conclude that IL-21R controls both antigen transport by DCs and the crucial beacon function of CD4(+) cells for autoreactive CD8(+) cells to reach the islets. |
| 8135 | 22596049 | Adoptive transfer of naive CD4(+) T cells in Rag1(-/-) mice led to a predominant Th1 response in adipose tissue. |
| 8136 | 22596049 | In contrast, during obesity DCs (human CD11c(+)CD1c(+) and mouse CD11c(high)F4/80(low)) accumulated in adipose tissue. |
| 8137 | 22596049 | In patients, the presence of CD11c(+)CD1c(+) DCs correlated with the BMI and with an elevation in Th17 cells. |
| 8138 | 22596049 | CD1c gene expression further correlated with homeostatic model assessment-insulin resistance in the subcutaneous adipose tissue of obese patients. |
| 8139 | 22649557 | Interestingly, the latter delay or protection from T1D is associated with the enhanced secretion of IL-10 rather than IFN-g by C24:0-treated CD4(+) T cells and the deviation of the islet-reactive diabetogenic T cell response. |
| 8140 | 22661285 | From an immunological standpoint, AG490 induced the expression of Foxp3 in CD4(+)CD25(-) T-cells and down-regulated expression of co-stimulatory molecules in dendritic cells (DC) both in vitro and in vivo. |
| 8141 | 22661285 | AG490 treated CD4+CD25- T-cells and DC in vitro, acquired regulatory functions; namely, the ability to suppress proliferation of a responding cell population in vitro. |
| 8142 | 22661285 | From an immunological standpoint, AG490 induced the expression of Foxp3 in CD4(+)CD25(-) T-cells and down-regulated expression of co-stimulatory molecules in dendritic cells (DC) both in vitro and in vivo. |
| 8143 | 22661285 | AG490 treated CD4+CD25- T-cells and DC in vitro, acquired regulatory functions; namely, the ability to suppress proliferation of a responding cell population in vitro. |
| 8144 | 22684085 | Flow cytometric analysis of Tregs was performed using the following markers: CD4, CD25, CD127, FoxP3, IL-10, and TGF-β. |
| 8145 | 22684085 | There was lower frequency of CD4(+)CD25(high)CD127(low)FoxP3(+) Tregs in T1D children <5 years than ≥5 years of age (0.87 vs. 1.56 %, respectively, p = 0.017). |
| 8146 | 22684085 | Diabetic children <5 years had lower CD4(+)CD25(high)CD127(low)FoxP3(+), CD4(+)CD25(high)IL-10, and CD4(+)CD25(high)TGF-β Tregs compared to age-matched controls. |
| 8147 | 22684085 | Flow cytometric analysis of Tregs was performed using the following markers: CD4, CD25, CD127, FoxP3, IL-10, and TGF-β. |
| 8148 | 22684085 | There was lower frequency of CD4(+)CD25(high)CD127(low)FoxP3(+) Tregs in T1D children <5 years than ≥5 years of age (0.87 vs. 1.56 %, respectively, p = 0.017). |
| 8149 | 22684085 | Diabetic children <5 years had lower CD4(+)CD25(high)CD127(low)FoxP3(+), CD4(+)CD25(high)IL-10, and CD4(+)CD25(high)TGF-β Tregs compared to age-matched controls. |
| 8150 | 22684085 | Flow cytometric analysis of Tregs was performed using the following markers: CD4, CD25, CD127, FoxP3, IL-10, and TGF-β. |
| 8151 | 22684085 | There was lower frequency of CD4(+)CD25(high)CD127(low)FoxP3(+) Tregs in T1D children <5 years than ≥5 years of age (0.87 vs. 1.56 %, respectively, p = 0.017). |
| 8152 | 22684085 | Diabetic children <5 years had lower CD4(+)CD25(high)CD127(low)FoxP3(+), CD4(+)CD25(high)IL-10, and CD4(+)CD25(high)TGF-β Tregs compared to age-matched controls. |
| 8153 | 22688334 | ADMSC treatment reversed the hyperglycemia of early-onset diabetes in 78% of diabetic NOD mice, and this effect was associated with higher serum insulin, amylin, and glucagon-like peptide 1 levels compared with untreated controls. |
| 8154 | 22688334 | This improved outcome was associated with downregulation of the CD4(+) Th1-biased immune response and expansion of regulatory T cells (Tregs) in the pancreatic lymph nodes. |
| 8155 | 22688334 | Within the pancreas, inflammatory cell infiltration and interferon-γ levels were reduced, while insulin, pancreatic duodenal homeobox-1, and active transforming growth factor-β1 expression were increased. |
| 8156 | 22693523 | In type 1 diabetes (T1D), CD8+ cytotoxic T lymphocytes, in conjunction with CD4+ T helper cells, destroy the insulin-producing β cells within the pancreatic islets of Langerhans. |
| 8157 | 22723880 | We also observed sensitization of the Th1 differentiation machinery through co-localization of IL-2Rα, IL-4Rα, and IL-12Rβ2 subunits with GM1 positive lipid rafts, and increased STAT-4 and STAT-5 phosphorylation following membrane cholesterol enrichment. |
| 8158 | 22723880 | Antigen stimulation or CD3/CD28 polyclonal stimulation of membrane cholesterol-enriched, resting CD4 T-cells followed a path of Th1 differentiation, which was more vigorous in the presence of increased IL-12 secretion by APCs enriched in membrane cholesterol. |
| 8159 | 22723880 | However, membrane cholesterol enrichment in CD4(+)Foxp3(+) T-reg cells did not alter their suppressogenic function. |
| 8160 | 22723880 | We also observed sensitization of the Th1 differentiation machinery through co-localization of IL-2Rα, IL-4Rα, and IL-12Rβ2 subunits with GM1 positive lipid rafts, and increased STAT-4 and STAT-5 phosphorylation following membrane cholesterol enrichment. |
| 8161 | 22723880 | Antigen stimulation or CD3/CD28 polyclonal stimulation of membrane cholesterol-enriched, resting CD4 T-cells followed a path of Th1 differentiation, which was more vigorous in the presence of increased IL-12 secretion by APCs enriched in membrane cholesterol. |
| 8162 | 22723880 | However, membrane cholesterol enrichment in CD4(+)Foxp3(+) T-reg cells did not alter their suppressogenic function. |
| 8163 | 22728763 | Targeting Janus tyrosine kinase 3 (JAK3) with an inhibitor induces secretion of TGF-β by CD4+ T cells. |
| 8164 | 22728763 | Here, we show that the JAK3 inhibitor 4-(4'-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P131) suppresses proliferation of short-term cultured NOD CD4(+) T cells through induction of apoptosis, while promoting survival of a particular population of long-term cultured cells. |
| 8165 | 22728763 | It was found that the surviving cells were not of the CD4(+)CD25(+)FoxP3(+) phenotype. |
| 8166 | 22728763 | They secreted decreased amounts of IL-10, IL-4 and interferon (IFN)-γ compared to the cells not exposed to the optimal concentrations of JAK3 inhibitor. |
| 8167 | 22728763 | In vivo treatment of prediabetic NOD mice with WHI-P131 did not affect the frequency and number of splenic and pancreatic lymph node CD4(+)FoxP3(+) Tregs, while generating an elevated numbers of CD4(+)FoxP3(-) TGF-β-secreting T cells. |
| 8168 | 22728763 | In conclusion, our data suggest an induction of TGF-β-secreting CD4(+) T cells as the underlying mechanism for antidiabetogenic effects obtained by the treatment with a JAK3 inhibitor. |
| 8169 | 22728763 | Targeting Janus tyrosine kinase 3 (JAK3) with an inhibitor induces secretion of TGF-β by CD4+ T cells. |
| 8170 | 22728763 | Here, we show that the JAK3 inhibitor 4-(4'-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P131) suppresses proliferation of short-term cultured NOD CD4(+) T cells through induction of apoptosis, while promoting survival of a particular population of long-term cultured cells. |
| 8171 | 22728763 | It was found that the surviving cells were not of the CD4(+)CD25(+)FoxP3(+) phenotype. |
| 8172 | 22728763 | They secreted decreased amounts of IL-10, IL-4 and interferon (IFN)-γ compared to the cells not exposed to the optimal concentrations of JAK3 inhibitor. |
| 8173 | 22728763 | In vivo treatment of prediabetic NOD mice with WHI-P131 did not affect the frequency and number of splenic and pancreatic lymph node CD4(+)FoxP3(+) Tregs, while generating an elevated numbers of CD4(+)FoxP3(-) TGF-β-secreting T cells. |
| 8174 | 22728763 | In conclusion, our data suggest an induction of TGF-β-secreting CD4(+) T cells as the underlying mechanism for antidiabetogenic effects obtained by the treatment with a JAK3 inhibitor. |
| 8175 | 22728763 | Targeting Janus tyrosine kinase 3 (JAK3) with an inhibitor induces secretion of TGF-β by CD4+ T cells. |
| 8176 | 22728763 | Here, we show that the JAK3 inhibitor 4-(4'-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P131) suppresses proliferation of short-term cultured NOD CD4(+) T cells through induction of apoptosis, while promoting survival of a particular population of long-term cultured cells. |
| 8177 | 22728763 | It was found that the surviving cells were not of the CD4(+)CD25(+)FoxP3(+) phenotype. |
| 8178 | 22728763 | They secreted decreased amounts of IL-10, IL-4 and interferon (IFN)-γ compared to the cells not exposed to the optimal concentrations of JAK3 inhibitor. |
| 8179 | 22728763 | In vivo treatment of prediabetic NOD mice with WHI-P131 did not affect the frequency and number of splenic and pancreatic lymph node CD4(+)FoxP3(+) Tregs, while generating an elevated numbers of CD4(+)FoxP3(-) TGF-β-secreting T cells. |
| 8180 | 22728763 | In conclusion, our data suggest an induction of TGF-β-secreting CD4(+) T cells as the underlying mechanism for antidiabetogenic effects obtained by the treatment with a JAK3 inhibitor. |
| 8181 | 22728763 | Targeting Janus tyrosine kinase 3 (JAK3) with an inhibitor induces secretion of TGF-β by CD4+ T cells. |
| 8182 | 22728763 | Here, we show that the JAK3 inhibitor 4-(4'-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P131) suppresses proliferation of short-term cultured NOD CD4(+) T cells through induction of apoptosis, while promoting survival of a particular population of long-term cultured cells. |
| 8183 | 22728763 | It was found that the surviving cells were not of the CD4(+)CD25(+)FoxP3(+) phenotype. |
| 8184 | 22728763 | They secreted decreased amounts of IL-10, IL-4 and interferon (IFN)-γ compared to the cells not exposed to the optimal concentrations of JAK3 inhibitor. |
| 8185 | 22728763 | In vivo treatment of prediabetic NOD mice with WHI-P131 did not affect the frequency and number of splenic and pancreatic lymph node CD4(+)FoxP3(+) Tregs, while generating an elevated numbers of CD4(+)FoxP3(-) TGF-β-secreting T cells. |
| 8186 | 22728763 | In conclusion, our data suggest an induction of TGF-β-secreting CD4(+) T cells as the underlying mechanism for antidiabetogenic effects obtained by the treatment with a JAK3 inhibitor. |
| 8187 | 22728763 | Targeting Janus tyrosine kinase 3 (JAK3) with an inhibitor induces secretion of TGF-β by CD4+ T cells. |
| 8188 | 22728763 | Here, we show that the JAK3 inhibitor 4-(4'-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P131) suppresses proliferation of short-term cultured NOD CD4(+) T cells through induction of apoptosis, while promoting survival of a particular population of long-term cultured cells. |
| 8189 | 22728763 | It was found that the surviving cells were not of the CD4(+)CD25(+)FoxP3(+) phenotype. |
| 8190 | 22728763 | They secreted decreased amounts of IL-10, IL-4 and interferon (IFN)-γ compared to the cells not exposed to the optimal concentrations of JAK3 inhibitor. |
| 8191 | 22728763 | In vivo treatment of prediabetic NOD mice with WHI-P131 did not affect the frequency and number of splenic and pancreatic lymph node CD4(+)FoxP3(+) Tregs, while generating an elevated numbers of CD4(+)FoxP3(-) TGF-β-secreting T cells. |
| 8192 | 22728763 | In conclusion, our data suggest an induction of TGF-β-secreting CD4(+) T cells as the underlying mechanism for antidiabetogenic effects obtained by the treatment with a JAK3 inhibitor. |
| 8193 | 22730534 | This is accompanied by an increased IFN-γ production of autoreactive splenic cells and a decreased presence of regulatory CD4(+)CD25(+)Foxp3(+) T cells. |
| 8194 | 22730534 | In contrast, transfer of CD4(+)CD25(+)Foxp3(+) T cells could correct the defect after denileukin diftitox treatment. |
| 8195 | 22730534 | This is accompanied by an increased IFN-γ production of autoreactive splenic cells and a decreased presence of regulatory CD4(+)CD25(+)Foxp3(+) T cells. |
| 8196 | 22730534 | In contrast, transfer of CD4(+)CD25(+)Foxp3(+) T cells could correct the defect after denileukin diftitox treatment. |
| 8197 | 22733483 | On the other hand, a differential role for CD4(+) Th1 and CD4(+) Th2 cells has been suggested. |
| 8198 | 22733769 | IL-7 increases, whereas IL-7Rα antibody therapy reduces, the IFN-γ-producing CD4(+) (T(H)1) and IFN-γ-producing CD8(+) T cells. |
| 8199 | 22733769 | Conversely, IL-7 decreases and IL-7Rα antibody enhances the inhibitory receptor Programmed Death 1 (PD-1) expression in the effector T cells. |
| 8200 | 22789848 | Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells. |
| 8201 | 22789848 | The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. |
| 8202 | 22789848 | Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl. |
| 8203 | 22789848 | Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. |
| 8204 | 22789848 | Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells. |
| 8205 | 22789848 | Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells. |
| 8206 | 22789848 | The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. |
| 8207 | 22789848 | Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl. |
| 8208 | 22789848 | Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. |
| 8209 | 22789848 | Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells. |
| 8210 | 22789848 | Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells. |
| 8211 | 22789848 | The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. |
| 8212 | 22789848 | Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl. |
| 8213 | 22789848 | Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. |
| 8214 | 22789848 | Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells. |
| 8215 | 22789848 | Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells. |
| 8216 | 22789848 | The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. |
| 8217 | 22789848 | Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl. |
| 8218 | 22789848 | Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. |
| 8219 | 22789848 | Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells. |
| 8220 | 22789848 | Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells. |
| 8221 | 22789848 | The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. |
| 8222 | 22789848 | Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl. |
| 8223 | 22789848 | Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. |
| 8224 | 22789848 | Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells. |
| 8225 | 22794701 | Type IV has four major categories: type IVa is CD4(+)Th1 lymphocyte mediated with activation of macrophages (granuloma formation and type I diabetes mellitus); type IVb is CD4(+)Th2 lymphocyte mediated with eosinophilic involvement (persistent asthma and allergic rhinitis); type IVc is cytotoxic CD8(+) T lymphocyte with involvement of perforin-granzme B in apoptosis (Stevens-Johnson syndrome and toxic epidermal necrolysis); type IVd is T-lymphocyte-driven neutrophilic inflammation (pustular psoriasis and acute generalized exanthematous pustulosis). |
| 8226 | 22851544 | Cytokine therapy with interleukin-2/anti-interleukin-2 monoclonal antibody complexes expands CD4+CD25+Foxp3+ regulatory T cells and attenuates development and progression of atherosclerosis. |
| 8227 | 22864396 | Combination therapy with Rosiglitazone and Gemcitabine modulated T cell populations by enhancing circulating CD8(+) T cells and intra-tumoral CD4(+) and CD8(+) T cells while limiting T regulatory cells. |
| 8228 | 22865049 | IFN-γ receptor deficiency prevents diabetes induction by diabetogenic CD4+, but not CD8+, T cells. |
| 8229 | 22865049 | In the current study, an adoptive transfer model was employed to define the contribution of IFN-γ in CD4(+) versus CD8(+) T cell-mediated β-cell autoimmunity. |
| 8230 | 22865049 | On the other hand, CD4(+) T cells indirectly promoted β-cell destruction by providing help to CD8(+) T cells in NOD.scid.IFNγRB(null) recipients. |
| 8231 | 22865049 | IFN-γ receptor deficiency prevents diabetes induction by diabetogenic CD4+, but not CD8+, T cells. |
| 8232 | 22865049 | In the current study, an adoptive transfer model was employed to define the contribution of IFN-γ in CD4(+) versus CD8(+) T cell-mediated β-cell autoimmunity. |
| 8233 | 22865049 | On the other hand, CD4(+) T cells indirectly promoted β-cell destruction by providing help to CD8(+) T cells in NOD.scid.IFNγRB(null) recipients. |
| 8234 | 22865049 | IFN-γ receptor deficiency prevents diabetes induction by diabetogenic CD4+, but not CD8+, T cells. |
| 8235 | 22865049 | In the current study, an adoptive transfer model was employed to define the contribution of IFN-γ in CD4(+) versus CD8(+) T cell-mediated β-cell autoimmunity. |
| 8236 | 22865049 | On the other hand, CD4(+) T cells indirectly promoted β-cell destruction by providing help to CD8(+) T cells in NOD.scid.IFNγRB(null) recipients. |
| 8237 | 22903683 | Twenty-five consecutive middle-aged (<55 years) out-patients with CHD (acute myocardial infarction in the previous 3 months) and stable clinical conditions (>1 month) underwent venous blood sampling in order to determinate CD3+ (T-lymphocytes), CD19+ (B-lymphocytes), CD4+ (helper/inducer lymphocytes) and CD8+ (suppressor/cytotoxic lymphocytes) populations. |
| 8238 | 22903683 | CHD patients showed lower CD3+ levels (70.96 ± 4.72 vs. 74.12 ± 4.93 %, p < 0.05) and CD8+ (37.80 ± 7.15 vs. 46.36 ± 5.22 %, p < 0.001) but higher CD4+ (37.32 ± 7.99 vs. 31.64 ± 4.72 %, p < 0.01) and CD4+/CD8+ ratio (1.06 ± 0.43 vs. 0.69 ± 0.13, p < 0.001). |
| 8239 | 22903683 | Subjects with an impaired (≤55 %) left ventricular ejection fraction were characterized by lower levels of CD8+ (33.23 ± 7.04 vs. 43.76 ± 7.40 %, p < 0.05) and higher levels of CD4+ (38.31 ± 8.23 vs. 32.73 ± 6.08 %, p < 0.05) and CD4+/CD8+ ratio (1.06 ± 0.38 vs. 0.79 ± 0.34, p < 0.05). |
| 8240 | 22903683 | In conclusion, subjects with early clinical presentation of CHD are characterized by an altered CD4+/CD8+ ratio and lower CD3+ levels. |
| 8241 | 22903683 | Twenty-five consecutive middle-aged (<55 years) out-patients with CHD (acute myocardial infarction in the previous 3 months) and stable clinical conditions (>1 month) underwent venous blood sampling in order to determinate CD3+ (T-lymphocytes), CD19+ (B-lymphocytes), CD4+ (helper/inducer lymphocytes) and CD8+ (suppressor/cytotoxic lymphocytes) populations. |
| 8242 | 22903683 | CHD patients showed lower CD3+ levels (70.96 ± 4.72 vs. 74.12 ± 4.93 %, p < 0.05) and CD8+ (37.80 ± 7.15 vs. 46.36 ± 5.22 %, p < 0.001) but higher CD4+ (37.32 ± 7.99 vs. 31.64 ± 4.72 %, p < 0.01) and CD4+/CD8+ ratio (1.06 ± 0.43 vs. 0.69 ± 0.13, p < 0.001). |
| 8243 | 22903683 | Subjects with an impaired (≤55 %) left ventricular ejection fraction were characterized by lower levels of CD8+ (33.23 ± 7.04 vs. 43.76 ± 7.40 %, p < 0.05) and higher levels of CD4+ (38.31 ± 8.23 vs. 32.73 ± 6.08 %, p < 0.05) and CD4+/CD8+ ratio (1.06 ± 0.38 vs. 0.79 ± 0.34, p < 0.05). |
| 8244 | 22903683 | In conclusion, subjects with early clinical presentation of CHD are characterized by an altered CD4+/CD8+ ratio and lower CD3+ levels. |
| 8245 | 22903683 | Twenty-five consecutive middle-aged (<55 years) out-patients with CHD (acute myocardial infarction in the previous 3 months) and stable clinical conditions (>1 month) underwent venous blood sampling in order to determinate CD3+ (T-lymphocytes), CD19+ (B-lymphocytes), CD4+ (helper/inducer lymphocytes) and CD8+ (suppressor/cytotoxic lymphocytes) populations. |
| 8246 | 22903683 | CHD patients showed lower CD3+ levels (70.96 ± 4.72 vs. 74.12 ± 4.93 %, p < 0.05) and CD8+ (37.80 ± 7.15 vs. 46.36 ± 5.22 %, p < 0.001) but higher CD4+ (37.32 ± 7.99 vs. 31.64 ± 4.72 %, p < 0.01) and CD4+/CD8+ ratio (1.06 ± 0.43 vs. 0.69 ± 0.13, p < 0.001). |
| 8247 | 22903683 | Subjects with an impaired (≤55 %) left ventricular ejection fraction were characterized by lower levels of CD8+ (33.23 ± 7.04 vs. 43.76 ± 7.40 %, p < 0.05) and higher levels of CD4+ (38.31 ± 8.23 vs. 32.73 ± 6.08 %, p < 0.05) and CD4+/CD8+ ratio (1.06 ± 0.38 vs. 0.79 ± 0.34, p < 0.05). |
| 8248 | 22903683 | In conclusion, subjects with early clinical presentation of CHD are characterized by an altered CD4+/CD8+ ratio and lower CD3+ levels. |
| 8249 | 22903683 | Twenty-five consecutive middle-aged (<55 years) out-patients with CHD (acute myocardial infarction in the previous 3 months) and stable clinical conditions (>1 month) underwent venous blood sampling in order to determinate CD3+ (T-lymphocytes), CD19+ (B-lymphocytes), CD4+ (helper/inducer lymphocytes) and CD8+ (suppressor/cytotoxic lymphocytes) populations. |
| 8250 | 22903683 | CHD patients showed lower CD3+ levels (70.96 ± 4.72 vs. 74.12 ± 4.93 %, p < 0.05) and CD8+ (37.80 ± 7.15 vs. 46.36 ± 5.22 %, p < 0.001) but higher CD4+ (37.32 ± 7.99 vs. 31.64 ± 4.72 %, p < 0.01) and CD4+/CD8+ ratio (1.06 ± 0.43 vs. 0.69 ± 0.13, p < 0.001). |
| 8251 | 22903683 | Subjects with an impaired (≤55 %) left ventricular ejection fraction were characterized by lower levels of CD8+ (33.23 ± 7.04 vs. 43.76 ± 7.40 %, p < 0.05) and higher levels of CD4+ (38.31 ± 8.23 vs. 32.73 ± 6.08 %, p < 0.05) and CD4+/CD8+ ratio (1.06 ± 0.38 vs. 0.79 ± 0.34, p < 0.05). |
| 8252 | 22903683 | In conclusion, subjects with early clinical presentation of CHD are characterized by an altered CD4+/CD8+ ratio and lower CD3+ levels. |
| 8253 | 22912420 | Chromogranin A (ChgA) has been identified as the antigen target for three NOD-derived, diabetogenic CD4 T-cell clones, including the well-known BDC-2.5. |
| 8254 | 22912420 | The WE14 responses of three NOD-derived CD4 T-cell clones, each with different T-cell receptors (TCRs), and of T cells from BDC-2.5 TCR transgenic mice are increased after TGase conversion of the peptide. |
| 8255 | 22912420 | Primary CD4 T cells isolated from NOD mice also respond to high concentrations of WE14 and significantly lower concentrations of TGase-treated WE14. |
| 8256 | 22912420 | Chromogranin A (ChgA) has been identified as the antigen target for three NOD-derived, diabetogenic CD4 T-cell clones, including the well-known BDC-2.5. |
| 8257 | 22912420 | The WE14 responses of three NOD-derived CD4 T-cell clones, each with different T-cell receptors (TCRs), and of T cells from BDC-2.5 TCR transgenic mice are increased after TGase conversion of the peptide. |
| 8258 | 22912420 | Primary CD4 T cells isolated from NOD mice also respond to high concentrations of WE14 and significantly lower concentrations of TGase-treated WE14. |
| 8259 | 22912420 | Chromogranin A (ChgA) has been identified as the antigen target for three NOD-derived, diabetogenic CD4 T-cell clones, including the well-known BDC-2.5. |
| 8260 | 22912420 | The WE14 responses of three NOD-derived CD4 T-cell clones, each with different T-cell receptors (TCRs), and of T cells from BDC-2.5 TCR transgenic mice are increased after TGase conversion of the peptide. |
| 8261 | 22912420 | Primary CD4 T cells isolated from NOD mice also respond to high concentrations of WE14 and significantly lower concentrations of TGase-treated WE14. |
| 8262 | 22966003 | Foxp3(+) CD4(+) T helper cells called regulatory T (T reg) cells play a key role in controlling reactivity to self-antigens and onset of autoimmunity. |
| 8263 | 22983906 | G6PC2, also known as islet-specific glucose 6-phosphatase catalytic subunit-related protein (IGRP), is a major target of autoreactive CD8(+) T cells in both diabetic human subjects and the non-obese diabetic (NOD) mouse. |
| 8264 | 22983906 | However, in contrast to the abundant literature regarding the CD8(+) response to this antigen, much less is known about the potential involvement of IGRP-reactive CD4(+) T cells in diabetogenesis. |
| 8265 | 22983906 | To address this issue, we immunized NOD mice with membranes from insect cells overexpressing full-length recombinant mouse IGRP and measured recall responses of purified CD4(+) T cells using a library of overlapping peptides encompassing the entire 355-aa primary sequence. |
| 8266 | 22983906 | G6PC2, also known as islet-specific glucose 6-phosphatase catalytic subunit-related protein (IGRP), is a major target of autoreactive CD8(+) T cells in both diabetic human subjects and the non-obese diabetic (NOD) mouse. |
| 8267 | 22983906 | However, in contrast to the abundant literature regarding the CD8(+) response to this antigen, much less is known about the potential involvement of IGRP-reactive CD4(+) T cells in diabetogenesis. |
| 8268 | 22983906 | To address this issue, we immunized NOD mice with membranes from insect cells overexpressing full-length recombinant mouse IGRP and measured recall responses of purified CD4(+) T cells using a library of overlapping peptides encompassing the entire 355-aa primary sequence. |
| 8269 | 22984077 | We used ONX 0914-treated wild-type CD4(+) T cells and also LMP7(-/-) CD4(+) T cells under different Th cell-polarizing conditions, focusing on the effector cytokines and transcription factors involved, and compared them with wild-type CD4(+) T cells. |
| 8270 | 23027613 | While ODNR01 shows no effect on diabetes in lymphocyte-free Rag1-deficient DIO mice, it enhances glucose tolerance and insulin sensitivity in CD4(+) T-cell-reconstituted Rag1-deficient DIO mice, suggesting its beneficial effect on insulin resistance is T-cell-dependent. |
| 8271 | 23065740 | This protection is peptide-restricted, independent of IL-10 secretion by DCs and of CD4(+) T cells. |
| 8272 | 23142275 | Cyclophosphamide (CY) in the dose of 175 mg/kg b.w. eliminated CD4+Foxp3+ regulatory T cells (Tregs) and enhanced disease severity in C57/BL6 mice, but it did not overcome resistance to diabetes in BALB/c mice and did not affect diabetes progression in ST2 knock-out (ST2KO) mice. |
| 8273 | 23142275 | This treatment eliminated Tregs in pancreatic lymph nodes in ST2KO mice, while markedly increasing the influx of CD8+, CD4+TNF-α+, and CD4+IFN-γ+ effector T cells (Teffs) in pancreata. |
| 8274 | 23142275 | Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation. |
| 8275 | 23142275 | Cyclophosphamide (CY) in the dose of 175 mg/kg b.w. eliminated CD4+Foxp3+ regulatory T cells (Tregs) and enhanced disease severity in C57/BL6 mice, but it did not overcome resistance to diabetes in BALB/c mice and did not affect diabetes progression in ST2 knock-out (ST2KO) mice. |
| 8276 | 23142275 | This treatment eliminated Tregs in pancreatic lymph nodes in ST2KO mice, while markedly increasing the influx of CD8+, CD4+TNF-α+, and CD4+IFN-γ+ effector T cells (Teffs) in pancreata. |
| 8277 | 23142275 | Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation. |
| 8278 | 23142275 | Cyclophosphamide (CY) in the dose of 175 mg/kg b.w. eliminated CD4+Foxp3+ regulatory T cells (Tregs) and enhanced disease severity in C57/BL6 mice, but it did not overcome resistance to diabetes in BALB/c mice and did not affect diabetes progression in ST2 knock-out (ST2KO) mice. |
| 8279 | 23142275 | This treatment eliminated Tregs in pancreatic lymph nodes in ST2KO mice, while markedly increasing the influx of CD8+, CD4+TNF-α+, and CD4+IFN-γ+ effector T cells (Teffs) in pancreata. |
| 8280 | 23142275 | Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation. |
| 8281 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 8282 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 8283 | 23180662 | A reduction in Il2 transcription results in impaired FoxP3(+) CD4(+) Treg-cell recruitment and function, and accounts for the association between murine Il2 and type 1 diabetes (T1D). |
| 8284 | 23180662 | The progression of T1D elicits a disease-countering negative feedback regulatory loop that involves the differentiation of low-avidity autoreactive CD8(+) T cells into memory-like autoregulatory T cells in a CD4(+) Th-dependent manner. |
| 8285 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 8286 | 23180662 | Surprisingly, we also find that a reduction in IL-2 production capacity increases memory autoregulatory CD8(+) T-cell formation indirectly, by decreasing the development and function of FoxP3(+) Treg cells in nonobese diabetic mice. |
| 8287 | 23180662 | These results illustrate a complex homeostatic interplay between IL-2, CD4(+) Th cells, FoxP3(+) CD4(+) Treg cells and autoregulatory CD8(+) T-cell memory whereby IL-2 controls the function of both Treg-cell subsets, but IL-2-potentiation of FoxP3(+) CD4(+) Treg-cell function results in the suppression of CD4(+) Th-cell activation and autoregulatory memory CD8(+) T-cell formation. |
| 8288 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 8289 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 8290 | 23180662 | A reduction in Il2 transcription results in impaired FoxP3(+) CD4(+) Treg-cell recruitment and function, and accounts for the association between murine Il2 and type 1 diabetes (T1D). |
| 8291 | 23180662 | The progression of T1D elicits a disease-countering negative feedback regulatory loop that involves the differentiation of low-avidity autoreactive CD8(+) T cells into memory-like autoregulatory T cells in a CD4(+) Th-dependent manner. |
| 8292 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 8293 | 23180662 | Surprisingly, we also find that a reduction in IL-2 production capacity increases memory autoregulatory CD8(+) T-cell formation indirectly, by decreasing the development and function of FoxP3(+) Treg cells in nonobese diabetic mice. |
| 8294 | 23180662 | These results illustrate a complex homeostatic interplay between IL-2, CD4(+) Th cells, FoxP3(+) CD4(+) Treg cells and autoregulatory CD8(+) T-cell memory whereby IL-2 controls the function of both Treg-cell subsets, but IL-2-potentiation of FoxP3(+) CD4(+) Treg-cell function results in the suppression of CD4(+) Th-cell activation and autoregulatory memory CD8(+) T-cell formation. |
| 8295 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 8296 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 8297 | 23180662 | A reduction in Il2 transcription results in impaired FoxP3(+) CD4(+) Treg-cell recruitment and function, and accounts for the association between murine Il2 and type 1 diabetes (T1D). |
| 8298 | 23180662 | The progression of T1D elicits a disease-countering negative feedback regulatory loop that involves the differentiation of low-avidity autoreactive CD8(+) T cells into memory-like autoregulatory T cells in a CD4(+) Th-dependent manner. |
| 8299 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 8300 | 23180662 | Surprisingly, we also find that a reduction in IL-2 production capacity increases memory autoregulatory CD8(+) T-cell formation indirectly, by decreasing the development and function of FoxP3(+) Treg cells in nonobese diabetic mice. |
| 8301 | 23180662 | These results illustrate a complex homeostatic interplay between IL-2, CD4(+) Th cells, FoxP3(+) CD4(+) Treg cells and autoregulatory CD8(+) T-cell memory whereby IL-2 controls the function of both Treg-cell subsets, but IL-2-potentiation of FoxP3(+) CD4(+) Treg-cell function results in the suppression of CD4(+) Th-cell activation and autoregulatory memory CD8(+) T-cell formation. |
| 8302 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 8303 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 8304 | 23180662 | A reduction in Il2 transcription results in impaired FoxP3(+) CD4(+) Treg-cell recruitment and function, and accounts for the association between murine Il2 and type 1 diabetes (T1D). |
| 8305 | 23180662 | The progression of T1D elicits a disease-countering negative feedback regulatory loop that involves the differentiation of low-avidity autoreactive CD8(+) T cells into memory-like autoregulatory T cells in a CD4(+) Th-dependent manner. |
| 8306 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 8307 | 23180662 | Surprisingly, we also find that a reduction in IL-2 production capacity increases memory autoregulatory CD8(+) T-cell formation indirectly, by decreasing the development and function of FoxP3(+) Treg cells in nonobese diabetic mice. |
| 8308 | 23180662 | These results illustrate a complex homeostatic interplay between IL-2, CD4(+) Th cells, FoxP3(+) CD4(+) Treg cells and autoregulatory CD8(+) T-cell memory whereby IL-2 controls the function of both Treg-cell subsets, but IL-2-potentiation of FoxP3(+) CD4(+) Treg-cell function results in the suppression of CD4(+) Th-cell activation and autoregulatory memory CD8(+) T-cell formation. |
| 8309 | 23195956 | Consistent with the hypothesis that anti-clade B serpin activity blocks the serpin from binding, exposure to exogenous anti-serpin B13 mAb or endogenous anti-serpin B13 autoantibodies resulted in cleavage of the surface molecules CD4 and CD19 in lymphocytes that accumulated in the pancreatic islets and pancreatic lymph nodes but not in the inguinal lymph nodes. |
| 8310 | 23200226 | One set, called type A, reacted like conventional CD4 T cells, recognizing both processed insulin protein and soluble B:9-23 peptide presented by APC. |
| 8311 | 23200226 | The second set, called type B, did not recognize processed insulin protein presented by APC, but reacted strongly to the presentation of soluble B:9-23 peptide. |
| 8312 | 23200226 | In the islets of Langerhans, beta cells constitutively generated proteolyzed peptides from insulin, which were taken up by intra-islet APC and presented to peptide-specific type B T cells. |
| 8313 | 23246831 | T1D is an autoimmune disorder, which involves the CD4(+) as well as CD8(+) T-cell-mediated destruction of β cells. |
| 8314 | 23246831 | In addition, the altered function of APCs and a subset of monocytes which spontaneously secrete IL-1β and IL-6 in T1D determine the abnormal expansion of Th17 as well. |
| 8315 | 23251685 | Autoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage. |
| 8316 | 23251685 | Islet transplantation provides a "cure" for type 1 diabetes but is limited in part by recurrent autoimmunity mediated by β cell-specific CD4(+) and CD8(+) T cells. |
| 8317 | 23251685 | Naïve CD4(+) and CD8(+) T cells exhibited a diverse TCR repertoire, which was similar in all tissues examined in NOD recipients including the pancreas and islet grafts. |
| 8318 | 23251685 | Similarly, islet graft- infiltrating effector/memory CD4(+) T cells expressed a limited number of prevalent TCR Vβ chains, although generally TCR repertoire diversity was increased compared to effector/memory CD8(+) T cells. |
| 8319 | 23251685 | Importantly, TCR Vβ usage by effector/memory CD4(+) and CD8(+) T cells infiltrating the islet graft exhibited greater similarity to the repertoire found in the pancreas as opposed to the draining renal lymph node, pancreatic lymph node, or spleen. |
| 8320 | 23251685 | Together these results demonstrate that effector/memory CD4(+) and CD8(+) T cells mediating autoimmune rejection of islet grafts are characterized by restricted TCR Vβ chain usage, and are similar to T cells that drive destruction of the endogenous islets. |
| 8321 | 23251685 | Autoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage. |
| 8322 | 23251685 | Islet transplantation provides a "cure" for type 1 diabetes but is limited in part by recurrent autoimmunity mediated by β cell-specific CD4(+) and CD8(+) T cells. |
| 8323 | 23251685 | Naïve CD4(+) and CD8(+) T cells exhibited a diverse TCR repertoire, which was similar in all tissues examined in NOD recipients including the pancreas and islet grafts. |
| 8324 | 23251685 | Similarly, islet graft- infiltrating effector/memory CD4(+) T cells expressed a limited number of prevalent TCR Vβ chains, although generally TCR repertoire diversity was increased compared to effector/memory CD8(+) T cells. |
| 8325 | 23251685 | Importantly, TCR Vβ usage by effector/memory CD4(+) and CD8(+) T cells infiltrating the islet graft exhibited greater similarity to the repertoire found in the pancreas as opposed to the draining renal lymph node, pancreatic lymph node, or spleen. |
| 8326 | 23251685 | Together these results demonstrate that effector/memory CD4(+) and CD8(+) T cells mediating autoimmune rejection of islet grafts are characterized by restricted TCR Vβ chain usage, and are similar to T cells that drive destruction of the endogenous islets. |
| 8327 | 23251685 | Autoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage. |
| 8328 | 23251685 | Islet transplantation provides a "cure" for type 1 diabetes but is limited in part by recurrent autoimmunity mediated by β cell-specific CD4(+) and CD8(+) T cells. |
| 8329 | 23251685 | Naïve CD4(+) and CD8(+) T cells exhibited a diverse TCR repertoire, which was similar in all tissues examined in NOD recipients including the pancreas and islet grafts. |
| 8330 | 23251685 | Similarly, islet graft- infiltrating effector/memory CD4(+) T cells expressed a limited number of prevalent TCR Vβ chains, although generally TCR repertoire diversity was increased compared to effector/memory CD8(+) T cells. |
| 8331 | 23251685 | Importantly, TCR Vβ usage by effector/memory CD4(+) and CD8(+) T cells infiltrating the islet graft exhibited greater similarity to the repertoire found in the pancreas as opposed to the draining renal lymph node, pancreatic lymph node, or spleen. |
| 8332 | 23251685 | Together these results demonstrate that effector/memory CD4(+) and CD8(+) T cells mediating autoimmune rejection of islet grafts are characterized by restricted TCR Vβ chain usage, and are similar to T cells that drive destruction of the endogenous islets. |
| 8333 | 23251685 | Autoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage. |
| 8334 | 23251685 | Islet transplantation provides a "cure" for type 1 diabetes but is limited in part by recurrent autoimmunity mediated by β cell-specific CD4(+) and CD8(+) T cells. |
| 8335 | 23251685 | Naïve CD4(+) and CD8(+) T cells exhibited a diverse TCR repertoire, which was similar in all tissues examined in NOD recipients including the pancreas and islet grafts. |
| 8336 | 23251685 | Similarly, islet graft- infiltrating effector/memory CD4(+) T cells expressed a limited number of prevalent TCR Vβ chains, although generally TCR repertoire diversity was increased compared to effector/memory CD8(+) T cells. |
| 8337 | 23251685 | Importantly, TCR Vβ usage by effector/memory CD4(+) and CD8(+) T cells infiltrating the islet graft exhibited greater similarity to the repertoire found in the pancreas as opposed to the draining renal lymph node, pancreatic lymph node, or spleen. |
| 8338 | 23251685 | Together these results demonstrate that effector/memory CD4(+) and CD8(+) T cells mediating autoimmune rejection of islet grafts are characterized by restricted TCR Vβ chain usage, and are similar to T cells that drive destruction of the endogenous islets. |
| 8339 | 23251685 | Autoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage. |
| 8340 | 23251685 | Islet transplantation provides a "cure" for type 1 diabetes but is limited in part by recurrent autoimmunity mediated by β cell-specific CD4(+) and CD8(+) T cells. |
| 8341 | 23251685 | Naïve CD4(+) and CD8(+) T cells exhibited a diverse TCR repertoire, which was similar in all tissues examined in NOD recipients including the pancreas and islet grafts. |
| 8342 | 23251685 | Similarly, islet graft- infiltrating effector/memory CD4(+) T cells expressed a limited number of prevalent TCR Vβ chains, although generally TCR repertoire diversity was increased compared to effector/memory CD8(+) T cells. |
| 8343 | 23251685 | Importantly, TCR Vβ usage by effector/memory CD4(+) and CD8(+) T cells infiltrating the islet graft exhibited greater similarity to the repertoire found in the pancreas as opposed to the draining renal lymph node, pancreatic lymph node, or spleen. |
| 8344 | 23251685 | Together these results demonstrate that effector/memory CD4(+) and CD8(+) T cells mediating autoimmune rejection of islet grafts are characterized by restricted TCR Vβ chain usage, and are similar to T cells that drive destruction of the endogenous islets. |
| 8345 | 23251685 | Autoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage. |
| 8346 | 23251685 | Islet transplantation provides a "cure" for type 1 diabetes but is limited in part by recurrent autoimmunity mediated by β cell-specific CD4(+) and CD8(+) T cells. |
| 8347 | 23251685 | Naïve CD4(+) and CD8(+) T cells exhibited a diverse TCR repertoire, which was similar in all tissues examined in NOD recipients including the pancreas and islet grafts. |
| 8348 | 23251685 | Similarly, islet graft- infiltrating effector/memory CD4(+) T cells expressed a limited number of prevalent TCR Vβ chains, although generally TCR repertoire diversity was increased compared to effector/memory CD8(+) T cells. |
| 8349 | 23251685 | Importantly, TCR Vβ usage by effector/memory CD4(+) and CD8(+) T cells infiltrating the islet graft exhibited greater similarity to the repertoire found in the pancreas as opposed to the draining renal lymph node, pancreatic lymph node, or spleen. |
| 8350 | 23251685 | Together these results demonstrate that effector/memory CD4(+) and CD8(+) T cells mediating autoimmune rejection of islet grafts are characterized by restricted TCR Vβ chain usage, and are similar to T cells that drive destruction of the endogenous islets. |
| 8351 | 23261674 | Low-dose alcohol administration reversed the immune response, decreasing inflammatory responses and the increment of adaptive immunity mainly related to CD4(+) T cells, but not CD8(+) T cells, to normal background levels. |
| 8352 | 23291488 | IPEX (immune dysregulation, polyendocrinopathy, enteropathy, and X-linked) syndrome is a rare immune disorder characterized by endocrinopathy such as insulin-dependent diabetes and hypothyroidism, intractable diarrhea, and recurrent infections. |
| 8353 | 23291488 | Having suffered from insulin-dependent diabetes since age two with hypothyroidism developing one year later, her clinical symptoms were quite reminiscent of IPEX syndrome. |
| 8354 | 23291488 | Although flow cytometry analysis revealed low expression of Foxp3 in CD4(+)CD25(+) T cells compared with healthy controls, no genetic mutation was found in the FOXP3 gene. |
| 8355 | 23293979 | Transient depletion of CD4+ CD25+ regulatory T cells results in multiple autoimmune diseases in wild-type and B-cell-deficient NOD mice. |
| 8356 | 23293979 | Under normal conditions, activation of self-reactive T cells in the periphery is limited by CD4(+) CD25(+) natural regulatory T (Treg) cells. |
| 8357 | 23293979 | To test the hypothesis that increased Treg cell activity in B(-/-) mice contributes to their resistance to other autoimmune diseases, WT and B(-/-) NOD mice were given anti-CD25 to transiently deplete CD4(+) CD25(+) Treg cells. |
| 8358 | 23293979 | Transient depletion of CD4+ CD25+ regulatory T cells results in multiple autoimmune diseases in wild-type and B-cell-deficient NOD mice. |
| 8359 | 23293979 | Under normal conditions, activation of self-reactive T cells in the periphery is limited by CD4(+) CD25(+) natural regulatory T (Treg) cells. |
| 8360 | 23293979 | To test the hypothesis that increased Treg cell activity in B(-/-) mice contributes to their resistance to other autoimmune diseases, WT and B(-/-) NOD mice were given anti-CD25 to transiently deplete CD4(+) CD25(+) Treg cells. |
| 8361 | 23293979 | Transient depletion of CD4+ CD25+ regulatory T cells results in multiple autoimmune diseases in wild-type and B-cell-deficient NOD mice. |
| 8362 | 23293979 | Under normal conditions, activation of self-reactive T cells in the periphery is limited by CD4(+) CD25(+) natural regulatory T (Treg) cells. |
| 8363 | 23293979 | To test the hypothesis that increased Treg cell activity in B(-/-) mice contributes to their resistance to other autoimmune diseases, WT and B(-/-) NOD mice were given anti-CD25 to transiently deplete CD4(+) CD25(+) Treg cells. |
| 8364 | 23306367 | Advax™ provided antigen-sparing, significantly enhanced both anti-HBs antibody titers, and anti-HBs CD4 and CD8 T-cells, with increases in Th1, Th2 and Th17 cytokine responses. |
| 8365 | 23349493 | We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. |
| 8366 | 23349493 | Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. |
| 8367 | 23349493 | VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. |
| 8368 | 23349493 | Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. |
| 8369 | 23349493 | In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. |
| 8370 | 23349493 | Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. |
| 8371 | 23395729 | Loss of the balance between CD4(+)Foxp3(+) regulatory T cells and CD4(+)IL17A(+) Th17 cells in patients with type 1 diabetes. |
| 8372 | 23396943 | The data show that 1) insulin is captured and rapidly internalized by 125Tg BCRs, 2) these Ag-exposed B cells are competent to activate both experienced and naive CD4(+) T cells, 3) anergic 125Tg B cells are more efficient than naive B cells at activating T cells when Ag is limiting, and 4) 125Tg B cells are competent to generate low-affinity insulin B chain epitopes necessary for activation of diabetogenic anti-insulin BDC12-4.1 T cells, indicating the pathological relevance of anergic B cells in type 1 diabetes. |
| 8373 | 23401506 | Here, we show that the antidiabetogenic MHC class II molecule I-A(b) affords diabetes resistance by promoting the differentiation of MHC-promiscuous autoreactive CD4(+) T cells into disease-suppressing natural regulatory T cells, in a β56-67-regulated manner. |
| 8374 | 23405091 | In the prevention studies, anti-CD20 plus proinsulin resulted in modest increases in Tregs in pancreatic lymph nodes and elevated levels of proinsulin-specific CD4+ T-cells that produced IL-4. |
| 8375 | 23405091 | Thus, combination therapy with anti-CD20 and either oral insulin or proinsulin does not protect hyperglycemic NOD mice, but the combination with proinsulin offers limited efficacy in T1D prevention, potentially by augmentation of proinsulin-specific IL-4 production. |
| 8376 | 23415873 | Stimulation of human T cells with PHA or CD3/CD28 induced IL-2 mRNA expression and activated the endoplasmic reticulum (ER) stress response. |
| 8377 | 23415873 | The treatment of T cells with curcumin induced the unfolded protein response (UPR) signaling pathway, initiated by the phosphorylation of PERK and IRE1. |
| 8378 | 23415873 | Furthermore, curcumin increased the expression of the ER stress associated transcriptional factors XBP-1, cleaved p50ATF6α and C/EBP homologous protein (CHOP) in human CD4+ and Jurkat T cells. |
| 8379 | 23415873 | In PHA-activated T cells, curcumin further enhanced PHA-induced CHOP expression and reduced the expression of the anti-apoptotic protein Bcl-2. |
| 8380 | 23418596 | Interestingly the mutation results in increased proportional representation of CD4(+)Foxp3(+) regulatory T cells and the absence of pathogenic CD4(+) T effectors. |
| 8381 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 8382 | 23418630 | In this study we present evidence that the frequency of naive CD4 T cells that express CD25 (IL-2 receptor α-chain) increases with age on subsets of both CD31(+) and CD31(-) naive CD4 T cells. |
| 8383 | 23418630 | Analyses of TCR excision circles from sorted subsets indicate that CD25(+) naive CD4 T cells have undergone more rounds of homeostatic proliferation than their CD25(-) counterparts in both the CD31(+) and CD31(-) subsets, indicating that CD25 is a marker of naive CD4 T cells that have preferentially responded to survival signals from self-Ags or cytokines. |
| 8384 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 8385 | 23418630 | Although CD25(+) naive T cells respond to lower concentrations of IL-2 as compared with their CD25(-) counterparts, IL-2 responsiveness is further increased in CD31(-) naive T cells by their expression of the signaling IL-2 receptor β-chain CD122, forming with common γ-chain functional high-affinity IL-2 receptors. |
| 8386 | 23418630 | CD25 plays a role during activation: CD25(+) naive T cells stimulated in an APC-dependent manner were shown to produce increased levels of IL-2 as compared with their CD25(-) counterparts. |
| 8387 | 23418630 | This study establishes CD25(+) naive CD4 T cells, which are further delineated by CD31 expression, as a major functionally distinct immune cell subset in humans that warrants further characterization in health and disease. |
| 8388 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 8389 | 23418630 | In this study we present evidence that the frequency of naive CD4 T cells that express CD25 (IL-2 receptor α-chain) increases with age on subsets of both CD31(+) and CD31(-) naive CD4 T cells. |
| 8390 | 23418630 | Analyses of TCR excision circles from sorted subsets indicate that CD25(+) naive CD4 T cells have undergone more rounds of homeostatic proliferation than their CD25(-) counterparts in both the CD31(+) and CD31(-) subsets, indicating that CD25 is a marker of naive CD4 T cells that have preferentially responded to survival signals from self-Ags or cytokines. |
| 8391 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 8392 | 23418630 | Although CD25(+) naive T cells respond to lower concentrations of IL-2 as compared with their CD25(-) counterparts, IL-2 responsiveness is further increased in CD31(-) naive T cells by their expression of the signaling IL-2 receptor β-chain CD122, forming with common γ-chain functional high-affinity IL-2 receptors. |
| 8393 | 23418630 | CD25 plays a role during activation: CD25(+) naive T cells stimulated in an APC-dependent manner were shown to produce increased levels of IL-2 as compared with their CD25(-) counterparts. |
| 8394 | 23418630 | This study establishes CD25(+) naive CD4 T cells, which are further delineated by CD31 expression, as a major functionally distinct immune cell subset in humans that warrants further characterization in health and disease. |
| 8395 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 8396 | 23418630 | In this study we present evidence that the frequency of naive CD4 T cells that express CD25 (IL-2 receptor α-chain) increases with age on subsets of both CD31(+) and CD31(-) naive CD4 T cells. |
| 8397 | 23418630 | Analyses of TCR excision circles from sorted subsets indicate that CD25(+) naive CD4 T cells have undergone more rounds of homeostatic proliferation than their CD25(-) counterparts in both the CD31(+) and CD31(-) subsets, indicating that CD25 is a marker of naive CD4 T cells that have preferentially responded to survival signals from self-Ags or cytokines. |
| 8398 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 8399 | 23418630 | Although CD25(+) naive T cells respond to lower concentrations of IL-2 as compared with their CD25(-) counterparts, IL-2 responsiveness is further increased in CD31(-) naive T cells by their expression of the signaling IL-2 receptor β-chain CD122, forming with common γ-chain functional high-affinity IL-2 receptors. |
| 8400 | 23418630 | CD25 plays a role during activation: CD25(+) naive T cells stimulated in an APC-dependent manner were shown to produce increased levels of IL-2 as compared with their CD25(-) counterparts. |
| 8401 | 23418630 | This study establishes CD25(+) naive CD4 T cells, which are further delineated by CD31 expression, as a major functionally distinct immune cell subset in humans that warrants further characterization in health and disease. |
| 8402 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 8403 | 23418630 | In this study we present evidence that the frequency of naive CD4 T cells that express CD25 (IL-2 receptor α-chain) increases with age on subsets of both CD31(+) and CD31(-) naive CD4 T cells. |
| 8404 | 23418630 | Analyses of TCR excision circles from sorted subsets indicate that CD25(+) naive CD4 T cells have undergone more rounds of homeostatic proliferation than their CD25(-) counterparts in both the CD31(+) and CD31(-) subsets, indicating that CD25 is a marker of naive CD4 T cells that have preferentially responded to survival signals from self-Ags or cytokines. |
| 8405 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 8406 | 23418630 | Although CD25(+) naive T cells respond to lower concentrations of IL-2 as compared with their CD25(-) counterparts, IL-2 responsiveness is further increased in CD31(-) naive T cells by their expression of the signaling IL-2 receptor β-chain CD122, forming with common γ-chain functional high-affinity IL-2 receptors. |
| 8407 | 23418630 | CD25 plays a role during activation: CD25(+) naive T cells stimulated in an APC-dependent manner were shown to produce increased levels of IL-2 as compared with their CD25(-) counterparts. |
| 8408 | 23418630 | This study establishes CD25(+) naive CD4 T cells, which are further delineated by CD31 expression, as a major functionally distinct immune cell subset in humans that warrants further characterization in health and disease. |
| 8409 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 8410 | 23418630 | In this study we present evidence that the frequency of naive CD4 T cells that express CD25 (IL-2 receptor α-chain) increases with age on subsets of both CD31(+) and CD31(-) naive CD4 T cells. |
| 8411 | 23418630 | Analyses of TCR excision circles from sorted subsets indicate that CD25(+) naive CD4 T cells have undergone more rounds of homeostatic proliferation than their CD25(-) counterparts in both the CD31(+) and CD31(-) subsets, indicating that CD25 is a marker of naive CD4 T cells that have preferentially responded to survival signals from self-Ags or cytokines. |
| 8412 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 8413 | 23418630 | Although CD25(+) naive T cells respond to lower concentrations of IL-2 as compared with their CD25(-) counterparts, IL-2 responsiveness is further increased in CD31(-) naive T cells by their expression of the signaling IL-2 receptor β-chain CD122, forming with common γ-chain functional high-affinity IL-2 receptors. |
| 8414 | 23418630 | CD25 plays a role during activation: CD25(+) naive T cells stimulated in an APC-dependent manner were shown to produce increased levels of IL-2 as compared with their CD25(-) counterparts. |
| 8415 | 23418630 | This study establishes CD25(+) naive CD4 T cells, which are further delineated by CD31 expression, as a major functionally distinct immune cell subset in humans that warrants further characterization in health and disease. |
| 8416 | 23447122 | Of note, the oral anti-CD3 treatment induced a fraction of interleukin (IL)-10-producing CD4 T cells in the small intestine through IL-10- and IL-27-producing dendritic cells. |
| 8417 | 23461175 | The following of cells subsets: CD19+, CD3+, CD3+CD4+, CD3+CD8+, CD3-CD16+CD56+, CD3+CD16+CD56+, CD3+CD25+, CD3+HLA-DR+, CD45+CD95+ were investigated. |
| 8418 | 23461175 | In this research was establish the rise of immunoregulatory index (CD3+CD4+/CD3+CD8+) in consequence of decrease the percentages of cytotoxic T-lymphocytes in patients with DM2 and obesity in comparison with the healthy persons. |
| 8419 | 23461175 | The direct correlation was found between the increased quantity of NKT-cells (CD3+CD16+CD56+) and contain of triglicerides in the peripheral blood of patients with DM2. |
| 8420 | 23461175 | The following of cells subsets: CD19+, CD3+, CD3+CD4+, CD3+CD8+, CD3-CD16+CD56+, CD3+CD16+CD56+, CD3+CD25+, CD3+HLA-DR+, CD45+CD95+ were investigated. |
| 8421 | 23461175 | In this research was establish the rise of immunoregulatory index (CD3+CD4+/CD3+CD8+) in consequence of decrease the percentages of cytotoxic T-lymphocytes in patients with DM2 and obesity in comparison with the healthy persons. |
| 8422 | 23461175 | The direct correlation was found between the increased quantity of NKT-cells (CD3+CD16+CD56+) and contain of triglicerides in the peripheral blood of patients with DM2. |
| 8423 | 23466550 | Impact of culture medium on CD4(+) CD25(high)CD127(lo/neg) Treg expansion for the purpose of clinical application. |
| 8424 | 23466550 | We compared Treg fold of expansion and their phenotypical characteristics including expression of FoxP3, CD25, CD127, CD62L and CD45RA in three commercially available culture media (RPMI 1640 (Cellgro; Manassas VA, USA), SCGM (Cellgenix; Freiburg, Germany), and X-VIVO 20 (Lonza; Walkersville, MD, USA)) with addition of human serum (HS, 10%) or fetal bovine serum (FBS, 10%). |
| 8425 | 23466550 | Among the tested media, X-VIVO 20 supplemented with HS produced the highest yield after 17days of in vitro expansion (a median of 86-fold expansion, range 30-1365) and highest level of FoxP3 expression (a median of 66.8% of positive cells, range 56-84.8%) in CD4(+) CD25(hi)CD127(lo/neg) FACS sorted polyclonal Tregs. |
| 8426 | 23466550 | Impact of culture medium on CD4(+) CD25(high)CD127(lo/neg) Treg expansion for the purpose of clinical application. |
| 8427 | 23466550 | We compared Treg fold of expansion and their phenotypical characteristics including expression of FoxP3, CD25, CD127, CD62L and CD45RA in three commercially available culture media (RPMI 1640 (Cellgro; Manassas VA, USA), SCGM (Cellgenix; Freiburg, Germany), and X-VIVO 20 (Lonza; Walkersville, MD, USA)) with addition of human serum (HS, 10%) or fetal bovine serum (FBS, 10%). |
| 8428 | 23466550 | Among the tested media, X-VIVO 20 supplemented with HS produced the highest yield after 17days of in vitro expansion (a median of 86-fold expansion, range 30-1365) and highest level of FoxP3 expression (a median of 66.8% of positive cells, range 56-84.8%) in CD4(+) CD25(hi)CD127(lo/neg) FACS sorted polyclonal Tregs. |
| 8429 | 23469279 | Glucagon-like peptide-1(9-36) inhibits chemokine-induced migration of human CD4-positive lymphocytes. |
| 8430 | 23534927 | Obesity, a chronic, low-grade inflammatory disease, is associated with alterations of multiple immune-cell components in the visceral adipose tissue (VAT), in which CD4(+) Foxp3(+) regulatory T cells (Tregs) have been suggested to be a critical regulator. |
| 8431 | 23537861 | The interaction between the components of the trimolecular complex (CD4(+) T cell receptors, self-peptide, and MHC class II molecules) plays a pivotal role in autoimmune disease pathogenesis. |
| 8432 | 23537861 | This review focuses on the components of the anti-insulin trimolecular complex, registers of insulin peptide binding to 'diabetogenic' MHC class II molecules, and therapies targeting each component of the trimolecular complex. |
| 8433 | 23545706 | PD-1, but not PD-L1, expressed by islet-reactive CD4+ T cells suppresses infiltration of the pancreas during type 1 diabetes. |
| 8434 | 23545706 | However, how PD-1 influences diabetogenic CD4(+) T cells during natural diabetes is not fully understood. |
| 8435 | 23545706 | Transferred BDC2.5 T cells became activated, differentiated into T-bet(+) IFN-γ-producing cells, and infiltrated the pancreas. |
| 8436 | 23545706 | In this model, loss of PD-1, but not programmed death ligand-1 (PD-L1), on the antigen-specific CD4(+) T cell resulted in increased cell numbers in the spleen, pancreas-draining lymph node, and pancreas. |
| 8437 | 23545706 | PD-1 deficiency also increased expression of the chemokine receptor CXCR3. |
| 8438 | 23545706 | These data support a model by which PD-1 regulates islet-reactive CD4(+) T cells in a cell intrinsic manner by suppressing proliferation, inhibiting infiltration of the pancreas, and limiting diabetes. |
| 8439 | 23545706 | PD-1, but not PD-L1, expressed by islet-reactive CD4+ T cells suppresses infiltration of the pancreas during type 1 diabetes. |
| 8440 | 23545706 | However, how PD-1 influences diabetogenic CD4(+) T cells during natural diabetes is not fully understood. |
| 8441 | 23545706 | Transferred BDC2.5 T cells became activated, differentiated into T-bet(+) IFN-γ-producing cells, and infiltrated the pancreas. |
| 8442 | 23545706 | In this model, loss of PD-1, but not programmed death ligand-1 (PD-L1), on the antigen-specific CD4(+) T cell resulted in increased cell numbers in the spleen, pancreas-draining lymph node, and pancreas. |
| 8443 | 23545706 | PD-1 deficiency also increased expression of the chemokine receptor CXCR3. |
| 8444 | 23545706 | These data support a model by which PD-1 regulates islet-reactive CD4(+) T cells in a cell intrinsic manner by suppressing proliferation, inhibiting infiltration of the pancreas, and limiting diabetes. |
| 8445 | 23545706 | PD-1, but not PD-L1, expressed by islet-reactive CD4+ T cells suppresses infiltration of the pancreas during type 1 diabetes. |
| 8446 | 23545706 | However, how PD-1 influences diabetogenic CD4(+) T cells during natural diabetes is not fully understood. |
| 8447 | 23545706 | Transferred BDC2.5 T cells became activated, differentiated into T-bet(+) IFN-γ-producing cells, and infiltrated the pancreas. |
| 8448 | 23545706 | In this model, loss of PD-1, but not programmed death ligand-1 (PD-L1), on the antigen-specific CD4(+) T cell resulted in increased cell numbers in the spleen, pancreas-draining lymph node, and pancreas. |
| 8449 | 23545706 | PD-1 deficiency also increased expression of the chemokine receptor CXCR3. |
| 8450 | 23545706 | These data support a model by which PD-1 regulates islet-reactive CD4(+) T cells in a cell intrinsic manner by suppressing proliferation, inhibiting infiltration of the pancreas, and limiting diabetes. |
| 8451 | 23545706 | PD-1, but not PD-L1, expressed by islet-reactive CD4+ T cells suppresses infiltration of the pancreas during type 1 diabetes. |
| 8452 | 23545706 | However, how PD-1 influences diabetogenic CD4(+) T cells during natural diabetes is not fully understood. |
| 8453 | 23545706 | Transferred BDC2.5 T cells became activated, differentiated into T-bet(+) IFN-γ-producing cells, and infiltrated the pancreas. |
| 8454 | 23545706 | In this model, loss of PD-1, but not programmed death ligand-1 (PD-L1), on the antigen-specific CD4(+) T cell resulted in increased cell numbers in the spleen, pancreas-draining lymph node, and pancreas. |
| 8455 | 23545706 | PD-1 deficiency also increased expression of the chemokine receptor CXCR3. |
| 8456 | 23545706 | These data support a model by which PD-1 regulates islet-reactive CD4(+) T cells in a cell intrinsic manner by suppressing proliferation, inhibiting infiltration of the pancreas, and limiting diabetes. |
| 8457 | 23562076 | Improved insulin sensitivity despite increased visceral adiposity in mice deficient for the immune cell transcription factor T-bet. |
| 8458 | 23562076 | We report that mice deficient in the immune cell transcription factor T-bet have lower energy expenditure and increased visceral fat compared with wild-type mice, yet paradoxically are more insulin sensitive. |
| 8459 | 23562076 | Indeed, adoptive transfer of T-bet-deficient, but not wild-type, CD4(+) T cells to Rag2(-/-) mice improved insulin sensitivity. |
| 8460 | 23562076 | Our results reveal a role for T-bet in metabolic physiology and obesity-associated insulin resistance. |
| 8461 | 23589231 | MicroRNA expressions in PMBCs, CD4+, and CD8+ T-cells from patients suffering from autoimmune Addison's disease. |
| 8462 | 23589231 | In CD4+ T-cells miRNA 181a*_1 (18.02 in AD vs. 11.99 in CG, p=0.0047) is significantly increased whereas miRNA 200a_1 (12.48 in AD vs. 19.40 in CG, p=0.0003) and miRNA 200a_2* (8.59 in AD vs. 17.94 in CG, p=0.0160) are significantly decreased. miRNA 200a_1 (12.37 in AD group vs. 18.12 in control group, p=0.001) and miRNA 200a_2* (10.72 in AD group vs. 17.84 in control group, p=0.022) are also significantly decreased in CD8+ T-cells. |
| 8463 | 23589231 | This study could show for the first time a significant change of three defined miRNAs in PBMCs, CD4+, and CD8+ T-cells of autoimmune AD patients in vivo. |
| 8464 | 23589231 | MicroRNA expressions in PMBCs, CD4+, and CD8+ T-cells from patients suffering from autoimmune Addison's disease. |
| 8465 | 23589231 | In CD4+ T-cells miRNA 181a*_1 (18.02 in AD vs. 11.99 in CG, p=0.0047) is significantly increased whereas miRNA 200a_1 (12.48 in AD vs. 19.40 in CG, p=0.0003) and miRNA 200a_2* (8.59 in AD vs. 17.94 in CG, p=0.0160) are significantly decreased. miRNA 200a_1 (12.37 in AD group vs. 18.12 in control group, p=0.001) and miRNA 200a_2* (10.72 in AD group vs. 17.84 in control group, p=0.022) are also significantly decreased in CD8+ T-cells. |
| 8466 | 23589231 | This study could show for the first time a significant change of three defined miRNAs in PBMCs, CD4+, and CD8+ T-cells of autoimmune AD patients in vivo. |
| 8467 | 23589231 | MicroRNA expressions in PMBCs, CD4+, and CD8+ T-cells from patients suffering from autoimmune Addison's disease. |
| 8468 | 23589231 | In CD4+ T-cells miRNA 181a*_1 (18.02 in AD vs. 11.99 in CG, p=0.0047) is significantly increased whereas miRNA 200a_1 (12.48 in AD vs. 19.40 in CG, p=0.0003) and miRNA 200a_2* (8.59 in AD vs. 17.94 in CG, p=0.0160) are significantly decreased. miRNA 200a_1 (12.37 in AD group vs. 18.12 in control group, p=0.001) and miRNA 200a_2* (10.72 in AD group vs. 17.84 in control group, p=0.022) are also significantly decreased in CD8+ T-cells. |
| 8469 | 23589231 | This study could show for the first time a significant change of three defined miRNAs in PBMCs, CD4+, and CD8+ T-cells of autoimmune AD patients in vivo. |
| 8470 | 23593036 | Functional IL6R 358Ala allele impairs classical IL-6 receptor signaling and influences risk of diverse inflammatory diseases. |
| 8471 | 23593036 | Although a common, non-synonymous variant in the IL-6 receptor gene (IL6R Asp358Ala; rs2228145 A>C) is associated with the risk of several common diseases, with the 358Ala allele conferring protection from coronary heart disease (CHD), rheumatoid arthritis (RA), atrial fibrillation (AF), abdominal aortic aneurysm (AAA), and increased susceptibility to asthma, the variant's effect on IL-6 signaling is not known. |
| 8472 | 23593036 | We demonstrate that, although 358Ala increases transcription of the soluble IL6R isoform (P = 8.3×10⁻²²) and not the membrane-bound isoform, 358Ala reduces surface expression of IL-6R on CD4+ T cells and monocytes (up to 28% reduction per allele; P≤5.6×10⁻²²). |
| 8473 | 23593036 | Importantly, reduced expression of membrane-bound IL-6R resulted in impaired IL-6 responsiveness, as measured by decreased phosphorylation of the transcription factors STAT3 and STAT1 following stimulation with IL-6 (P≤5.2×10⁻⁷). |
| 8474 | 23593036 | Our findings elucidate the regulation of IL-6 signaling by IL-6R, which is causally relevant to several complex diseases, identify mechanisms for new approaches to target the IL-6/IL-6R axis, and anticipate differences in treatment response to IL-6 therapies based on this common IL6R variant. |
| 8475 | 23600827 | Glutamic acid decarboxylase (GAD)(65) formulated with aluminium hydroxide (GAD-alum) was effective in preserving insulin secretion in a Phase II clinical trial in children and adolescents with recent-onset type 1 diabetes. |
| 8476 | 23600827 | In addition, GAD-alum treated patients increased CD4(+) CD25(hi) forkhead box protein 3(+) (FoxP3(+)) cell numbers in response to in-vitro GAD(65) stimulation. |
| 8477 | 23600827 | Regulatory T cells (CD4(+) CD25(hi) CD127(lo)) and effector T cells (CD4(+) CD25(-) CD127(+)) were further sorted, expanded and used in suppression assays to assess regulatory T cell function after GAD-alum treatment. |
| 8478 | 23600827 | GAD-alum-treated patients displayed higher frequencies of in-vitro GAD(65) -induced CD4(+) CD25(+) CD127(+) as well as CD4(+) CD25(hi) CD127(lo) and CD4(+) FoxP3(+) cells compared to placebo. |
| 8479 | 23600827 | Moreover, GAD(65) stimulation induced a population of CD4(hi) cells consisting mainly of CD25(+) CD127(+) , which was specific of GAD-alum-treated patients (16 of 25 versus one of 25 in placebo). |
| 8480 | 23600827 | In conclusion, GAD-alum treatment induced both GAD(65) -reactive CD25(+) CD127(+) and CD25(hi) CD127(lo) cells, but no difference in regulatory T cell function 4 years after GAD-alum treatment. |
| 8481 | 23600827 | Glutamic acid decarboxylase (GAD)(65) formulated with aluminium hydroxide (GAD-alum) was effective in preserving insulin secretion in a Phase II clinical trial in children and adolescents with recent-onset type 1 diabetes. |
| 8482 | 23600827 | In addition, GAD-alum treated patients increased CD4(+) CD25(hi) forkhead box protein 3(+) (FoxP3(+)) cell numbers in response to in-vitro GAD(65) stimulation. |
| 8483 | 23600827 | Regulatory T cells (CD4(+) CD25(hi) CD127(lo)) and effector T cells (CD4(+) CD25(-) CD127(+)) were further sorted, expanded and used in suppression assays to assess regulatory T cell function after GAD-alum treatment. |
| 8484 | 23600827 | GAD-alum-treated patients displayed higher frequencies of in-vitro GAD(65) -induced CD4(+) CD25(+) CD127(+) as well as CD4(+) CD25(hi) CD127(lo) and CD4(+) FoxP3(+) cells compared to placebo. |
| 8485 | 23600827 | Moreover, GAD(65) stimulation induced a population of CD4(hi) cells consisting mainly of CD25(+) CD127(+) , which was specific of GAD-alum-treated patients (16 of 25 versus one of 25 in placebo). |
| 8486 | 23600827 | In conclusion, GAD-alum treatment induced both GAD(65) -reactive CD25(+) CD127(+) and CD25(hi) CD127(lo) cells, but no difference in regulatory T cell function 4 years after GAD-alum treatment. |
| 8487 | 23600827 | Glutamic acid decarboxylase (GAD)(65) formulated with aluminium hydroxide (GAD-alum) was effective in preserving insulin secretion in a Phase II clinical trial in children and adolescents with recent-onset type 1 diabetes. |
| 8488 | 23600827 | In addition, GAD-alum treated patients increased CD4(+) CD25(hi) forkhead box protein 3(+) (FoxP3(+)) cell numbers in response to in-vitro GAD(65) stimulation. |
| 8489 | 23600827 | Regulatory T cells (CD4(+) CD25(hi) CD127(lo)) and effector T cells (CD4(+) CD25(-) CD127(+)) were further sorted, expanded and used in suppression assays to assess regulatory T cell function after GAD-alum treatment. |
| 8490 | 23600827 | GAD-alum-treated patients displayed higher frequencies of in-vitro GAD(65) -induced CD4(+) CD25(+) CD127(+) as well as CD4(+) CD25(hi) CD127(lo) and CD4(+) FoxP3(+) cells compared to placebo. |
| 8491 | 23600827 | Moreover, GAD(65) stimulation induced a population of CD4(hi) cells consisting mainly of CD25(+) CD127(+) , which was specific of GAD-alum-treated patients (16 of 25 versus one of 25 in placebo). |
| 8492 | 23600827 | In conclusion, GAD-alum treatment induced both GAD(65) -reactive CD25(+) CD127(+) and CD25(hi) CD127(lo) cells, but no difference in regulatory T cell function 4 years after GAD-alum treatment. |
| 8493 | 23600827 | Glutamic acid decarboxylase (GAD)(65) formulated with aluminium hydroxide (GAD-alum) was effective in preserving insulin secretion in a Phase II clinical trial in children and adolescents with recent-onset type 1 diabetes. |
| 8494 | 23600827 | In addition, GAD-alum treated patients increased CD4(+) CD25(hi) forkhead box protein 3(+) (FoxP3(+)) cell numbers in response to in-vitro GAD(65) stimulation. |
| 8495 | 23600827 | Regulatory T cells (CD4(+) CD25(hi) CD127(lo)) and effector T cells (CD4(+) CD25(-) CD127(+)) were further sorted, expanded and used in suppression assays to assess regulatory T cell function after GAD-alum treatment. |
| 8496 | 23600827 | GAD-alum-treated patients displayed higher frequencies of in-vitro GAD(65) -induced CD4(+) CD25(+) CD127(+) as well as CD4(+) CD25(hi) CD127(lo) and CD4(+) FoxP3(+) cells compared to placebo. |
| 8497 | 23600827 | Moreover, GAD(65) stimulation induced a population of CD4(hi) cells consisting mainly of CD25(+) CD127(+) , which was specific of GAD-alum-treated patients (16 of 25 versus one of 25 in placebo). |
| 8498 | 23600827 | In conclusion, GAD-alum treatment induced both GAD(65) -reactive CD25(+) CD127(+) and CD25(hi) CD127(lo) cells, but no difference in regulatory T cell function 4 years after GAD-alum treatment. |
| 8499 | 23607886 | CD4(+) forkhead box protein 3 (FoxP3)(+) T cells are composed of three phenotypically and functionally distinct subpopulations; CD45RA(+) FoxP3(low) resting T(regs) (r-T(regs)), CD45RA(-) FoxP3(high) activated T(regs) (a-T(regs)) and CD45RA(-) FoxP3(low) non-suppressive T cells (non-T(regs)). |
| 8500 | 23607886 | We aimed to clarify the frequency of these three subpopulations in CD4(+) FoxP3(+) T cells and the function of a-T(regs) with reference to subtypes of type 1 diabetes. |
| 8501 | 23607886 | Further, the proportion of a-T(regs) among CD4(+) FoxP3(+) T cells was significantly higher in patients with type 1A diabetes with detectable C-peptide but not in patients with type 1A diabetes without it and with fulminant type 1 diabetes. |
| 8502 | 23607886 | CD4(+) forkhead box protein 3 (FoxP3)(+) T cells are composed of three phenotypically and functionally distinct subpopulations; CD45RA(+) FoxP3(low) resting T(regs) (r-T(regs)), CD45RA(-) FoxP3(high) activated T(regs) (a-T(regs)) and CD45RA(-) FoxP3(low) non-suppressive T cells (non-T(regs)). |
| 8503 | 23607886 | We aimed to clarify the frequency of these three subpopulations in CD4(+) FoxP3(+) T cells and the function of a-T(regs) with reference to subtypes of type 1 diabetes. |
| 8504 | 23607886 | Further, the proportion of a-T(regs) among CD4(+) FoxP3(+) T cells was significantly higher in patients with type 1A diabetes with detectable C-peptide but not in patients with type 1A diabetes without it and with fulminant type 1 diabetes. |
| 8505 | 23607886 | CD4(+) forkhead box protein 3 (FoxP3)(+) T cells are composed of three phenotypically and functionally distinct subpopulations; CD45RA(+) FoxP3(low) resting T(regs) (r-T(regs)), CD45RA(-) FoxP3(high) activated T(regs) (a-T(regs)) and CD45RA(-) FoxP3(low) non-suppressive T cells (non-T(regs)). |
| 8506 | 23607886 | We aimed to clarify the frequency of these three subpopulations in CD4(+) FoxP3(+) T cells and the function of a-T(regs) with reference to subtypes of type 1 diabetes. |
| 8507 | 23607886 | Further, the proportion of a-T(regs) among CD4(+) FoxP3(+) T cells was significantly higher in patients with type 1A diabetes with detectable C-peptide but not in patients with type 1A diabetes without it and with fulminant type 1 diabetes. |
| 8508 | 23611977 | CD4/CD8 ratio remained stable in treated subjects but declined in control subjects (P = .03). |
| 8509 | 23638232 | Immunohistochemically, the lymphoid cells were positive for vimentin, CD3, CD4, CD5, CD8, CD10, CD15, CD20, CD23, CD30, CD43, CD38, CD138, CD45RO, CD79α, bcl-2, bcl-6, κ-chain, λ-chain, and Ki-67 (labeling index=7%). |
| 8510 | 23638232 | The lymphoblastic cells were positively labeled for CD15 and CD30. |
| 8511 | 23638232 | They were negative for cytokeratin (CK) CAM5.2, CKAE1/3, CK34BE12, CK5/6, CK7, CK8, CK18, CK19, CK20, EMA, CEA, CD56, CD57, p53, KIT, PDGFRA, and cyclin D1. |
| 8512 | 23638232 | The low Ki-67 labeling and negative p53 also suggested the diagnosis. |
| 8513 | 23650440 | Results from gene signature analyses, quantification of STAT5 phosphorylation levels, cytokine neutralization experiments, cytokine supplementation studies, and evaluations of intracellular cytokine levels collectively argue for a scenario in which T reg cells regulate NK cell functions by controlling the bioavailability of limiting amounts of IL-2 in the islets, generated mainly by infiltrating CD4(+) T cells. |
| 8514 | 23657001 | Treg cells endowed with enhanced killing activity through decoration with Fas-ligand (FasL) protein (killer Treg) have been effective in delay of hyperglycemia in prediabetic non-obese diabetic (NOD) mice. |
| 8515 | 23657001 | A second mechanism of action consisted of increased fractions of CD4(+)CD25(-)FoxP3(+) T cells in the pancreas and all lymphoid organs. |
| 8516 | 23657001 | Immunomodulation with FasL rather than Treg cells enhanced the expression of CD25 and FoxP3 in the thymus, suggesting a possible contribution of thymic output to prolonged stabilization of the glucose levels. |
| 8517 | 23663075 | Expression of GzmA and Fas was enhanced in the islets from pre-diabetic NOD.GzmB(-/-) mice. |
| 8518 | 23663075 | Cyclophosphamide treatment led to a significantly lower percentage of apoptotic CD4(+) , CD8(+) and CD4(+) CD25(+) T cells in SPCs from NOD.GzmB(-/-) mice than those from wt-NOD mice. |
| 8519 | 23685786 | T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10. |
| 8520 | 23685786 | CD52(hi)CD4(+) T cells were distinct from CD4(+)CD25(+)Foxp3(+) regulatory T cells. |
| 8521 | 23685786 | Their suppression was mediated by soluble CD52 released by phospholipase C. |
| 8522 | 23685786 | Soluble CD52 bound to the inhibitory receptor Siglec-10 and impaired phosphorylation of the T cell receptor-associated kinases Lck and Zap70 and T cell activation. |
| 8523 | 23685786 | Humans with type 1 diabetes had a lower frequency and diminished function of CD52(hi)CD4(+) T cells responsive to the autoantigen GAD65. |
| 8524 | 23685786 | T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10. |
| 8525 | 23685786 | CD52(hi)CD4(+) T cells were distinct from CD4(+)CD25(+)Foxp3(+) regulatory T cells. |
| 8526 | 23685786 | Their suppression was mediated by soluble CD52 released by phospholipase C. |
| 8527 | 23685786 | Soluble CD52 bound to the inhibitory receptor Siglec-10 and impaired phosphorylation of the T cell receptor-associated kinases Lck and Zap70 and T cell activation. |
| 8528 | 23685786 | Humans with type 1 diabetes had a lower frequency and diminished function of CD52(hi)CD4(+) T cells responsive to the autoantigen GAD65. |
| 8529 | 23691523 | In recent years, increasing evidence has implicated CD4(+)CD25(+) regulatory T (Treg) cells expressing the transcription factor Foxp3 in both the breakdown of self-tolerance and the restoration of immune homeostasis in T1D. |
| 8530 | 23707515 | Other pro-inflammatory cells found in AT include neutrophils, Th1 CD4 T cells, CD8 T cells, B cells, DCs, and mast cells. |
| 8531 | 23709681 | Thymic damage, impaired negative selection, and development of chronic graft-versus-host disease caused by donor CD4+ and CD8+ T cells. |
| 8532 | 23709681 | Donor CD8(+) T cells were more potent than CD4(+) T cells for inducing cGVHD. |
| 8533 | 23709681 | The recipient thymus and de novo-generated, donor-derived CD4(+) T cells were required for induction of cGVHD by donor CD8(+) T cells but not by donor CD4(+) T cells. |
| 8534 | 23709681 | Donor CD8(+) T cells preferentially damaged recipient medullary thymic epithelial cells and impaired negative selection, resulting in production of autoreactive CD4(+) T cells that perpetuated damage to the thymus and augmented the development of cGVHD. |
| 8535 | 23709681 | These results demonstrate that donor CD8(+) T cells cause cGVHD solely through thymic-dependent mechanisms, whereas CD4(+) T cells can cause cGVHD through either thymic-dependent or independent mechanisms. |
| 8536 | 23709681 | Thymic damage, impaired negative selection, and development of chronic graft-versus-host disease caused by donor CD4+ and CD8+ T cells. |
| 8537 | 23709681 | Donor CD8(+) T cells were more potent than CD4(+) T cells for inducing cGVHD. |
| 8538 | 23709681 | The recipient thymus and de novo-generated, donor-derived CD4(+) T cells were required for induction of cGVHD by donor CD8(+) T cells but not by donor CD4(+) T cells. |
| 8539 | 23709681 | Donor CD8(+) T cells preferentially damaged recipient medullary thymic epithelial cells and impaired negative selection, resulting in production of autoreactive CD4(+) T cells that perpetuated damage to the thymus and augmented the development of cGVHD. |
| 8540 | 23709681 | These results demonstrate that donor CD8(+) T cells cause cGVHD solely through thymic-dependent mechanisms, whereas CD4(+) T cells can cause cGVHD through either thymic-dependent or independent mechanisms. |
| 8541 | 23709681 | Thymic damage, impaired negative selection, and development of chronic graft-versus-host disease caused by donor CD4+ and CD8+ T cells. |
| 8542 | 23709681 | Donor CD8(+) T cells were more potent than CD4(+) T cells for inducing cGVHD. |
| 8543 | 23709681 | The recipient thymus and de novo-generated, donor-derived CD4(+) T cells were required for induction of cGVHD by donor CD8(+) T cells but not by donor CD4(+) T cells. |
| 8544 | 23709681 | Donor CD8(+) T cells preferentially damaged recipient medullary thymic epithelial cells and impaired negative selection, resulting in production of autoreactive CD4(+) T cells that perpetuated damage to the thymus and augmented the development of cGVHD. |
| 8545 | 23709681 | These results demonstrate that donor CD8(+) T cells cause cGVHD solely through thymic-dependent mechanisms, whereas CD4(+) T cells can cause cGVHD through either thymic-dependent or independent mechanisms. |
| 8546 | 23709681 | Thymic damage, impaired negative selection, and development of chronic graft-versus-host disease caused by donor CD4+ and CD8+ T cells. |
| 8547 | 23709681 | Donor CD8(+) T cells were more potent than CD4(+) T cells for inducing cGVHD. |
| 8548 | 23709681 | The recipient thymus and de novo-generated, donor-derived CD4(+) T cells were required for induction of cGVHD by donor CD8(+) T cells but not by donor CD4(+) T cells. |
| 8549 | 23709681 | Donor CD8(+) T cells preferentially damaged recipient medullary thymic epithelial cells and impaired negative selection, resulting in production of autoreactive CD4(+) T cells that perpetuated damage to the thymus and augmented the development of cGVHD. |
| 8550 | 23709681 | These results demonstrate that donor CD8(+) T cells cause cGVHD solely through thymic-dependent mechanisms, whereas CD4(+) T cells can cause cGVHD through either thymic-dependent or independent mechanisms. |
| 8551 | 23709681 | Thymic damage, impaired negative selection, and development of chronic graft-versus-host disease caused by donor CD4+ and CD8+ T cells. |
| 8552 | 23709681 | Donor CD8(+) T cells were more potent than CD4(+) T cells for inducing cGVHD. |
| 8553 | 23709681 | The recipient thymus and de novo-generated, donor-derived CD4(+) T cells were required for induction of cGVHD by donor CD8(+) T cells but not by donor CD4(+) T cells. |
| 8554 | 23709681 | Donor CD8(+) T cells preferentially damaged recipient medullary thymic epithelial cells and impaired negative selection, resulting in production of autoreactive CD4(+) T cells that perpetuated damage to the thymus and augmented the development of cGVHD. |
| 8555 | 23709681 | These results demonstrate that donor CD8(+) T cells cause cGVHD solely through thymic-dependent mechanisms, whereas CD4(+) T cells can cause cGVHD through either thymic-dependent or independent mechanisms. |
| 8556 | 23715623 | In vitro exposure of bone marrow-derived DCs to TGF-β reduced expression of costimulatory molecules CD80 and CD86, as well as production of proinflammatory cytokines such as interleukin-12 p70 in DCs, but did not alter levels of major histocompatibility complex classes I and II. |
| 8557 | 23715623 | Furthermore, the capacity of TGF-β-treated bone marrow-derived DCs to activate both CD4(+) and CD8(+) T cells was reduced. |
| 8558 | 23724162 | Type 1 diabetes mellitus (T1DM) is characterized by recognition of beta cell proteins as self-antigens, called autoantigens (AAgs), by patients' own CD4+ and CD8+ T cells and/or the products of self-reactive B cells, called autoantibodies. |
| 8559 | 23724162 | Since many excellent reviews have covered the previously identified T1DM-associated AAgs exhaustedly, here we only focus on several recently discovered T1DM-AAgs (PDX1, ZnT8, CHGA, and IAAP). |
| 8560 | 23728300 | Here, by studying mice in which the Bach2 gene is disrupted, we define BACH2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programs of multiple effector lineages in CD4(+) T cells. |
| 8561 | 23728300 | These findings identify BACH2 as a key regulator of CD4(+) T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity. |
| 8562 | 23728300 | Here, by studying mice in which the Bach2 gene is disrupted, we define BACH2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programs of multiple effector lineages in CD4(+) T cells. |
| 8563 | 23728300 | These findings identify BACH2 as a key regulator of CD4(+) T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity. |
| 8564 | 23730508 | The hepatic sinusoidal lymphoid cells were strongly positive for CD2, CD3 and CD5 whereas CD4, CD8 stained only minor subsets of the T cells. |
| 8565 | 23730508 | Subsequent flow cytometric immunophenotypying of peripheral blood identified T-cell receptor alpha/beta positive cells that lacked CD4 and CD8 (double negative alpha/beta T cells). |
| 8566 | 23730508 | The hepatic sinusoidal lymphoid cells were strongly positive for CD2, CD3 and CD5 whereas CD4, CD8 stained only minor subsets of the T cells. |
| 8567 | 23730508 | Subsequent flow cytometric immunophenotypying of peripheral blood identified T-cell receptor alpha/beta positive cells that lacked CD4 and CD8 (double negative alpha/beta T cells). |
| 8568 | 23733197 | However, weight cycling did increase the number of CD4(+) and CD8(+) T cells in AT. |
| 8569 | 23735590 | Five patients showed CD4-/CD8+/bF-1+ phenotype with TIA-1 expression. |
| 8570 | 23740949 | In this study, we show that expression of I-E on dendritic cells (DCs) of NOD mice promotes the differentiation of MHC promiscuous autoreactive CD4(+) clonotypes into antidiabetogenic autoregulatory T cells. |
| 8571 | 23740949 | We expressed an I-Eα(kloxP) transgene in NOD mice and used cell type-specific I-E ablation to show that I-E-expressing DCs, but not B cells, promote the generation of autoreactive CD4(+)Foxp3(+) regulatory T cells (Tregs) and their accumulation in the pancreas-draining lymph nodes. |
| 8572 | 23740949 | There, these Tregs suppress the presentation of β cell Ags to naive autoreactive CD4(+) and CD8(+) T cells restricted by diabetogenic MHC molecules in an I-E-independent manner. |
| 8573 | 23740949 | In this study, we show that expression of I-E on dendritic cells (DCs) of NOD mice promotes the differentiation of MHC promiscuous autoreactive CD4(+) clonotypes into antidiabetogenic autoregulatory T cells. |
| 8574 | 23740949 | We expressed an I-Eα(kloxP) transgene in NOD mice and used cell type-specific I-E ablation to show that I-E-expressing DCs, but not B cells, promote the generation of autoreactive CD4(+)Foxp3(+) regulatory T cells (Tregs) and their accumulation in the pancreas-draining lymph nodes. |
| 8575 | 23740949 | There, these Tregs suppress the presentation of β cell Ags to naive autoreactive CD4(+) and CD8(+) T cells restricted by diabetogenic MHC molecules in an I-E-independent manner. |
| 8576 | 23740949 | In this study, we show that expression of I-E on dendritic cells (DCs) of NOD mice promotes the differentiation of MHC promiscuous autoreactive CD4(+) clonotypes into antidiabetogenic autoregulatory T cells. |
| 8577 | 23740949 | We expressed an I-Eα(kloxP) transgene in NOD mice and used cell type-specific I-E ablation to show that I-E-expressing DCs, but not B cells, promote the generation of autoreactive CD4(+)Foxp3(+) regulatory T cells (Tregs) and their accumulation in the pancreas-draining lymph nodes. |
| 8578 | 23740949 | There, these Tregs suppress the presentation of β cell Ags to naive autoreactive CD4(+) and CD8(+) T cells restricted by diabetogenic MHC molecules in an I-E-independent manner. |
| 8579 | 23741311 | We also found that there was a higher percentage of Sema4D(high) CD3(+) (P<0.01), CD4(+) (P<0.001), and CD8(+) (P<0.01) T-cells in samples from HF patients, but no changes in Sema4D expression levels in B cells and platelets. |
| 8580 | 23750800 | Delayed anti-CD3 therapy results in depletion of alloreactive T cells and the dominance of Foxp3+ CD4+ graft infiltrating cells. |
| 8581 | 23752610 | The transgenic mice had a significantly lower incidence of spontaneous autoimmune diabetes, which was accompanied by fewer IFN-γ-producing T cells, and an increased ratio of CD4(+)Foxp3(+) T(regs)to CD4(+)IFN-γ(+) or to CD8(+)IFN-γ(+) T cells, respectively, in pancreatic islets. |
| 8582 | 23752610 | To examine further the pathogenic features of transgenic T cells, we generated Ptpn22/BDC2.5 doubly transgenic mice and found reduced proliferation and Th1 differentiation in CD4(+) T lymphocytes with additional Pep in pancreatic lymph nodes but not in inguinal lymph nodes of NOD/SCID recipients. |
| 8583 | 23752610 | The transgenic mice had a significantly lower incidence of spontaneous autoimmune diabetes, which was accompanied by fewer IFN-γ-producing T cells, and an increased ratio of CD4(+)Foxp3(+) T(regs)to CD4(+)IFN-γ(+) or to CD8(+)IFN-γ(+) T cells, respectively, in pancreatic islets. |
| 8584 | 23752610 | To examine further the pathogenic features of transgenic T cells, we generated Ptpn22/BDC2.5 doubly transgenic mice and found reduced proliferation and Th1 differentiation in CD4(+) T lymphocytes with additional Pep in pancreatic lymph nodes but not in inguinal lymph nodes of NOD/SCID recipients. |
| 8585 | 23776180 | Although defining pathogenic effector T cells in autoimmunity has been inconsistent, CD4(+) cells expressing the CD40 receptor (Th40 cells) are highly diabetogenic in NOD mice, and NOD.BDC2.5.TCR.Tg mice possess large numbers of these cells. |
| 8586 | 23776180 | Regulatory T cells, CD4(+)CD25(hi)Foxp3(+), develop normally, but pathogenic effector cells are severely reduced in number. |
| 8587 | 23776180 | Mechanistically, Foxp3(+) cells produce IL-17 but do not produce IFN-γ, whereas Foxp3(-) Th40 cells produce IFN-γ and IL-2. |
| 8588 | 23776180 | Although defining pathogenic effector T cells in autoimmunity has been inconsistent, CD4(+) cells expressing the CD40 receptor (Th40 cells) are highly diabetogenic in NOD mice, and NOD.BDC2.5.TCR.Tg mice possess large numbers of these cells. |
| 8589 | 23776180 | Regulatory T cells, CD4(+)CD25(hi)Foxp3(+), develop normally, but pathogenic effector cells are severely reduced in number. |
| 8590 | 23776180 | Mechanistically, Foxp3(+) cells produce IL-17 but do not produce IFN-γ, whereas Foxp3(-) Th40 cells produce IFN-γ and IL-2. |
| 8591 | 23795893 | These host-derived CD4(+) T cells were enriched for conventional regulatory T cells (Tregs ) (CD25(+) forkhead box protein 3 (FoxP3)(+)] and also for host- derived CD4(+)CD25(-)FoxP3(-) T cells that express markers of suppressive function, CD73, FR4 and CD39. |
| 8592 | 23803704 | No significant changes were noted in interferon-γ, interleukin-4 (IL-4), or IL-10 production in CD4 T cells. |
| 8593 | 23834659 | Whereas CD4(+) CD25(-) T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. |
| 8594 | 23878307 | CD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response. |
| 8595 | 23878307 | We show that the transcription factor DEC1 is highly induced in a CD28-dependent manner upon T cell activation, is involved in essential CD4(+) effector T cell functions, and participates in the transcriptional regulation of several T cell activation pathways, including a large group of CD28-regulated genes. |
| 8596 | 23878307 | Antigen-specific, DEC1-deficient CD4(+) T cells have cell-intrinsic defects in survival and proliferation. |
| 8597 | 23878307 | Furthermore, we found that DEC1 is required for the development of experimental autoimmune encephalomyelitis because of its critical role in the production of the proinflammatory cytokines GM-CSF, IFN-γ, and IL-2. |
| 8598 | 23878307 | Thus, we identify DEC1 as a critical transcriptional mediator in the activation of naive CD4(+) T cells that is required for the development of a T cell-mediated autoimmune disease. |
| 8599 | 23878307 | CD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response. |
| 8600 | 23878307 | We show that the transcription factor DEC1 is highly induced in a CD28-dependent manner upon T cell activation, is involved in essential CD4(+) effector T cell functions, and participates in the transcriptional regulation of several T cell activation pathways, including a large group of CD28-regulated genes. |
| 8601 | 23878307 | Antigen-specific, DEC1-deficient CD4(+) T cells have cell-intrinsic defects in survival and proliferation. |
| 8602 | 23878307 | Furthermore, we found that DEC1 is required for the development of experimental autoimmune encephalomyelitis because of its critical role in the production of the proinflammatory cytokines GM-CSF, IFN-γ, and IL-2. |
| 8603 | 23878307 | Thus, we identify DEC1 as a critical transcriptional mediator in the activation of naive CD4(+) T cells that is required for the development of a T cell-mediated autoimmune disease. |
| 8604 | 23878307 | CD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response. |
| 8605 | 23878307 | We show that the transcription factor DEC1 is highly induced in a CD28-dependent manner upon T cell activation, is involved in essential CD4(+) effector T cell functions, and participates in the transcriptional regulation of several T cell activation pathways, including a large group of CD28-regulated genes. |
| 8606 | 23878307 | Antigen-specific, DEC1-deficient CD4(+) T cells have cell-intrinsic defects in survival and proliferation. |
| 8607 | 23878307 | Furthermore, we found that DEC1 is required for the development of experimental autoimmune encephalomyelitis because of its critical role in the production of the proinflammatory cytokines GM-CSF, IFN-γ, and IL-2. |
| 8608 | 23878307 | Thus, we identify DEC1 as a critical transcriptional mediator in the activation of naive CD4(+) T cells that is required for the development of a T cell-mediated autoimmune disease. |
| 8609 | 23878307 | CD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response. |
| 8610 | 23878307 | We show that the transcription factor DEC1 is highly induced in a CD28-dependent manner upon T cell activation, is involved in essential CD4(+) effector T cell functions, and participates in the transcriptional regulation of several T cell activation pathways, including a large group of CD28-regulated genes. |
| 8611 | 23878307 | Antigen-specific, DEC1-deficient CD4(+) T cells have cell-intrinsic defects in survival and proliferation. |
| 8612 | 23878307 | Furthermore, we found that DEC1 is required for the development of experimental autoimmune encephalomyelitis because of its critical role in the production of the proinflammatory cytokines GM-CSF, IFN-γ, and IL-2. |
| 8613 | 23878307 | Thus, we identify DEC1 as a critical transcriptional mediator in the activation of naive CD4(+) T cells that is required for the development of a T cell-mediated autoimmune disease. |
| 8614 | 23878314 | CCL22-producing CD8α- myeloid dendritic cells mediate regulatory T cell recruitment in response to G-CSF treatment. |
| 8615 | 23878314 | We demonstrate in this study that the adoptive transfer of CD11c(high)CD8α(-) DCs isolated from pegylated G-CSF (pegG-CSF) recipients, but not that of other DC subtypes, enhanced the pancreatic recruitment of CD4(+)CD25(+)Foxp3(+) Tregs, which generated increased amounts of TGF-β. |
| 8616 | 23878314 | PegG-CSF was more efficient at enhancing the synthesis of CCL22 by CD11c(high)CD8α(-) DCs from the pancreatic lymph nodes compared with those from the spleen. |
| 8617 | 23878314 | These data assign a key role to CD8α(-) DCs and CCL22 in Treg recruitment in the protection of NOD mice against type 1 diabetes following the treatment with G-CSF. |
| 8618 | 23890479 | Sitagliptin is a dipeptidyl peptidase IV (DPP-IV) inhibitor that exerts an anti-hyperglycaemic effect by preventing degradation of glucagon-like peptide 1 with subsequent β-cell stimulation and potential regeneration. |
| 8619 | 23890479 | While compared to diabetic controls sitagliptin prevented increase of the CD8+/CD4+ ratio in pancreatic nodes after four weeks (0.443 ± 0.067 vs. 0.544 ± 0.131; P < 0.05), the population of Tregs in lymph nodes increased from day 0 to 28 in both treated and non-treated diabetic groups (8 ± 1.76 vs. 13.45 ± 5.07 % and 8 ± 1.76 vs. 13.19 ± 5.58 %, respectively). |
| 8620 | 23899994 | Pam3CSK(4) enhanced beta cell loss and diabetogenesis: the roles of IFN-gamma and IL-17. |
| 8621 | 23899994 | FACS analysis of isolated pancreatic lymph node cells revealed significant increased number of macrophages, dendritic cells, CD4(+) TNF-α(+), CD4(+) IFN-γ(+) and most significantly, CD4(+) IL-17(+) and reduced number of CD25(+)Fox p3(+) T cells after Pam3CSK4 treatment. |
| 8622 | 23925934 | Here, using tetramer analysis, we investigated how oral delivery of CTB fused to two CD4(+) T-cell epitopes, the BDC-2.5 T-cell 2.5 mi mimotope and glutamic acid decarboxylase (GAD) 286-300, affected diabetogenic CD4(+) T cells in nonobese diabetic (NOD) mice. |
| 8623 | 23927943 | Impaired CD4+ and T-helper 17 cell memory response to Streptococcus pneumoniae is associated with elevated glucose and percent glycated hemoglobin A1c in Mexican Americans with type 2 diabetes mellitus. |
| 8624 | 23927943 | Measurement of specific subsets indicated that those with diabetes had, low intracellular levels of interleukin (IL)-17, and lower pathogen-specific memory CD4+ and IL-17+ cell numbers. |
| 8625 | 23927943 | Impaired CD4+ and T-helper 17 cell memory response to Streptococcus pneumoniae is associated with elevated glucose and percent glycated hemoglobin A1c in Mexican Americans with type 2 diabetes mellitus. |
| 8626 | 23927943 | Measurement of specific subsets indicated that those with diabetes had, low intracellular levels of interleukin (IL)-17, and lower pathogen-specific memory CD4+ and IL-17+ cell numbers. |
| 8627 | 23928796 | Circulating primary CD4(+) or CD8(+) T cells were quantified with 5-color flow cytometry. |
| 8628 | 23928796 | Serum IL-22 and IL-17 levels were examined by ELISA. |
| 8629 | 23928796 | Serum autoantibodies were measured by radio-binding assays, using (35)S-labeled glutamic acid decarboxylase-65 (GAD65), protein tyrosine phosphatase-2 (IA-2), and zinc transporter 8 (ZnT8). |
| 8630 | 23928796 | However, we did not find any correlation between IL-17 and IL-22 in sera. |
| 8631 | 23929911 | A fine cytometric analysis was designed for their characterization, using a panel of markers including FOXP3, CTLA4, glucocorticoid-induced TNFR family related (GITR) and CD127. |
| 8632 | 23929911 | The frequency of peripheral CD4(+)CD25(hi) T(reg) cells was similar between samples. |
| 8633 | 23939393 | STAT4 deficiency reduces obesity-induced insulin resistance and adipose tissue inflammation. |
| 8634 | 23939393 | STAT4 has a prominent role in mediating interleukin-12-induced T-helper cell type 1 lineage differentiation. |
| 8635 | 23939393 | We sought to determine the role of STAT4 in AT inflammation in obesity-induced insulin resistance. |
| 8636 | 23939393 | We have found that STAT4(-/-)C57Bl6/J mice develop high-fat diet-induced obesity (DIO) similar to wild-type controls, but that they have significantly improved insulin sensitivity and better glucose tolerance. |
| 8637 | 23939393 | Using flow cytometry and real-time PCR, we show that STAT4(-/-) mice with DIO produce significantly reduced numbers of inflammatory cytokines and chemokines in adipocytes, have reduced numbers of CD8(+) cells, and display increased alternative (M2) macrophage polarization. |
| 8638 | 23939393 | CD8(+) cells, but not CD4(+) cells, from STAT4(-/-) mice displayed reduced in vitro migration. |
| 8639 | 23939393 | Also, we found that adipocyte inflammation is reduced and insulin signaling is improved in STAT4(-/-) mice with DIO. |
| 8640 | 23939393 | We have identified STAT4 as a key contributor to insulin resistance and AT inflammation in DIO. |
| 8641 | 23939393 | Targeting STAT4 activation could be a novel approach to reducing AT inflammation and insulin resistance in obesity. |
| 8642 | 23974926 | In vitro assays suggested that CD137 deficiency had a limited effect on the suppressive function of CD4(+)CD25(+) regulatory T-cells (Tregs). |
| 8643 | 23981600 | In a cohort of patients aged 60 years or older with excellent antiretroviral therapy adherence, correlates to cognitive impairment were apolipoprotein (Apo) E4 genotype and a novel measure of the effectiveness of antiretroviral drugs in monocytes, the monocyte efficacy (ME) score, with trend associations for diabetes and nadir CD4+ cell count. |
| 8644 | 23987037 | After CCT there are noted the inhibition of predominantly cellular link of immunity, accompanied by reduction of the CD3+ lymphocytes quantity, as well as lymphocytes of the main subpopulations CD4+ and CD8+, CD16+, reduction of the neutrophils phagocytic activity, a complement titer enhancement. |
| 8645 | 24016298 | Fluorescent-labelled antibodies to CD3, CD4 and CD8 cell marker proteins were utilized to determine proliferative responses of CD3, CD4 and CD8 T cells. |
| 8646 | 24016298 | PEP treatment had no significant effect on CD8 T cell reactivity to the peptic-trytic digest of wheat gluten. |