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Gene Information
Gene symbol: IL2
Gene name: interleukin 2
HGNC ID: 6001
Synonyms: IL-2, TCGF
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1309355 | CD4-/CD8-/TCR gamma, delta + T lymphocytes were observed within the islets. |
| 2 | 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+). |
| 3 | 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. |
| 4 | 1346344 | In view of the importance of the IL-2 receptors in the expression of antiallograft immunity and the currently existing controversy regarding the effect of CsA on the induction of IL-2 receptors, we explored the effect of cyclosporine on the induction of interleukin-2 receptor alpha and beta in normal human T cells. |
| 5 | 1374102 | Prostaglandin E2 and other cyclic AMP-elevating agents modulate IL-2 and IL-2R alpha gene expression at multiple levels. |
| 6 | 1374102 | cAMP is an intracellular second messenger that conveys inhibitory signals for T cell activation and clonal proliferation. cAMP also inhibits the production of IL-2 and IL-2R alpha-chain expression. |
| 7 | 1374102 | Nuclear run-off assays showed that the inhibitory effect of cAMP on IL-2 and IL-2R alpha gene expression is mediated at the transcriptional level. |
| 8 | 1374102 | H-8, an inhibitor of protein kinase A, reversed the inhibitory effect of cAMP on nuclear transcription of the IL-2 gene, suggesting that this is mediated through activation of protein kinase A. |
| 9 | 1374102 | Prostaglandin E2 and other cyclic AMP-elevating agents modulate IL-2 and IL-2R alpha gene expression at multiple levels. |
| 10 | 1374102 | cAMP is an intracellular second messenger that conveys inhibitory signals for T cell activation and clonal proliferation. cAMP also inhibits the production of IL-2 and IL-2R alpha-chain expression. |
| 11 | 1374102 | Nuclear run-off assays showed that the inhibitory effect of cAMP on IL-2 and IL-2R alpha gene expression is mediated at the transcriptional level. |
| 12 | 1374102 | H-8, an inhibitor of protein kinase A, reversed the inhibitory effect of cAMP on nuclear transcription of the IL-2 gene, suggesting that this is mediated through activation of protein kinase A. |
| 13 | 1374102 | Prostaglandin E2 and other cyclic AMP-elevating agents modulate IL-2 and IL-2R alpha gene expression at multiple levels. |
| 14 | 1374102 | cAMP is an intracellular second messenger that conveys inhibitory signals for T cell activation and clonal proliferation. cAMP also inhibits the production of IL-2 and IL-2R alpha-chain expression. |
| 15 | 1374102 | Nuclear run-off assays showed that the inhibitory effect of cAMP on IL-2 and IL-2R alpha gene expression is mediated at the transcriptional level. |
| 16 | 1374102 | H-8, an inhibitor of protein kinase A, reversed the inhibitory effect of cAMP on nuclear transcription of the IL-2 gene, suggesting that this is mediated through activation of protein kinase A. |
| 17 | 1374102 | Prostaglandin E2 and other cyclic AMP-elevating agents modulate IL-2 and IL-2R alpha gene expression at multiple levels. |
| 18 | 1374102 | cAMP is an intracellular second messenger that conveys inhibitory signals for T cell activation and clonal proliferation. cAMP also inhibits the production of IL-2 and IL-2R alpha-chain expression. |
| 19 | 1374102 | Nuclear run-off assays showed that the inhibitory effect of cAMP on IL-2 and IL-2R alpha gene expression is mediated at the transcriptional level. |
| 20 | 1374102 | H-8, an inhibitor of protein kinase A, reversed the inhibitory effect of cAMP on nuclear transcription of the IL-2 gene, suggesting that this is mediated through activation of protein kinase A. |
| 21 | 1388634 | T cell activation is dependent upon calcium influx and protein kinase C activation, with subsequent lymphocyte proliferation dependent upon IL-2. |
| 22 | 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. |
| 23 | 1388637 | We observed increased percentages of activated splenic CD5+ T cells expressing the IL-2 receptor and MHC class II antigen in DP and D rats compared with DR animals. |
| 24 | 1424744 | The presence of interleukin 6 (IL-6), interleukin 1 (IL-1), interleukin 2 (IL-2) and tumour necrosis factor (TNF) was investigated in vitreous and aqueous aspirates from eyes undergoing vitrectomy for the treatment of different inflammatory conditions. |
| 25 | 1424744 | The present observations suggest that cytokines, particularly IL-6 and IL-1, may act as local amplification signals in pathological processes associated with chronic eye inflammation. |
| 26 | 1466799 | Thus, cytokines, such as tumor necrosis factor-alpha, are implicated in the pathogenesis of rheumatoid arthritis based on in vitro studies on synovial tissue from patients with rheumatoid arthritis, which suggest that the effects of tumor necrosis factor-alpha are amplified by its potential to induce other pro-inflammatory cytokines, such as interleukin-1 and granulocyte-macrophage colony-stimulating factor. |
| 27 | 1466799 | Interleukin-2 has also been identified by transgenic technology as a cytokine involved in the pathogenesis of insulin-dependent diabetes mellitus through the activation and stimulation of growth of autoreactive T cells. |
| 28 | 1491835 | The lactoperoxidase/glucoseoxidase technique was the labelling method of choice leading to immunoreactive IL-2 with high specific activity. |
| 29 | 1528876 | An anergic, islet-infiltrating T-cell clone that suppresses murine diabetes secretes a factor that blocks interleukin 2/interleukin 4-dependent proliferation. |
| 30 | 1528876 | As we previously reported, an accelerated form of diabetogenic autoimmunity in nonobese diabetic mice can be blocked by passive transfer of a CD3+, CD8+, beta-chain variable region 11-positive islet-infiltrating T-cell clone (IS-2.15). |
| 31 | 1528876 | Moreover, these T cells secrete an inhibitory factor(s) that irreversibly inhibits interleukin (IL) 2/IL-4-driven proliferation of IL-2/IL-4 indicator T-cell lines. |
| 32 | 1528876 | These data indicate that at least some anergic T cells can play an active role in peripheral tolerance by secreting suppressor factor(s) that regulate IL-2/IL-4-dependent proliferation. |
| 33 | 1528876 | An anergic, islet-infiltrating T-cell clone that suppresses murine diabetes secretes a factor that blocks interleukin 2/interleukin 4-dependent proliferation. |
| 34 | 1528876 | As we previously reported, an accelerated form of diabetogenic autoimmunity in nonobese diabetic mice can be blocked by passive transfer of a CD3+, CD8+, beta-chain variable region 11-positive islet-infiltrating T-cell clone (IS-2.15). |
| 35 | 1528876 | Moreover, these T cells secrete an inhibitory factor(s) that irreversibly inhibits interleukin (IL) 2/IL-4-driven proliferation of IL-2/IL-4 indicator T-cell lines. |
| 36 | 1528876 | These data indicate that at least some anergic T cells can play an active role in peripheral tolerance by secreting suppressor factor(s) that regulate IL-2/IL-4-dependent proliferation. |
| 37 | 1528876 | An anergic, islet-infiltrating T-cell clone that suppresses murine diabetes secretes a factor that blocks interleukin 2/interleukin 4-dependent proliferation. |
| 38 | 1528876 | As we previously reported, an accelerated form of diabetogenic autoimmunity in nonobese diabetic mice can be blocked by passive transfer of a CD3+, CD8+, beta-chain variable region 11-positive islet-infiltrating T-cell clone (IS-2.15). |
| 39 | 1528876 | Moreover, these T cells secrete an inhibitory factor(s) that irreversibly inhibits interleukin (IL) 2/IL-4-driven proliferation of IL-2/IL-4 indicator T-cell lines. |
| 40 | 1528876 | These data indicate that at least some anergic T cells can play an active role in peripheral tolerance by secreting suppressor factor(s) that regulate IL-2/IL-4-dependent proliferation. |
| 41 | 1547815 | Interleukin 2 receptor targeted fusion toxin (DAB486-IL-2) treatment blocks diabetogenic autoimmunity in non-obese diabetic mice. |
| 42 | 1547815 | Insulin-dependent diabetes mellitus (IDDM) is strikingly similar in the non-obese diabetic (NOD) mouse and humans. |
| 43 | 1547815 | In IDDM, the systematic autoimmune destruction of insulin-producing beta cells within the pancreas is dependent on autoreactive T cells. |
| 44 | 1547815 | In a previous study we established that interleukin 2 receptor (IL 2R)-bearing cells propagated from pre-diabetic NOD mice promote IDDM. |
| 45 | 1547815 | We set DAB486-IL-2 the challenging task of preventing fulminant IDDM accelerated by the adoptive transfer of diabetic spleen cells. |
| 46 | 1547815 | Taken together, these studies strongly support the concept that IL 2R-bearing T cells are essential for the induction of IDDM and suggest that DAB486-IL-2 would be a promising therapeutic approach in the treatment of human IDDM. |
| 47 | 1547815 | Interleukin 2 receptor targeted fusion toxin (DAB486-IL-2) treatment blocks diabetogenic autoimmunity in non-obese diabetic mice. |
| 48 | 1547815 | Insulin-dependent diabetes mellitus (IDDM) is strikingly similar in the non-obese diabetic (NOD) mouse and humans. |
| 49 | 1547815 | In IDDM, the systematic autoimmune destruction of insulin-producing beta cells within the pancreas is dependent on autoreactive T cells. |
| 50 | 1547815 | In a previous study we established that interleukin 2 receptor (IL 2R)-bearing cells propagated from pre-diabetic NOD mice promote IDDM. |
| 51 | 1547815 | We set DAB486-IL-2 the challenging task of preventing fulminant IDDM accelerated by the adoptive transfer of diabetic spleen cells. |
| 52 | 1547815 | Taken together, these studies strongly support the concept that IL 2R-bearing T cells are essential for the induction of IDDM and suggest that DAB486-IL-2 would be a promising therapeutic approach in the treatment of human IDDM. |
| 53 | 1547815 | Interleukin 2 receptor targeted fusion toxin (DAB486-IL-2) treatment blocks diabetogenic autoimmunity in non-obese diabetic mice. |
| 54 | 1547815 | Insulin-dependent diabetes mellitus (IDDM) is strikingly similar in the non-obese diabetic (NOD) mouse and humans. |
| 55 | 1547815 | In IDDM, the systematic autoimmune destruction of insulin-producing beta cells within the pancreas is dependent on autoreactive T cells. |
| 56 | 1547815 | In a previous study we established that interleukin 2 receptor (IL 2R)-bearing cells propagated from pre-diabetic NOD mice promote IDDM. |
| 57 | 1547815 | We set DAB486-IL-2 the challenging task of preventing fulminant IDDM accelerated by the adoptive transfer of diabetic spleen cells. |
| 58 | 1547815 | Taken together, these studies strongly support the concept that IL 2R-bearing T cells are essential for the induction of IDDM and suggest that DAB486-IL-2 would be a promising therapeutic approach in the treatment of human IDDM. |
| 59 | 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. |
| 60 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 61 | 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. |
| 62 | 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). |
| 63 | 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. |
| 64 | 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+. |
| 65 | 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. |
| 66 | 1679332 | After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7. |
| 67 | 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. |
| 68 | 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). |
| 69 | 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. |
| 70 | 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+. |
| 71 | 1687810 | Analysis of IL-2 receptor positive CD8(+)-T-lymphocytes grown from islets of NOD mice. |
| 72 | 1687810 | Of 13 lines obtained after limiting dilution all were positive for the T-cell marker Thy-1 and for CD8. |
| 73 | 1687810 | We conclude that IL-2 receptor positive CD8+ T-lymphocytes from NOD islets are heterogenous with respect to V beta T-cell receptor usage. |
| 74 | 1687810 | Analysis of IL-2 receptor positive CD8(+)-T-lymphocytes grown from islets of NOD mice. |
| 75 | 1687810 | Of 13 lines obtained after limiting dilution all were positive for the T-cell marker Thy-1 and for CD8. |
| 76 | 1687810 | We conclude that IL-2 receptor positive CD8+ T-lymphocytes from NOD islets are heterogenous with respect to V beta T-cell receptor usage. |
| 77 | 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. |
| 78 | 1696864 | Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. |
| 79 | 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. |
| 80 | 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. |
| 81 | 1696864 | In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. |
| 82 | 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. |
| 83 | 1727731 | T-lymphocyte lines specific for glutamic acid decarboxylase (GAD) the 64K beta-cell antigen of IDDM. |
| 84 | 1727731 | Insulin-dependent diabetes mellitus (IDDM) is viewed as a thymus-dependent autoimmune disease, although the specific beta-cell autoantigen or autoantigens remain unknown. |
| 85 | 1727731 | In this study, we describe the isolation of GAD-specific T-lymphocyte lines from BB rats, an animal model of IDDM. |
| 86 | 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. |
| 87 | 1727731 | Four stable, CD4+, MHC (RT1u)-restricted T-lymphocyte lines were isolated. |
| 88 | 1727731 | They proliferate selectively in the presence of GAD and secrete interleukin 2 and interferon-gamma. |
| 89 | 1727731 | T-lymphocyte lines specific for glutamic acid decarboxylase (GAD) the 64K beta-cell antigen of IDDM. |
| 90 | 1727731 | Insulin-dependent diabetes mellitus (IDDM) is viewed as a thymus-dependent autoimmune disease, although the specific beta-cell autoantigen or autoantigens remain unknown. |
| 91 | 1727731 | In this study, we describe the isolation of GAD-specific T-lymphocyte lines from BB rats, an animal model of IDDM. |
| 92 | 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. |
| 93 | 1727731 | Four stable, CD4+, MHC (RT1u)-restricted T-lymphocyte lines were isolated. |
| 94 | 1727731 | They proliferate selectively in the presence of GAD and secrete interleukin 2 and interferon-gamma. |
| 95 | 1747949 | We have recently reported that systemic and chronic administration of recombinant tumour necrosis factor alpha (TNF-alpha), as well as streptococcal preparation (OK-432), inhibits development of insulin-dependent diabetes mellitus (IDDM) in NOD mice and BB rats, models of IDDM. |
| 96 | 1747949 | In this study we examined whether serum containing endogenous TNF induced by OK-432 injection could inhibit IDDM in NOD mice. |
| 97 | 1747949 | Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). |
| 98 | 1747949 | The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF. |
| 99 | 1821052 | The resulting immunological network involves monocytes activation, interleukin-1 secretion, T-lymphocyte activation, secretion of interleukin-2 and other lymphokines which activate cytotoxic cells to induce beta-cell lysis. |
| 100 | 1825939 | Cell surface phenotyping of 58 newly diagnosed diabetic children and 25 controls confirmed the presence of activated T cells, expressing HLA class II antigens or receptors for interleukin-2 (IL-2R, CD25) in the majority of the patients. |
| 101 | 1838123 | The subsets of Leu11+Leu7+, Leu11-Leu7+ and Leu7+Leu2+ were decreased significantly in peripheral Natural Killer cells. |
| 102 | 1838123 | The CD4/CD8 ratio, and the IL2+Leu2+ subset, showed a negative regressions with HbA1, and the diabetic duration, respectively. |
| 103 | 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. |
| 104 | 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. |
| 105 | 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. |
| 106 | 1902177 | An interleukin 2 (IL 2)-dependent noncytolytic, V beta 11+ CD8+. |
| 107 | 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. |
| 108 | 1914257 | Insulin-dependent diabetes mellitus (IDDM) is believed to be a consequence of an autoimmune attack on beta cells by T cells. |
| 109 | 1914257 | We have previously reported that T cells from the majority of patients with IDDM produced decreased levels of interleukin-2 (IL-2) following activation with phytohemagglutinin. |
| 110 | 1914257 | Second, we examined steady-state levels of IL-2 mRNA in IDDMs and controls. |
| 111 | 1914257 | Preliminary experiments demonstrated that G0/G1 cells from IDDMs reproduced the IL-2 defect seen originally with PBL. |
| 112 | 1914257 | A comparison of steady-state levels of IL-2 mRNA from activated T cells of IDDMs and age-matched controls, however, demonstrated lower levels of IL-2 mRNA in IDDMs compared to controls. |
| 113 | 1914257 | Finally, we observed that the IL-2 mRNA in IDDM T cells was less stabile than that in the control cells, suggesting a possible mechanism for the defect. |
| 114 | 1914257 | Insulin-dependent diabetes mellitus (IDDM) is believed to be a consequence of an autoimmune attack on beta cells by T cells. |
| 115 | 1914257 | We have previously reported that T cells from the majority of patients with IDDM produced decreased levels of interleukin-2 (IL-2) following activation with phytohemagglutinin. |
| 116 | 1914257 | Second, we examined steady-state levels of IL-2 mRNA in IDDMs and controls. |
| 117 | 1914257 | Preliminary experiments demonstrated that G0/G1 cells from IDDMs reproduced the IL-2 defect seen originally with PBL. |
| 118 | 1914257 | A comparison of steady-state levels of IL-2 mRNA from activated T cells of IDDMs and age-matched controls, however, demonstrated lower levels of IL-2 mRNA in IDDMs compared to controls. |
| 119 | 1914257 | Finally, we observed that the IL-2 mRNA in IDDM T cells was less stabile than that in the control cells, suggesting a possible mechanism for the defect. |
| 120 | 1914257 | Insulin-dependent diabetes mellitus (IDDM) is believed to be a consequence of an autoimmune attack on beta cells by T cells. |
| 121 | 1914257 | We have previously reported that T cells from the majority of patients with IDDM produced decreased levels of interleukin-2 (IL-2) following activation with phytohemagglutinin. |
| 122 | 1914257 | Second, we examined steady-state levels of IL-2 mRNA in IDDMs and controls. |
| 123 | 1914257 | Preliminary experiments demonstrated that G0/G1 cells from IDDMs reproduced the IL-2 defect seen originally with PBL. |
| 124 | 1914257 | A comparison of steady-state levels of IL-2 mRNA from activated T cells of IDDMs and age-matched controls, however, demonstrated lower levels of IL-2 mRNA in IDDMs compared to controls. |
| 125 | 1914257 | Finally, we observed that the IL-2 mRNA in IDDM T cells was less stabile than that in the control cells, suggesting a possible mechanism for the defect. |
| 126 | 1914257 | Insulin-dependent diabetes mellitus (IDDM) is believed to be a consequence of an autoimmune attack on beta cells by T cells. |
| 127 | 1914257 | We have previously reported that T cells from the majority of patients with IDDM produced decreased levels of interleukin-2 (IL-2) following activation with phytohemagglutinin. |
| 128 | 1914257 | Second, we examined steady-state levels of IL-2 mRNA in IDDMs and controls. |
| 129 | 1914257 | Preliminary experiments demonstrated that G0/G1 cells from IDDMs reproduced the IL-2 defect seen originally with PBL. |
| 130 | 1914257 | A comparison of steady-state levels of IL-2 mRNA from activated T cells of IDDMs and age-matched controls, however, demonstrated lower levels of IL-2 mRNA in IDDMs compared to controls. |
| 131 | 1914257 | Finally, we observed that the IL-2 mRNA in IDDM T cells was less stabile than that in the control cells, suggesting a possible mechanism for the defect. |
| 132 | 1914257 | Insulin-dependent diabetes mellitus (IDDM) is believed to be a consequence of an autoimmune attack on beta cells by T cells. |
| 133 | 1914257 | We have previously reported that T cells from the majority of patients with IDDM produced decreased levels of interleukin-2 (IL-2) following activation with phytohemagglutinin. |
| 134 | 1914257 | Second, we examined steady-state levels of IL-2 mRNA in IDDMs and controls. |
| 135 | 1914257 | Preliminary experiments demonstrated that G0/G1 cells from IDDMs reproduced the IL-2 defect seen originally with PBL. |
| 136 | 1914257 | A comparison of steady-state levels of IL-2 mRNA from activated T cells of IDDMs and age-matched controls, however, demonstrated lower levels of IL-2 mRNA in IDDMs compared to controls. |
| 137 | 1914257 | Finally, we observed that the IL-2 mRNA in IDDM T cells was less stabile than that in the control cells, suggesting a possible mechanism for the defect. |
| 138 | 1934594 | Cytokines are known to play an important role in autoimmunity and have been suggested to be involved in the pathogenesis of insulin-dependent diabetes (IDDM). |
| 139 | 1934594 | In the present study we have measured IL-1, IL-2, IL-4, IL-6, interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) (using both immunoassays and bioassays) in sera from 50 patients affected by IDDM at the time of clinical diagnosis and 51 age and sex matched controls. |
| 140 | 1934594 | Detectable levels of IL-1, IL-2, IL-6 and IFN-gamma were found in the serum of a small percentage of subjects and were not significantly different between patients and controls. |
| 141 | 1934594 | IL-4 was detectable in a higher number of both patients and controls and circulating TNF-alpha (greater than 1 U/ml) was found in a percentage of patients (24%) significantly higher than controls (P less than 0.01). |
| 142 | 1934594 | Cytokines are known to play an important role in autoimmunity and have been suggested to be involved in the pathogenesis of insulin-dependent diabetes (IDDM). |
| 143 | 1934594 | In the present study we have measured IL-1, IL-2, IL-4, IL-6, interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) (using both immunoassays and bioassays) in sera from 50 patients affected by IDDM at the time of clinical diagnosis and 51 age and sex matched controls. |
| 144 | 1934594 | Detectable levels of IL-1, IL-2, IL-6 and IFN-gamma were found in the serum of a small percentage of subjects and were not significantly different between patients and controls. |
| 145 | 1934594 | IL-4 was detectable in a higher number of both patients and controls and circulating TNF-alpha (greater than 1 U/ml) was found in a percentage of patients (24%) significantly higher than controls (P less than 0.01). |
| 146 | 1969186 | The L3 clone produces gamma-interferon and tumor necrosis factor but not IL-2 and IL-3. |
| 147 | 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. |
| 148 | 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. |
| 149 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 150 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 151 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 152 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 153 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 154 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 155 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 156 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 157 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 158 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 159 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 160 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 161 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 162 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 163 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 164 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 165 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 166 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 167 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 168 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 169 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 170 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 171 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 172 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 173 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 174 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 175 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 176 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 177 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 178 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 179 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 180 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 181 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 182 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 183 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 184 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 185 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 186 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 187 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 188 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 189 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 190 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 191 | 2022743 | Glucocorticosteroids have an inhibitory effect on the expression of interleukin 2 (IL-2) and interleukin 2 receptor (IL-2R) genes. |
| 192 | 2022743 | Nuclear transcription run-off assays showed that high doses of dexamethasone inhibited the transcription of the IL-2 gene but not that of the IL-2R gene. |
| 193 | 2022743 | Post-transcriptionally, high doses of dexamethasone (10(-4) M) were required to inhibit IL-2R mRNA levels by 50%, whereas lower doses (10(-6) M) inhibited by greater than 70% the accumulation of IL-2 mRNA. |
| 194 | 2022743 | At the protein product level, dexamethasone inhibited both IL-2 production, as well as cell surface and soluble forms of IL-2R. |
| 195 | 2022743 | In the presence of exogenous IL-2, dexamethasone failed to exert a significant effect on the production of IL-2R protein. |
| 196 | 2022743 | These data indicate that dexamethasone has a greater effect on the expression of the IL-2 gene than on the IL-2R gene. |
| 197 | 2022743 | The effect of dexamethasone on the IL-2R gene is post-transcriptional and may result indirectly from decreased IL-2 production. |
| 198 | 2104185 | Soluble interleukin-2 receptor secretion defect in vitro in HLA-B8, DR3 positive subjects. |
| 199 | 2110525 | When using monoclonal antibodies detecting activation markers (OX-17 for class II antigens; ART-18 for interleukin-2 receptor) a significant increase of OX-17+ cells and OX-17+ T-lymphocytes could be observed in lymph node lymphocytes from 24 h after transplantation until 7 days, whereas the peripheral lymphocytes behaved inconspicuously. |
| 200 | 2147547 | T-lymphocyte activation markers, HLA-DR/CD3 and interleukin-2 receptor (Tac) expression, were measured in peripheral blood mononuclear cells by dual- or single-colour flow cytometry. |
| 201 | 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. |
| 202 | 2204602 | T cells of the helper/inducer (CD4+) phenotype and interleukin 2 receptor positive lymphocytes were increased both at diagnosis and one year later. |
| 203 | 2252531 | Phenotyping of the T-lymphocyte subsets, levels of CD25 positive cells and interleukin-2 production by patients' lymphocytes, as well as remission rate and stimulated C-peptide levels, were serially assessed. |
| 204 | 2351412 | [Interleukin-2 modifies the development of insulin-dependent diabetes of BB rats]. |
| 205 | 2384189 | Even sufficient amounts of recombinant IL-2 (rIL-2) or IL-1 (rIL-1), added with mitogens to the preculture medium, failed to provoke normal proliferative responses from NOD/Shi/Kbe mouse cells. |
| 206 | 2429979 | Peripheral blood lymphocytes from 13 patients with established insulin-dependent diabetes mellitus (IDDM) and 2 prediabetic patients were examined for natural killer (NK) and antibody-dependent cellular cytotoxic activities (ADCC), lectin-dependent cellular cytotoxicity (LDCC), interferon- and interleukin-2-induced cytotoxicity, and concanavalin A-induced suppressor-cell activities in comparison with age-matched normal controls. |
| 207 | 2429979 | Interferon- and interleukin-2-induced NK activities were significantly higher with IDDM lymphocytes than with control cells. |
| 208 | 2429979 | The increased interferon- and interleukin-2-induced enhancement of NK activity and reduced suppressor activity of lymphocytes from IDDM patients may be involved in the pathogenesis of the disease. |
| 209 | 2429979 | Peripheral blood lymphocytes from 13 patients with established insulin-dependent diabetes mellitus (IDDM) and 2 prediabetic patients were examined for natural killer (NK) and antibody-dependent cellular cytotoxic activities (ADCC), lectin-dependent cellular cytotoxicity (LDCC), interferon- and interleukin-2-induced cytotoxicity, and concanavalin A-induced suppressor-cell activities in comparison with age-matched normal controls. |
| 210 | 2429979 | Interferon- and interleukin-2-induced NK activities were significantly higher with IDDM lymphocytes than with control cells. |
| 211 | 2429979 | The increased interferon- and interleukin-2-induced enhancement of NK activity and reduced suppressor activity of lymphocytes from IDDM patients may be involved in the pathogenesis of the disease. |
| 212 | 2429979 | Peripheral blood lymphocytes from 13 patients with established insulin-dependent diabetes mellitus (IDDM) and 2 prediabetic patients were examined for natural killer (NK) and antibody-dependent cellular cytotoxic activities (ADCC), lectin-dependent cellular cytotoxicity (LDCC), interferon- and interleukin-2-induced cytotoxicity, and concanavalin A-induced suppressor-cell activities in comparison with age-matched normal controls. |
| 213 | 2429979 | Interferon- and interleukin-2-induced NK activities were significantly higher with IDDM lymphocytes than with control cells. |
| 214 | 2429979 | The increased interferon- and interleukin-2-induced enhancement of NK activity and reduced suppressor activity of lymphocytes from IDDM patients may be involved in the pathogenesis of the disease. |
| 215 | 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. |
| 216 | 2493178 | A newly constructed chimeric IL-2 diphtheria toxin fusion protein specifically binds to and poisons activated T cells bearing the high-affinity IL-2R. |
| 217 | 2502462 | Persistent reduction of CD4/CD8 lymphocyte ratio and cell activation before the onset of type 1 (insulin-dependent) diabetes. |
| 218 | 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). |
| 219 | 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. |
| 220 | 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. |
| 221 | 2533502 | Treatment of mice with Poly [I:C] alone [50 micrograms twice weekly, an inducer of Interferon (IFN) alpha/beta] or in conjunction with rIL-2 was even more effective, completely preventing glycosuria for 20 weeks. |
| 222 | 2533502 | IL-2 treatment increased transcription of interleukin-1 (IL-1) mRNA in peritoneal macrophages and increased lipopolysaccharide (LPS)-stimulated IL-1 secretion in comparison to controls. |
| 223 | 2533502 | Peritoneal macrophages from Poly [I:C]-treated mice exhibited increased IFN alpha gene transcription and LPS-stimulated IL-1 secretion. |
| 224 | 2560916 | Interferon-gamma (IFN gamma) and interleukin 2 (IL-2) production by EMCV-D-infected spleen cell cultures were monitored at 4-hour intervals for 24 hours. |
| 225 | 2560916 | Addition of a monoclonal rat anti-mouse IL-2 to virus-infected cultures did not significantly affect the early (less than 16 hours PI) production of IFN gamma by spleen cells of females. |
| 226 | 2560916 | Treatment of the spleen cell donors with rabbit anti-asialo GM1 (AAGM1) abolished early production of IFN gamma in virus-infected female spleen cell cultures and reduced the early IL-2 production by infected male and female cells. |
| 227 | 2560916 | Interferon-gamma (IFN gamma) and interleukin 2 (IL-2) production by EMCV-D-infected spleen cell cultures were monitored at 4-hour intervals for 24 hours. |
| 228 | 2560916 | Addition of a monoclonal rat anti-mouse IL-2 to virus-infected cultures did not significantly affect the early (less than 16 hours PI) production of IFN gamma by spleen cells of females. |
| 229 | 2560916 | Treatment of the spleen cell donors with rabbit anti-asialo GM1 (AAGM1) abolished early production of IFN gamma in virus-infected female spleen cell cultures and reduced the early IL-2 production by infected male and female cells. |
| 230 | 2560916 | Interferon-gamma (IFN gamma) and interleukin 2 (IL-2) production by EMCV-D-infected spleen cell cultures were monitored at 4-hour intervals for 24 hours. |
| 231 | 2560916 | Addition of a monoclonal rat anti-mouse IL-2 to virus-infected cultures did not significantly affect the early (less than 16 hours PI) production of IFN gamma by spleen cells of females. |
| 232 | 2560916 | Treatment of the spleen cell donors with rabbit anti-asialo GM1 (AAGM1) abolished early production of IFN gamma in virus-infected female spleen cell cultures and reduced the early IL-2 production by infected male and female cells. |
| 233 | 2644144 | Effect of cyclosporin on interleukin 2-related T-lymphocyte parameters in IDDM patients. |
| 234 | 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. |
| 235 | 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. |
| 236 | 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). |
| 237 | 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). |
| 238 | 2644144 | Effect of cyclosporin on interleukin 2-related T-lymphocyte parameters in IDDM patients. |
| 239 | 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. |
| 240 | 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. |
| 241 | 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). |
| 242 | 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). |
| 243 | 2644144 | Effect of cyclosporin on interleukin 2-related T-lymphocyte parameters in IDDM patients. |
| 244 | 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. |
| 245 | 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. |
| 246 | 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). |
| 247 | 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). |
| 248 | 2654349 | Developmental regulation of serum interleukin-2 receptor concentrations: attenuation of the childhood peak in patients at risk for developing or having recently developed type I diabetes mellitus. |
| 249 | 2666213 | A higher percentage of activated cells was observed using another monoclonal antibody (7D4) directed against a different epitope of the interleukin 2 receptor, suggesting the presence of activated lymphocytes with interleukin 2 receptors saturated by interleukin 2. |
| 250 | 2676272 | Splenic T cells from NOD mice responded with IL-2 production and proliferation when both islet cell antigens from NOD mice and mitomycin C-treated spleen cells (source of antigen-presenting cells) from NOD mice or major histocompatibility complex (MHC)-compatible ILI mice were present. |
| 251 | 2783919 | In this study, we investigated whether an interleukin 2 (IL-2) secretion defect by peripheral blood mononuclear cells (PBMCs) after in vitro stimulation with phytohemagglutinin (PHA-M) occurs in either newly diagnosed or long-standing type I (insulin-dependent) diabetic patients and whether it is accompanied by a dysregulation of soluble IL-2-receptor (IL-2RS) production. |
| 252 | 2785066 | Evidence for macrophage-mediated suppression participating in the deficient function of splenic lymphocytes in this mouse model of insulin-dependent diabetes includes: 1) the restoration of mitogen-induced interleukin 2 production after the macrophages have been depleted by silica absorption form spleen cells; 2) the complete suppression of the cell proliferation by thioglycollate-stimulated peritoneal exudate cells from non-obese diabetic and control mice, and the partial suppression by spleen macrophages from non-obese diabetic mice; 3) the reversal of the suppression of interleukin 2 production by the prostaglandin synthetase inhibitor indomethacin (0.1-1 microgram/ml); 4) the partial suppression of interleukin 2 production, conversely, by the exogenous prostaglandins E1 and E2 (2.5 x 10(-6) mol/l). |
| 253 | 2792122 | We studied interleukin 1 (IL-1) and interleukin 2 (IL-2) production in unstimulated and stimulated cultures from 27 young diabetic patients and 21 age-matched healthy subjects. |
| 254 | 2792122 | IL-2 production was low or absent in unstimulated cultures from insulin-dependent diabetes mellitus (IDDM) patients and controls. |
| 255 | 2792122 | No correlation was observed between IL-1, IL-2 production and HbA1 levels or the presence of HLA-DR3 or DR4. |
| 256 | 2792122 | Our data on "spontaneous" IL-1 production support the hypothesis that monocytes from some newly diagnosed IDDM patients may circulate in a "preactivated" state. |
| 257 | 2792122 | We studied interleukin 1 (IL-1) and interleukin 2 (IL-2) production in unstimulated and stimulated cultures from 27 young diabetic patients and 21 age-matched healthy subjects. |
| 258 | 2792122 | IL-2 production was low or absent in unstimulated cultures from insulin-dependent diabetes mellitus (IDDM) patients and controls. |
| 259 | 2792122 | No correlation was observed between IL-1, IL-2 production and HbA1 levels or the presence of HLA-DR3 or DR4. |
| 260 | 2792122 | Our data on "spontaneous" IL-1 production support the hypothesis that monocytes from some newly diagnosed IDDM patients may circulate in a "preactivated" state. |
| 261 | 2792122 | We studied interleukin 1 (IL-1) and interleukin 2 (IL-2) production in unstimulated and stimulated cultures from 27 young diabetic patients and 21 age-matched healthy subjects. |
| 262 | 2792122 | IL-2 production was low or absent in unstimulated cultures from insulin-dependent diabetes mellitus (IDDM) patients and controls. |
| 263 | 2792122 | No correlation was observed between IL-1, IL-2 production and HbA1 levels or the presence of HLA-DR3 or DR4. |
| 264 | 2792122 | Our data on "spontaneous" IL-1 production support the hypothesis that monocytes from some newly diagnosed IDDM patients may circulate in a "preactivated" state. |
| 265 | 2824259 | Concanavalin A and recombinant interleukin 2, inducers of immune interferon, which in turn primes macrophages for activation and induces their expression of la antigens, protected the ICR Swiss male against the diabetogenic effects of EMCV-D. |
| 266 | 2887834 | The labelled IL2, which had a high specific activity (100-150 microCi/microgram) and retained its capacity for binding to the IL2 receptor on activated lymphocytes in vitro, was injected intravenously into BB/W diabetes-prone and normal rats. |
| 267 | 2887834 | Combined immunoperoxidase staining and autoradiography of organ sections revealed that labelled IL2 bound specifically in vivo to IL2-receptor-positive cells in the spleen of both normal and BB/W rats and to activated lymphocytes infiltrating the pancreas of BB/W rats. |
| 268 | 2887834 | The labelled IL2, which had a high specific activity (100-150 microCi/microgram) and retained its capacity for binding to the IL2 receptor on activated lymphocytes in vitro, was injected intravenously into BB/W diabetes-prone and normal rats. |
| 269 | 2887834 | Combined immunoperoxidase staining and autoradiography of organ sections revealed that labelled IL2 bound specifically in vivo to IL2-receptor-positive cells in the spleen of both normal and BB/W rats and to activated lymphocytes infiltrating the pancreas of BB/W rats. |
| 270 | 2897395 | A deficiency in cytokine release was not limited to IL-2, because peritoneal exudate cells from NOD exhibited a greatly diminished sensitivity to LPS-stimulated IL-1 release in comparison to SWR mice. |
| 271 | 2933286 | Results obtained by viability measurements and in vitro biological assays of lymphoid function, including proliferation in response to T- and B-cell mitogens, the production of interleukin-2 by T cells, and the production of interleukin-1 by macrophages indicated that direct exposure to alloxan for 48 h (at concentrations less than or equal to 14 mmol/l) had no adverse effects on lymphoid activity, while exposure to streptozotocin was routinely toxic at concentrations greater than or equal to 1 mmol/l. |
| 272 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 273 | 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. |
| 274 | 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. |
| 275 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 276 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 277 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 278 | 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. |
| 279 | 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. |
| 280 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 281 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 282 | 2972427 | The majority of the activated T cells in the blood of insulin-dependent diabetes mellitus (IDDM) patients are CD4+. |
| 283 | 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. |
| 284 | 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. |
| 285 | 2972427 | In recent onset insulin-dependent diabetes blood there was no lack of CD4 CD45R+ (suppressor/inducer) T cells. |
| 286 | 2972427 | The activated IL-2 receptor, expressing cells belonged to both CD4 subsets, 'helper inducer' (CD44B4) and 'suppressor inducer', (CD42H4). |
| 287 | 3093206 | The expression of activation antigens (transferrin receptor, IL-2 receptor and Ia antigen) on circulating T lymphocytes from Japanese children with Type 1 diabetes was studied using five monoclonal antibodies (Ab), OKT9, anti-Tac Ab, OKIa1, anti-human HLA-DR Ab and OKT3. |
| 288 | 3098471 | Monolayer cultures from 25 human pancreatic glands were supplemented with alpha-interferon (IFN), beta-IFN or gamma-IFN, interleukin 2 (IL-2) and supernatants from activated lymphocytes. |
| 289 | 3110074 | Previous studies have shown several immunoregulatory abnormalities in insulin-dependent diabetes mellitus (IDDM). |
| 290 | 3110074 | In this report we compared peripheral blood mononuclear cells (PBMC) from patients with IDDM complicated by end-stage renal disease (ESRD) to those from normal subjects and from patients with ESRD of different etiologies for their: natural killer (NK) and antibody-dependent cell-mediated cytotoxic (ADCC) activities; modulation of NK and ADCC activities by biological response modifiers (BRM) including purified human lymphoblastoid interferon, human recombinant alpha-2 interferon, human gamma interferon and human recombinant interleukin 2; proliferative response of T and B lymphocytes to concanavalin A (Con A), phytohemagglutinin and pokeweed mitogen, and ability to produce T-cell growth factor (interleukin 2; IL-2). |
| 291 | 3110074 | The proliferative responses to Con A, phytohemagglutinin and pokeweed mitogen as well as IL-2 production in response to Con A stimulation were significantly lower in the IDDM group. |
| 292 | 3110074 | Our results indicated that NK cells from patients with IDDM can respond to IL-2 with enhanced cytotoxicity, and, because activation of resting T cells by mitogenic stimuli depends on the production of IL-2 as well as the appearance of a receptor for IL-2, our finding of low levels of in vitro IL-2 production by PBMC from patients with IDDM may explain the depressed NK activity and the observed poor response to T-cell mitogens. |
| 293 | 3110074 | Previous studies have shown several immunoregulatory abnormalities in insulin-dependent diabetes mellitus (IDDM). |
| 294 | 3110074 | In this report we compared peripheral blood mononuclear cells (PBMC) from patients with IDDM complicated by end-stage renal disease (ESRD) to those from normal subjects and from patients with ESRD of different etiologies for their: natural killer (NK) and antibody-dependent cell-mediated cytotoxic (ADCC) activities; modulation of NK and ADCC activities by biological response modifiers (BRM) including purified human lymphoblastoid interferon, human recombinant alpha-2 interferon, human gamma interferon and human recombinant interleukin 2; proliferative response of T and B lymphocytes to concanavalin A (Con A), phytohemagglutinin and pokeweed mitogen, and ability to produce T-cell growth factor (interleukin 2; IL-2). |
| 295 | 3110074 | The proliferative responses to Con A, phytohemagglutinin and pokeweed mitogen as well as IL-2 production in response to Con A stimulation were significantly lower in the IDDM group. |
| 296 | 3110074 | Our results indicated that NK cells from patients with IDDM can respond to IL-2 with enhanced cytotoxicity, and, because activation of resting T cells by mitogenic stimuli depends on the production of IL-2 as well as the appearance of a receptor for IL-2, our finding of low levels of in vitro IL-2 production by PBMC from patients with IDDM may explain the depressed NK activity and the observed poor response to T-cell mitogens. |
| 297 | 3110074 | Previous studies have shown several immunoregulatory abnormalities in insulin-dependent diabetes mellitus (IDDM). |
| 298 | 3110074 | In this report we compared peripheral blood mononuclear cells (PBMC) from patients with IDDM complicated by end-stage renal disease (ESRD) to those from normal subjects and from patients with ESRD of different etiologies for their: natural killer (NK) and antibody-dependent cell-mediated cytotoxic (ADCC) activities; modulation of NK and ADCC activities by biological response modifiers (BRM) including purified human lymphoblastoid interferon, human recombinant alpha-2 interferon, human gamma interferon and human recombinant interleukin 2; proliferative response of T and B lymphocytes to concanavalin A (Con A), phytohemagglutinin and pokeweed mitogen, and ability to produce T-cell growth factor (interleukin 2; IL-2). |
| 299 | 3110074 | The proliferative responses to Con A, phytohemagglutinin and pokeweed mitogen as well as IL-2 production in response to Con A stimulation were significantly lower in the IDDM group. |
| 300 | 3110074 | Our results indicated that NK cells from patients with IDDM can respond to IL-2 with enhanced cytotoxicity, and, because activation of resting T cells by mitogenic stimuli depends on the production of IL-2 as well as the appearance of a receptor for IL-2, our finding of low levels of in vitro IL-2 production by PBMC from patients with IDDM may explain the depressed NK activity and the observed poor response to T-cell mitogens. |
| 301 | 3118853 | [Immunological studies on insulin-dependent diabetes mellitus (IDDM). 2. |
| 302 | 3118853 | Expression of interleukin-2 receptor by stimulation and interleukin-2 responsiveness]. |
| 303 | 3121415 | Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin, and interleukin 1. |
| 304 | 3121415 | When tested alone, murine (rat and mouse) interferon-gamma (mIFN-gamma) produced a small dose-dependent lysis of islet cells; human IFN-gamma, mouse IFN-alpha/beta, interleukins 1 and 2 (IL-1 and IL-2), tumor necrosis factor (TNF), and lymphotoxin (LT) were inactive. |
| 305 | 3121415 | When added together, the following combinations of cytokines showed synergistic cytotoxic effects: TNF (or LT) plus IL-1, TNF (or LT) plus mIFN-gamma, and IL-1 plus mIFN-gamma. |
| 306 | 3121415 | These results indicate that the cytokine products of mononuclear cells of the immune system, IFN-gamma, TNF, LT, and IL-1 have strong synergistic cytotoxic effects on islet cells and therefore may act as direct chemical mediators of islet beta-cell destruction in type I (insulin-dependent) diabetes. |
| 307 | 3134297 | IL-1 and IFN-gamma increase vascular permeability. |
| 308 | 3134297 | Injections of a mixture of recombinant interleukin-1 alpha and beta (Il-1 alpha, IL-1 beta) and interferon-gamma (IFN-gamma) caused a maximal increase of permeability after 30 min (delta PI = 2). |
| 309 | 3134297 | The administration of single recombinant cytokines revealed that the increase of permeability is mainly due to the action of IL-1 beta (delta PI = 1.4) and IFN-gamma (delta PI = 2.9) (P less than 0.001) at doses of 1-20 microU per injection site. |
| 310 | 3134297 | IL-1 alpha slightly increased vascular permeability, whereas recombinant IL-2 and recombinant tumour necrosis factor alpha had no significant effects. |
| 311 | 3134297 | Histological observations revealed significantly increased numbers of degranulated mast cells in skin sections pretreated with IL-1 beta (P less than 0.005) or IFN-gamma (P less than 0.001). |
| 312 | 3134297 | Our experiments indicate an important role of IL-1 beta and IFN-gamma as vasoactive substances besides their function as hormone-like messengers between leucocytes. |
| 313 | 3136960 | Interleukin-2 production and interleukin-2 receptor expression in children with newly diagnosed diabetes. |
| 314 | 3136960 | In the present study, we investigated the interleukin-2 (IL-2) production and the proliferative responses by peripheral blood mononuclear cells (PBMNC) of 23 children suffering from insulin-dependent diabetes mellitus (IDDM). |
| 315 | 3136960 | In addition, the presence of circulating activated T lymphocytes expressing the interleukin-2 receptor (IL-2 R) and HLA-DR antigens was evaluated. |
| 316 | 3136960 | Decreased IL-2 production by phytohemagglutinin (PHA)-activated PBMNC of IDDM patients was observed when compared to normal donors. |
| 317 | 3136960 | These results confirm the presence in IDDM patients of an imbalanced cellular immune response and demonstrate that the IL-2 deficiency is already present at the diagnosis and is not correlated with insulin administration. |
| 318 | 3136960 | Interleukin-2 production and interleukin-2 receptor expression in children with newly diagnosed diabetes. |
| 319 | 3136960 | In the present study, we investigated the interleukin-2 (IL-2) production and the proliferative responses by peripheral blood mononuclear cells (PBMNC) of 23 children suffering from insulin-dependent diabetes mellitus (IDDM). |
| 320 | 3136960 | In addition, the presence of circulating activated T lymphocytes expressing the interleukin-2 receptor (IL-2 R) and HLA-DR antigens was evaluated. |
| 321 | 3136960 | Decreased IL-2 production by phytohemagglutinin (PHA)-activated PBMNC of IDDM patients was observed when compared to normal donors. |
| 322 | 3136960 | These results confirm the presence in IDDM patients of an imbalanced cellular immune response and demonstrate that the IL-2 deficiency is already present at the diagnosis and is not correlated with insulin administration. |
| 323 | 3136960 | Interleukin-2 production and interleukin-2 receptor expression in children with newly diagnosed diabetes. |
| 324 | 3136960 | In the present study, we investigated the interleukin-2 (IL-2) production and the proliferative responses by peripheral blood mononuclear cells (PBMNC) of 23 children suffering from insulin-dependent diabetes mellitus (IDDM). |
| 325 | 3136960 | In addition, the presence of circulating activated T lymphocytes expressing the interleukin-2 receptor (IL-2 R) and HLA-DR antigens was evaluated. |
| 326 | 3136960 | Decreased IL-2 production by phytohemagglutinin (PHA)-activated PBMNC of IDDM patients was observed when compared to normal donors. |
| 327 | 3136960 | These results confirm the presence in IDDM patients of an imbalanced cellular immune response and demonstrate that the IL-2 deficiency is already present at the diagnosis and is not correlated with insulin administration. |
| 328 | 3136960 | Interleukin-2 production and interleukin-2 receptor expression in children with newly diagnosed diabetes. |
| 329 | 3136960 | In the present study, we investigated the interleukin-2 (IL-2) production and the proliferative responses by peripheral blood mononuclear cells (PBMNC) of 23 children suffering from insulin-dependent diabetes mellitus (IDDM). |
| 330 | 3136960 | In addition, the presence of circulating activated T lymphocytes expressing the interleukin-2 receptor (IL-2 R) and HLA-DR antigens was evaluated. |
| 331 | 3136960 | Decreased IL-2 production by phytohemagglutinin (PHA)-activated PBMNC of IDDM patients was observed when compared to normal donors. |
| 332 | 3136960 | These results confirm the presence in IDDM patients of an imbalanced cellular immune response and demonstrate that the IL-2 deficiency is already present at the diagnosis and is not correlated with insulin administration. |
| 333 | 3136960 | Interleukin-2 production and interleukin-2 receptor expression in children with newly diagnosed diabetes. |
| 334 | 3136960 | In the present study, we investigated the interleukin-2 (IL-2) production and the proliferative responses by peripheral blood mononuclear cells (PBMNC) of 23 children suffering from insulin-dependent diabetes mellitus (IDDM). |
| 335 | 3136960 | In addition, the presence of circulating activated T lymphocytes expressing the interleukin-2 receptor (IL-2 R) and HLA-DR antigens was evaluated. |
| 336 | 3136960 | Decreased IL-2 production by phytohemagglutinin (PHA)-activated PBMNC of IDDM patients was observed when compared to normal donors. |
| 337 | 3136960 | These results confirm the presence in IDDM patients of an imbalanced cellular immune response and demonstrate that the IL-2 deficiency is already present at the diagnosis and is not correlated with insulin administration. |
| 338 | 3138125 | There is ample evidence that cell-mediated immune mechanisms are crucial in the initiation of insulin-dependent diabetes mellitus (IDDM). |
| 339 | 3138125 | Interleukin 1 (IL 1) activity was measured by the thymocyte co-stimulator assay, and interleukin 2 (IL 2) using IL 2 dependent cell lines. |
| 340 | 3138125 | Peripheral blood T-lymphocyte IL 2 production at onset of IDDM was normal under basal conditions, and upon optimal stimulation with concanavalin A (ConA) and phorbol myristate acetate (PMA). |
| 341 | 3138125 | We conclude that monocytes and T-lymphocytes from patients with diabetes mellitus have a diminished capacity to release IL 1 and IL 2 only later in the course of the disease. |
| 342 | 3138125 | At the time of manifestation of disease, IL 1 and IL 2 production is normal in type-I diabetes mellitus. |
| 343 | 3138125 | There is ample evidence that cell-mediated immune mechanisms are crucial in the initiation of insulin-dependent diabetes mellitus (IDDM). |
| 344 | 3138125 | Interleukin 1 (IL 1) activity was measured by the thymocyte co-stimulator assay, and interleukin 2 (IL 2) using IL 2 dependent cell lines. |
| 345 | 3138125 | Peripheral blood T-lymphocyte IL 2 production at onset of IDDM was normal under basal conditions, and upon optimal stimulation with concanavalin A (ConA) and phorbol myristate acetate (PMA). |
| 346 | 3138125 | We conclude that monocytes and T-lymphocytes from patients with diabetes mellitus have a diminished capacity to release IL 1 and IL 2 only later in the course of the disease. |
| 347 | 3138125 | At the time of manifestation of disease, IL 1 and IL 2 production is normal in type-I diabetes mellitus. |
| 348 | 3138125 | There is ample evidence that cell-mediated immune mechanisms are crucial in the initiation of insulin-dependent diabetes mellitus (IDDM). |
| 349 | 3138125 | Interleukin 1 (IL 1) activity was measured by the thymocyte co-stimulator assay, and interleukin 2 (IL 2) using IL 2 dependent cell lines. |
| 350 | 3138125 | Peripheral blood T-lymphocyte IL 2 production at onset of IDDM was normal under basal conditions, and upon optimal stimulation with concanavalin A (ConA) and phorbol myristate acetate (PMA). |
| 351 | 3138125 | We conclude that monocytes and T-lymphocytes from patients with diabetes mellitus have a diminished capacity to release IL 1 and IL 2 only later in the course of the disease. |
| 352 | 3138125 | At the time of manifestation of disease, IL 1 and IL 2 production is normal in type-I diabetes mellitus. |
| 353 | 3138125 | There is ample evidence that cell-mediated immune mechanisms are crucial in the initiation of insulin-dependent diabetes mellitus (IDDM). |
| 354 | 3138125 | Interleukin 1 (IL 1) activity was measured by the thymocyte co-stimulator assay, and interleukin 2 (IL 2) using IL 2 dependent cell lines. |
| 355 | 3138125 | Peripheral blood T-lymphocyte IL 2 production at onset of IDDM was normal under basal conditions, and upon optimal stimulation with concanavalin A (ConA) and phorbol myristate acetate (PMA). |
| 356 | 3138125 | We conclude that monocytes and T-lymphocytes from patients with diabetes mellitus have a diminished capacity to release IL 1 and IL 2 only later in the course of the disease. |
| 357 | 3138125 | At the time of manifestation of disease, IL 1 and IL 2 production is normal in type-I diabetes mellitus. |
| 358 | 3150011 | Dissociated production of interleukin-2 and immune gamma-interferon by phytohaemoagglutinin stimulated peripheral mononuclear cells in type 1 (insulin-dependent) diabetes. |
| 359 | 3159965 | Some of the T cells were "activated" (positive for HLA-DR antigen, and the interleukin-2 receptor). |
| 360 | 3159965 | Increased expression of Class I (HLA-A, B, and C) molecules was observed in the affected islet cells, and in damaged islets showing scant lymphocytic infiltration, some beta cells (still producing insulin), but not glucagon or somatostatin cells, were HLA-DR positive. |
| 361 | 3265901 | Increased soluble interleukin-2 receptor levels in the sera of type 1 diabetic patients. |
| 362 | 3265901 | Our findings suggest a potentially significant role for the released IL-2R in the regulation of IL-2 dependent lymphocyte functions in Type 1 diabetes. |
| 363 | 3265901 | Increased soluble interleukin-2 receptor levels in the sera of type 1 diabetic patients. |
| 364 | 3265901 | Our findings suggest a potentially significant role for the released IL-2R in the regulation of IL-2 dependent lymphocyte functions in Type 1 diabetes. |
| 365 | 3266157 | To evaluate the role of zinc status in immune system dysfunction in diabetic animals, the interleukin-2 production and the lymphocyte mitogenic response to phytohaemagglutinin, concanavalin A and lipopolysaccharide were measured in streptozotocin-induced diabetic rats, diabetic rats treated with insulin and their non-diabetic controls maintained on low zinc, normal zinc and high zinc diets for 3 weeks. |
| 366 | 3266991 | Monoclonal antibodies (Mab) targeting certain T cell-surface proteins including the interleukin-2 (IL2) receptor molecule exert powerful immunosuppressive effects. |
| 367 | 3266991 | The induced antibodies are capable of blocking M7/20 binding to its target, the IL2 receptor, in vitro. |
| 368 | 3266991 | Monoclonal antibodies (Mab) targeting certain T cell-surface proteins including the interleukin-2 (IL2) receptor molecule exert powerful immunosuppressive effects. |
| 369 | 3266991 | The induced antibodies are capable of blocking M7/20 binding to its target, the IL2 receptor, in vitro. |
| 370 | 3311852 | Of several lymphokine products of ConA-stimulated lymphoid cells, interleukin 2 (IL-2), but not interleukin 1 or interferon-gamma, significantly activated splenic lymphoid cells cytotoxic to islet cells, and the lymphoid cells from diabetic rats were more sensitive to IL-2 (3 U/ml) than were the cells from DR rats (30 U/ml). |
| 371 | 3494640 | When compared to PBMC from 18 control subjects, mean PHA-stimulated IL-2 synthesis in the diabetic group was found unimpaired (1.2 +/- 0.1 vs 1.5 +/- 0.2 U/ml). |
| 372 | 3497274 | Lymphocyte responsiveness and interleukin 2 production in type 1 (insulin-dependent) diabetes mellitus. |
| 373 | 3514237 | Recombinant interleukin 2 enhances spontaneous insulin-dependent diabetes in BB rats. |
| 374 | 3514344 | Addition of highly purified human Interleukin-1 to the culture medium of isolated rat islets of Langerhans for 6 days led to 88% inhibition of glucose-induced insulin-release, reduction of islet contents of insulin and glucagon to 31% and 8% respectively, and disintegration of the islets. |
| 375 | 3514344 | Highly purified human Interleukin-2, Lymphotoxin, Leucocyte Migration Inhibitory Factor and Macrophage Migration Inhibitory Factor were ineffective. |
| 376 | 3514344 | These findings suggest that Interleukin-1 may play an important role in the molecular mechanisms underlying autoimmune B-cell destruction leading to Type 1 (insulin-dependent) diabetes mellitus. |
| 377 | 3531850 | We therefore measured interleukin-2 production in 27 patients with Type I diabetes, 20 patients with Type II diabetes (6 requiring insulin), 5 monozygotic twin pairs discordant for Type I diabetes, and 10 nondiabetic persons with islet-cell antibodies. |
| 378 | 3531850 | There was no correlation between glycosylated hemoglobin levels and interleukin-2 production in any diabetic group. |
| 379 | 3531850 | We conclude that patients with Type I diabetes have an acquired defect in interleukin-2 production, whereas patients with Type II diabetes do not, and that this defect is not correlated with an ongoing autoimmune process, with hyperglycemia, or with insulin administration or oral hypoglycemic therapy. |
| 380 | 3531850 | We therefore measured interleukin-2 production in 27 patients with Type I diabetes, 20 patients with Type II diabetes (6 requiring insulin), 5 monozygotic twin pairs discordant for Type I diabetes, and 10 nondiabetic persons with islet-cell antibodies. |
| 381 | 3531850 | There was no correlation between glycosylated hemoglobin levels and interleukin-2 production in any diabetic group. |
| 382 | 3531850 | We conclude that patients with Type I diabetes have an acquired defect in interleukin-2 production, whereas patients with Type II diabetes do not, and that this defect is not correlated with an ongoing autoimmune process, with hyperglycemia, or with insulin administration or oral hypoglycemic therapy. |
| 383 | 3531850 | We therefore measured interleukin-2 production in 27 patients with Type I diabetes, 20 patients with Type II diabetes (6 requiring insulin), 5 monozygotic twin pairs discordant for Type I diabetes, and 10 nondiabetic persons with islet-cell antibodies. |
| 384 | 3531850 | There was no correlation between glycosylated hemoglobin levels and interleukin-2 production in any diabetic group. |
| 385 | 3531850 | We conclude that patients with Type I diabetes have an acquired defect in interleukin-2 production, whereas patients with Type II diabetes do not, and that this defect is not correlated with an ongoing autoimmune process, with hyperglycemia, or with insulin administration or oral hypoglycemic therapy. |
| 386 | 6088584 | The stimulation of this response by TCGF may provide a tool by which enough cytotoxic effector cells could be obtained to establish their possible direct pathogenetic role in the induction of insulin-dependent diabetes. |
| 387 | 6239872 | The autologous mixed lymphocyte response (AMLR) and the allogeneic mixed lymphocyte response were deficient in a subset of patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM). |
| 388 | 6239872 | This suggests that the deficient AMLR in IDDM may be in part due to a deficiency in the production of interleukin-2. |
| 389 | 6368290 | Blood T-cells from 28 patients with type I (insulin-dependent) diabetes (IDDM) of variable duration were examined for the Tac antigen by immunofluorescence, and for proliferation in the presence of interleukin 2 (IL 2). |
| 390 | 6378703 | Such T-lymphocytes responded by proliferation and IL-2 secretion in the combined presence of islet cell antigens and major histocompatibility (MHC)-matched antigen-presenting cells. |
| 391 | 6607315 | This abnormality was not due solely to abnormal T cell numbers since: (a) addition of BB spleen cells of BB splenic macrophages to normal major histocompatibility complex (MHC)-matched Wistar Furth (WF) spleen cells resulted in severe suppression of concanavalin A (Con A)-, phytohemagglutinin (PHA)-, and pokeweed mitogen (PWM)-mediated proliferation, and IL-2 production; (b) macrophage depletion from BB spleen cells, but not B cell or T cell depletion, removed completely the suppressive effects of BB cells on WF cells; (c) macrophage depletion greatly enhanced the response of BB lymphocytes to T-dependent mitogens. |
| 392 | 6607315 | Furthermore, indomethacin (but not catalase or PMA) considerably augmented IL-2 secretion of Con A-stimulated BB spleen cells, but had little effect on WF spleen cells. |
| 393 | 6607315 | While IL-2 secretion was severely depressed in BB rats unstimulated and lipopolysaccharide (LPS)-stimulated IL-1 secretion by splenic macrophages was normal. |
| 394 | 6607315 | This abnormality was not due solely to abnormal T cell numbers since: (a) addition of BB spleen cells of BB splenic macrophages to normal major histocompatibility complex (MHC)-matched Wistar Furth (WF) spleen cells resulted in severe suppression of concanavalin A (Con A)-, phytohemagglutinin (PHA)-, and pokeweed mitogen (PWM)-mediated proliferation, and IL-2 production; (b) macrophage depletion from BB spleen cells, but not B cell or T cell depletion, removed completely the suppressive effects of BB cells on WF cells; (c) macrophage depletion greatly enhanced the response of BB lymphocytes to T-dependent mitogens. |
| 395 | 6607315 | Furthermore, indomethacin (but not catalase or PMA) considerably augmented IL-2 secretion of Con A-stimulated BB spleen cells, but had little effect on WF spleen cells. |
| 396 | 6607315 | While IL-2 secretion was severely depressed in BB rats unstimulated and lipopolysaccharide (LPS)-stimulated IL-1 secretion by splenic macrophages was normal. |
| 397 | 6607315 | This abnormality was not due solely to abnormal T cell numbers since: (a) addition of BB spleen cells of BB splenic macrophages to normal major histocompatibility complex (MHC)-matched Wistar Furth (WF) spleen cells resulted in severe suppression of concanavalin A (Con A)-, phytohemagglutinin (PHA)-, and pokeweed mitogen (PWM)-mediated proliferation, and IL-2 production; (b) macrophage depletion from BB spleen cells, but not B cell or T cell depletion, removed completely the suppressive effects of BB cells on WF cells; (c) macrophage depletion greatly enhanced the response of BB lymphocytes to T-dependent mitogens. |
| 398 | 6607315 | Furthermore, indomethacin (but not catalase or PMA) considerably augmented IL-2 secretion of Con A-stimulated BB spleen cells, but had little effect on WF spleen cells. |
| 399 | 6607315 | While IL-2 secretion was severely depressed in BB rats unstimulated and lipopolysaccharide (LPS)-stimulated IL-1 secretion by splenic macrophages was normal. |
| 400 | 6609855 | Decreased synthesis of interleukin-2 (IL-2) in insulin-dependent diabetes mellitus. |
| 401 | 6609855 | Synthesis of interleukin-2 (IL-2) by lymphocytes from 26 insulin-dependent diabetic subjects (IDDM) was compared with that by lymphocytes from 24 nondiabetic control subjects. |
| 402 | 6609855 | IL-2 synthesis by 6 non-insulin-dependent diabetic subjects (NIDDM) was not decreased (mean +/- SEM, 1.20 +/- 0.04 U/ml). |
| 403 | 6609855 | These data suggest that decreased IL-2 synthesis is specific for IDDM, not explainable solely as a consequence of poor metabolic control, and thus, might be involved in the pathogenesis of the disease. |
| 404 | 6609855 | Decreased synthesis of interleukin-2 (IL-2) in insulin-dependent diabetes mellitus. |
| 405 | 6609855 | Synthesis of interleukin-2 (IL-2) by lymphocytes from 26 insulin-dependent diabetic subjects (IDDM) was compared with that by lymphocytes from 24 nondiabetic control subjects. |
| 406 | 6609855 | IL-2 synthesis by 6 non-insulin-dependent diabetic subjects (NIDDM) was not decreased (mean +/- SEM, 1.20 +/- 0.04 U/ml). |
| 407 | 6609855 | These data suggest that decreased IL-2 synthesis is specific for IDDM, not explainable solely as a consequence of poor metabolic control, and thus, might be involved in the pathogenesis of the disease. |
| 408 | 6609855 | Decreased synthesis of interleukin-2 (IL-2) in insulin-dependent diabetes mellitus. |
| 409 | 6609855 | Synthesis of interleukin-2 (IL-2) by lymphocytes from 26 insulin-dependent diabetic subjects (IDDM) was compared with that by lymphocytes from 24 nondiabetic control subjects. |
| 410 | 6609855 | IL-2 synthesis by 6 non-insulin-dependent diabetic subjects (NIDDM) was not decreased (mean +/- SEM, 1.20 +/- 0.04 U/ml). |
| 411 | 6609855 | These data suggest that decreased IL-2 synthesis is specific for IDDM, not explainable solely as a consequence of poor metabolic control, and thus, might be involved in the pathogenesis of the disease. |
| 412 | 6609855 | Decreased synthesis of interleukin-2 (IL-2) in insulin-dependent diabetes mellitus. |
| 413 | 6609855 | Synthesis of interleukin-2 (IL-2) by lymphocytes from 26 insulin-dependent diabetic subjects (IDDM) was compared with that by lymphocytes from 24 nondiabetic control subjects. |
| 414 | 6609855 | IL-2 synthesis by 6 non-insulin-dependent diabetic subjects (NIDDM) was not decreased (mean +/- SEM, 1.20 +/- 0.04 U/ml). |
| 415 | 6609855 | These data suggest that decreased IL-2 synthesis is specific for IDDM, not explainable solely as a consequence of poor metabolic control, and thus, might be involved in the pathogenesis of the disease. |
| 416 | 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. |
| 417 | 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. |
| 418 | 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. |
| 419 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 420 | 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. |
| 421 | 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. |
| 422 | 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. |
| 423 | 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. |
| 424 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 425 | 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. |
| 426 | 7516851 | The percentage of CD57+ cells was similar in IDDM patients and controls, while the percentage of CD16+ cells was lower in IDDM patients (P < 0.05) than in controls. |
| 427 | 7516851 | The decreased NK cytotoxic activity observed in our patients, in particular in long-standing diabetics, with normal NK cell number, could be due to a qualitative defect of the NK cells, or to a deficient IL-2 and/or TNF-alpha production, or to a immunomodulatory or immunosuppressing effect of insulin. |
| 428 | 7540571 | We detect a significant increase in the level of expression of interferon (IFN)-alpha in the pancreases of the diabetic patients as compared with the control pancreases. |
| 429 | 7540571 | In contrast, IFN-beta was detected at comparable levels in both groups, while IFN-gamma was detected in three of four control pancreases and one of four pancreases from the diabetic individuals. |
| 430 | 7540571 | The IFN-alpha cDNAs generated by the RT-PCR were cloned and sequenced to determine which alpha-subtypes were being expressed. |
| 431 | 7540571 | We also examined these pancreases for the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-2, IL-4, and IL-6. |
| 432 | 7540571 | We found no detectable expression of TNF-alpha or IL-2 in any pancreases, and the expression of the other cytokines was variable, with no pattern emerging from the comparison of the diabetic and nondiabetic individuals. |
| 433 | 7540571 | We conclude that, of the cytokines examined, only IFN-alpha was significantly increased in the diabetic patients, a result that is consistent with the possibility that this cytokine is directly involved in the development of type I diabetes. |
| 434 | 7540571 | We detect a significant increase in the level of expression of interferon (IFN)-alpha in the pancreases of the diabetic patients as compared with the control pancreases. |
| 435 | 7540571 | In contrast, IFN-beta was detected at comparable levels in both groups, while IFN-gamma was detected in three of four control pancreases and one of four pancreases from the diabetic individuals. |
| 436 | 7540571 | The IFN-alpha cDNAs generated by the RT-PCR were cloned and sequenced to determine which alpha-subtypes were being expressed. |
| 437 | 7540571 | We also examined these pancreases for the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-2, IL-4, and IL-6. |
| 438 | 7540571 | We found no detectable expression of TNF-alpha or IL-2 in any pancreases, and the expression of the other cytokines was variable, with no pattern emerging from the comparison of the diabetic and nondiabetic individuals. |
| 439 | 7540571 | We conclude that, of the cytokines examined, only IFN-alpha was significantly increased in the diabetic patients, a result that is consistent with the possibility that this cytokine is directly involved in the development of type I diabetes. |
| 440 | 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. |
| 441 | 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. |
| 442 | 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). |
| 443 | 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). |
| 444 | 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. |
| 445 | 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. |
| 446 | 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). |
| 447 | 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. |
| 448 | 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. |
| 449 | 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. |
| 450 | 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. |
| 451 | 7647584 | Three IDDM patients had detectable IL-1 beta and this weakly so (< 3.5 pg/ml). |
| 452 | 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. |
| 453 | 7652767 | Combined therapy with interleukin-4 and interleukin-10 inhibits autoimmune diabetes recurrence in syngeneic islet-transplanted nonobese diabetic mice. |
| 454 | 7652767 | IL-4 and IL-10 are cytokines that inhibit cell-mediated immunity. |
| 455 | 7652767 | In this study, we evaluated the effects of IL-4 and IL-10 on the survival of syngeneic pancreatic islets transplanted into diabetic NOD mice. |
| 456 | 7652767 | Islet grafts survived beyond 18 days and normoglycemia was maintained in 67% (10 of 15) of mice treated with IL-4 plus IL-10, but in none (0 of 20) of vehicle-injected (control) mice. |
| 457 | 7652767 | Also, 40% (6 of 15) of the mice treated with IL-4 plus IL-10 were normoglycemic at 30 days after transplantation, compared with 14% (1 of 7) of the mice treated with IL-4 alone, 8% (1 of 13) of the mice treated with IL-10 alone, and none (0 of 20) of the control mice. |
| 458 | 7652767 | Histological examination of grafts at 10 days after transplantation revealed peri-islet accumulations of mononuclear leukocytes and intact islet beta cells in grafts from IL-4 plus IL-10-treated mice, whereas islets were infiltrated by leukocytes and the beta cell mass was greatly reduced in grafts from control mice. |
| 459 | 7652767 | Polymerase chain reaction (PCR) analysis of cytokine mRNA expression in the grafts revealed higher levels of IL-2, IFN gamma, and IL-10 mRNA in grafts of diabetic compared with normoglycemic control mice, whereas IFN gamma and TNF alpha mRNA levels were significantly decreased in grafts of IL-4 plus IL-10-treated mice compared with either normoglycemic or diabetic control mice. |
| 460 | 7652767 | These results suggest that T helper (Th)1 cells and their cytokine products (IL-2, IFN gamma, and TNF alpha) may promote islet beta cell destructive insulitis and autoimmune diabetes recurrence in syngeneic islet-transplanted NOD mice, and that administration of IL-4 plus IL-10 may inhibit diabetes recurrence by suppressing Th1 cytokine production in the islet grafts. |
| 461 | 7652767 | Combined therapy with interleukin-4 and interleukin-10 inhibits autoimmune diabetes recurrence in syngeneic islet-transplanted nonobese diabetic mice. |
| 462 | 7652767 | IL-4 and IL-10 are cytokines that inhibit cell-mediated immunity. |
| 463 | 7652767 | In this study, we evaluated the effects of IL-4 and IL-10 on the survival of syngeneic pancreatic islets transplanted into diabetic NOD mice. |
| 464 | 7652767 | Islet grafts survived beyond 18 days and normoglycemia was maintained in 67% (10 of 15) of mice treated with IL-4 plus IL-10, but in none (0 of 20) of vehicle-injected (control) mice. |
| 465 | 7652767 | Also, 40% (6 of 15) of the mice treated with IL-4 plus IL-10 were normoglycemic at 30 days after transplantation, compared with 14% (1 of 7) of the mice treated with IL-4 alone, 8% (1 of 13) of the mice treated with IL-10 alone, and none (0 of 20) of the control mice. |
| 466 | 7652767 | Histological examination of grafts at 10 days after transplantation revealed peri-islet accumulations of mononuclear leukocytes and intact islet beta cells in grafts from IL-4 plus IL-10-treated mice, whereas islets were infiltrated by leukocytes and the beta cell mass was greatly reduced in grafts from control mice. |
| 467 | 7652767 | Polymerase chain reaction (PCR) analysis of cytokine mRNA expression in the grafts revealed higher levels of IL-2, IFN gamma, and IL-10 mRNA in grafts of diabetic compared with normoglycemic control mice, whereas IFN gamma and TNF alpha mRNA levels were significantly decreased in grafts of IL-4 plus IL-10-treated mice compared with either normoglycemic or diabetic control mice. |
| 468 | 7652767 | These results suggest that T helper (Th)1 cells and their cytokine products (IL-2, IFN gamma, and TNF alpha) may promote islet beta cell destructive insulitis and autoimmune diabetes recurrence in syngeneic islet-transplanted NOD mice, and that administration of IL-4 plus IL-10 may inhibit diabetes recurrence by suppressing Th1 cytokine production in the islet grafts. |
| 469 | 7656336 | Previously we reported that the administration of human (h) lymphotoxin (h-LT) markedly protected NOD mice from insulin-dependent diabetes mellitus (IDDM) partly by affecting the generation phase of anti-islet effector cells, probably in the thymus. |
| 470 | 7656336 | The low c-Fos expression in the female NOD thymocytes was most prominent in CD3low thymocytes. c-Jun expression of the CD3low thymocytes was also lower in the female NOD mice. |
| 471 | 7656336 | Administrations of h-LT, h-TNF, and h-IL-2, which has been reported to prevent IDDM in NOD mice by systemic administration, significantly up-regulated c-Fos expression in CD3low thymocytes. |
| 472 | 7656336 | From these results, it is assumed that a relationship may exist between the high diabetes incidence and the defective c-Fos expression in female NOD mice and between the prevention of IDDM and the amelioration of the defective c-Fos expression with h-LT in female NOD mice. |
| 473 | 7718517 | Differential patterns of production of granulocyte macrophage colony stimulating factor, IL-2, IL-3 and IL-4 by cultured islets of Langerhans from non-obese diabetic and non-diabetic strains of mice. |
| 474 | 7718517 | Each of the cytokines studied, i.e. granulocyte-monocyte colony stimulating factor (GM-CSF), IL-2, IL-3 and IL-4, showed different patterns of production. |
| 475 | 7718517 | For NOD islets, GM-CSF and IL-3 levels correlated with the degree of infiltrate release, although production was not confined to islets that released mononuclear cells in vitro. |
| 476 | 7718517 | However, GM-CSF differed from IL-3 in that it was produced by islets from some non-diabetic strains of mice, whereas IL-3 production was confined to NOD islets. |
| 477 | 7718517 | Finally, male NOD islets produced more IL-4 than females, possibly related to the lower incidence of diabetes in males, but unlike GM-CSF and IL-3, IL-4 production did not correlate with the degree of infiltrate released in culture. |
| 478 | 7718517 | Differential patterns of production of granulocyte macrophage colony stimulating factor, IL-2, IL-3 and IL-4 by cultured islets of Langerhans from non-obese diabetic and non-diabetic strains of mice. |
| 479 | 7718517 | Each of the cytokines studied, i.e. granulocyte-monocyte colony stimulating factor (GM-CSF), IL-2, IL-3 and IL-4, showed different patterns of production. |
| 480 | 7718517 | For NOD islets, GM-CSF and IL-3 levels correlated with the degree of infiltrate release, although production was not confined to islets that released mononuclear cells in vitro. |
| 481 | 7718517 | However, GM-CSF differed from IL-3 in that it was produced by islets from some non-diabetic strains of mice, whereas IL-3 production was confined to NOD islets. |
| 482 | 7718517 | Finally, male NOD islets produced more IL-4 than females, possibly related to the lower incidence of diabetes in males, but unlike GM-CSF and IL-3, IL-4 production did not correlate with the degree of infiltrate released in culture. |
| 483 | 7722337 | We found that mRNA levels of IL-1 beta, IL-2, IL-4, IL-10, and IFN-gamma in mononuclear cells from islets of diabetes-prone female NOD mice increased progressively as these cells infiltrated the islets from age 5 wk to diabetes onset (> 13 wk). |
| 484 | 7722337 | Splenic cell mRNA levels of IFN-gamma and IL-4 were not different in the four groups of mice. |
| 485 | 7762070 | Glucocorticoids (GC) inhibit IL-2 gene transcription by interfering with the binding of the nuclear factor activator protein-1 on the IL-2 promoter. |
| 486 | 7762070 | Calcineurin, a Ca2+/calmodulin-dependent protein phosphatase, is an essential component of the T cell antigen receptor signal transduction pathway leading to IL-2 gene transcription. |
| 487 | 7762070 | Glucocorticoids (GC) inhibit IL-2 gene transcription by interfering with the binding of the nuclear factor activator protein-1 on the IL-2 promoter. |
| 488 | 7762070 | Calcineurin, a Ca2+/calmodulin-dependent protein phosphatase, is an essential component of the T cell antigen receptor signal transduction pathway leading to IL-2 gene transcription. |
| 489 | 7788961 | We have investigated the effects of interleukin-2 (IL-2) on the activation of suppressor T lymphocytes in autoimmune thyroid disease (AITD), with insulin-dependent diabetes mellitus (IDDM) as an autoimmune disease control; this was accomplished by measuring the expression of major histocompatibility complex class II (HLA-DR), CD25 (IL-2 alpha receptor (R)), and IL-2 beta R expression on their surfaces by flow cytometric analysis. |
| 490 | 7788961 | Peripheral blood mononuclear cells (PBMC), obtained from 10 patients with Graves' disease (GD), 11 with Hashimoto's thyroiditis (HT), 9 with insulin-dependent diabetes mellitus (IDDM), and 10 normal persons (N), were cultured for 7 d in the presence or absence of IL-2 at a final concentration of 50 U/mL. |
| 491 | 7788961 | CD8+ cells were isolated from cultured PBMC with immunomagnetic beads, and were stained with fluorescent-conjugated monoclonal antibodies (anti-CD11b, anti-IL-2 alpha R, anti-IL-2 beta R, and anti-HLA-DR); the activation of CD8+CD11b+ ("suppressor") T cells (Ts) by IL-2 was then analyzed on a flow cytometer. |
| 492 | 7788961 | In the absence of IL-2, i.e., in the autologous mixed lymphocyte reaction (AMLR), Ts from patients with GD, HT, and IDDM showed significantly lower activation as compared to N when analyzed by HLA-DR expression, but were not significantly different when IL-2R expression was measured. |
| 493 | 7788961 | With stimulation of 50 U/mL of IL-2, SI of HLA-DR+ Ts was significantly (p < 0.05 to 0.01) lower in GD, HT, and IDDM as compared with N. |
| 494 | 7788961 | We have investigated the effects of interleukin-2 (IL-2) on the activation of suppressor T lymphocytes in autoimmune thyroid disease (AITD), with insulin-dependent diabetes mellitus (IDDM) as an autoimmune disease control; this was accomplished by measuring the expression of major histocompatibility complex class II (HLA-DR), CD25 (IL-2 alpha receptor (R)), and IL-2 beta R expression on their surfaces by flow cytometric analysis. |
| 495 | 7788961 | Peripheral blood mononuclear cells (PBMC), obtained from 10 patients with Graves' disease (GD), 11 with Hashimoto's thyroiditis (HT), 9 with insulin-dependent diabetes mellitus (IDDM), and 10 normal persons (N), were cultured for 7 d in the presence or absence of IL-2 at a final concentration of 50 U/mL. |
| 496 | 7788961 | CD8+ cells were isolated from cultured PBMC with immunomagnetic beads, and were stained with fluorescent-conjugated monoclonal antibodies (anti-CD11b, anti-IL-2 alpha R, anti-IL-2 beta R, and anti-HLA-DR); the activation of CD8+CD11b+ ("suppressor") T cells (Ts) by IL-2 was then analyzed on a flow cytometer. |
| 497 | 7788961 | In the absence of IL-2, i.e., in the autologous mixed lymphocyte reaction (AMLR), Ts from patients with GD, HT, and IDDM showed significantly lower activation as compared to N when analyzed by HLA-DR expression, but were not significantly different when IL-2R expression was measured. |
| 498 | 7788961 | With stimulation of 50 U/mL of IL-2, SI of HLA-DR+ Ts was significantly (p < 0.05 to 0.01) lower in GD, HT, and IDDM as compared with N. |
| 499 | 7788961 | We have investigated the effects of interleukin-2 (IL-2) on the activation of suppressor T lymphocytes in autoimmune thyroid disease (AITD), with insulin-dependent diabetes mellitus (IDDM) as an autoimmune disease control; this was accomplished by measuring the expression of major histocompatibility complex class II (HLA-DR), CD25 (IL-2 alpha receptor (R)), and IL-2 beta R expression on their surfaces by flow cytometric analysis. |
| 500 | 7788961 | Peripheral blood mononuclear cells (PBMC), obtained from 10 patients with Graves' disease (GD), 11 with Hashimoto's thyroiditis (HT), 9 with insulin-dependent diabetes mellitus (IDDM), and 10 normal persons (N), were cultured for 7 d in the presence or absence of IL-2 at a final concentration of 50 U/mL. |
| 501 | 7788961 | CD8+ cells were isolated from cultured PBMC with immunomagnetic beads, and were stained with fluorescent-conjugated monoclonal antibodies (anti-CD11b, anti-IL-2 alpha R, anti-IL-2 beta R, and anti-HLA-DR); the activation of CD8+CD11b+ ("suppressor") T cells (Ts) by IL-2 was then analyzed on a flow cytometer. |
| 502 | 7788961 | In the absence of IL-2, i.e., in the autologous mixed lymphocyte reaction (AMLR), Ts from patients with GD, HT, and IDDM showed significantly lower activation as compared to N when analyzed by HLA-DR expression, but were not significantly different when IL-2R expression was measured. |
| 503 | 7788961 | With stimulation of 50 U/mL of IL-2, SI of HLA-DR+ Ts was significantly (p < 0.05 to 0.01) lower in GD, HT, and IDDM as compared with N. |
| 504 | 7788961 | We have investigated the effects of interleukin-2 (IL-2) on the activation of suppressor T lymphocytes in autoimmune thyroid disease (AITD), with insulin-dependent diabetes mellitus (IDDM) as an autoimmune disease control; this was accomplished by measuring the expression of major histocompatibility complex class II (HLA-DR), CD25 (IL-2 alpha receptor (R)), and IL-2 beta R expression on their surfaces by flow cytometric analysis. |
| 505 | 7788961 | Peripheral blood mononuclear cells (PBMC), obtained from 10 patients with Graves' disease (GD), 11 with Hashimoto's thyroiditis (HT), 9 with insulin-dependent diabetes mellitus (IDDM), and 10 normal persons (N), were cultured for 7 d in the presence or absence of IL-2 at a final concentration of 50 U/mL. |
| 506 | 7788961 | CD8+ cells were isolated from cultured PBMC with immunomagnetic beads, and were stained with fluorescent-conjugated monoclonal antibodies (anti-CD11b, anti-IL-2 alpha R, anti-IL-2 beta R, and anti-HLA-DR); the activation of CD8+CD11b+ ("suppressor") T cells (Ts) by IL-2 was then analyzed on a flow cytometer. |
| 507 | 7788961 | In the absence of IL-2, i.e., in the autologous mixed lymphocyte reaction (AMLR), Ts from patients with GD, HT, and IDDM showed significantly lower activation as compared to N when analyzed by HLA-DR expression, but were not significantly different when IL-2R expression was measured. |
| 508 | 7788961 | With stimulation of 50 U/mL of IL-2, SI of HLA-DR+ Ts was significantly (p < 0.05 to 0.01) lower in GD, HT, and IDDM as compared with N. |
| 509 | 7788961 | We have investigated the effects of interleukin-2 (IL-2) on the activation of suppressor T lymphocytes in autoimmune thyroid disease (AITD), with insulin-dependent diabetes mellitus (IDDM) as an autoimmune disease control; this was accomplished by measuring the expression of major histocompatibility complex class II (HLA-DR), CD25 (IL-2 alpha receptor (R)), and IL-2 beta R expression on their surfaces by flow cytometric analysis. |
| 510 | 7788961 | Peripheral blood mononuclear cells (PBMC), obtained from 10 patients with Graves' disease (GD), 11 with Hashimoto's thyroiditis (HT), 9 with insulin-dependent diabetes mellitus (IDDM), and 10 normal persons (N), were cultured for 7 d in the presence or absence of IL-2 at a final concentration of 50 U/mL. |
| 511 | 7788961 | CD8+ cells were isolated from cultured PBMC with immunomagnetic beads, and were stained with fluorescent-conjugated monoclonal antibodies (anti-CD11b, anti-IL-2 alpha R, anti-IL-2 beta R, and anti-HLA-DR); the activation of CD8+CD11b+ ("suppressor") T cells (Ts) by IL-2 was then analyzed on a flow cytometer. |
| 512 | 7788961 | In the absence of IL-2, i.e., in the autologous mixed lymphocyte reaction (AMLR), Ts from patients with GD, HT, and IDDM showed significantly lower activation as compared to N when analyzed by HLA-DR expression, but were not significantly different when IL-2R expression was measured. |
| 513 | 7788961 | With stimulation of 50 U/mL of IL-2, SI of HLA-DR+ Ts was significantly (p < 0.05 to 0.01) lower in GD, HT, and IDDM as compared with N. |
| 514 | 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. |
| 515 | 7798703 | IL-2 production in GII was significantly correlated to the number of CD4 positive lymphocytes, but this was not true in GI. |
| 516 | 7822811 | Here we 1) map the fine specificity of these T cells, 2) delineate a homologous peptide sequence near the N-terminus of p69, and 3) demonstrate T cell recognition of this p69 sequence (T cell epitope p69, Tep69) by patient T cells. |
| 517 | 7822811 | Whereas BSA triggers T cell proliferation, recombinant p69 and a synthetic Tep69 peptide induce early stages of T cell activation (IL-2R transcription) but insufficient IL-2 production and thus anergy. |
| 518 | 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. |
| 519 | 7860729 | Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. |
| 520 | 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. |
| 521 | 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. |
| 522 | 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. |
| 523 | 7860729 | Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. |
| 524 | 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. |
| 525 | 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. |
| 526 | 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. |
| 527 | 7860729 | Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. |
| 528 | 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. |
| 529 | 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. |
| 530 | 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. |
| 531 | 7860729 | Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. |
| 532 | 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. |
| 533 | 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. |
| 534 | 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. |
| 535 | 7865456 | The infiltrate consisted primarily of B cells and CD4+ and CD8+ T cells. |
| 536 | 7869038 | Calcium/calmodulin-dependent protein kinase II downregulates both calcineurin and protein kinase C-mediated pathways for cytokine gene transcription in human T cells. |
| 537 | 7869038 | Engagement of the T cell receptor for antigen activates phospholipase C resulting in an increase in intracellular free calcium concentration ([Ca2+]i) and activation of protein kinase C (PKC). |
| 538 | 7869038 | Recent studies have identified calcineurin as a key enzyme for interleukin (IL)-2 and IL-4 promoter activation. |
| 539 | 7869038 | The inhibitory effect of CaM-K II on IL-2 promoter was associated with decreased transcription of its AP-1 and NF-AT transactivating pathways. |
| 540 | 7869038 | Similar results were obtained when a construct containing the IL-4 promoter also was used. gamma B*CaM-K also downregulated the activation of AP-1 in response to transfection with a constitutively active mutant of PKC or stimulation with PMA. |
| 541 | 7869038 | Calcium/calmodulin-dependent protein kinase II downregulates both calcineurin and protein kinase C-mediated pathways for cytokine gene transcription in human T cells. |
| 542 | 7869038 | Engagement of the T cell receptor for antigen activates phospholipase C resulting in an increase in intracellular free calcium concentration ([Ca2+]i) and activation of protein kinase C (PKC). |
| 543 | 7869038 | Recent studies have identified calcineurin as a key enzyme for interleukin (IL)-2 and IL-4 promoter activation. |
| 544 | 7869038 | The inhibitory effect of CaM-K II on IL-2 promoter was associated with decreased transcription of its AP-1 and NF-AT transactivating pathways. |
| 545 | 7869038 | Similar results were obtained when a construct containing the IL-4 promoter also was used. gamma B*CaM-K also downregulated the activation of AP-1 in response to transfection with a constitutively active mutant of PKC or stimulation with PMA. |
| 546 | 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. |
| 547 | 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. |
| 548 | 7913115 | Insulin-dependent diabetes mellitus (IDDM), in which only the pancreatic beta cells are destroyed by the autoimmune response, is the paradigm of organ-specific autoimmunity. |
| 549 | 7913115 | The analysis of the correlation between class I overexpression, residual insulin, and insulitis suggests that the first event is the increase of HLA class I expression. |
| 550 | 7913115 | Of adhesion molecules, ICAM-1, VLA, VCAM, and LFA-3 were normal and only ICAM-1 was moderately overexpressed in and around the islets of case 1 insulitis, as was detected by immunofluorescence which showed that 18% of the islets of case 1 had CD8+ lymphocytes as the predominant population. |
| 551 | 7913115 | Reverse transcription-PCR demonstrated moderate V beta skewing and the profile of cytokines expected in CTLs: IL-2, IL-4, IL-10, and IFN-gamma negative, perforin positive. |
| 552 | 7913115 | In addition, IFN-alpha, IFN-beta, and IL-6 transcripts were detected in the case 1 pancreas, consistent with the existence of a silent viral infection. |
| 553 | 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. |
| 554 | 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. |
| 555 | 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. |
| 556 | 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. |
| 557 | 7951531 | The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved. |
| 558 | 7951531 | The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. |
| 559 | 7955566 | We performed limiting dilution culture of T cells from a patient affected by primary immunodeficiency as a result of complete lack of adenosine deaminase (ADA) activity and also affected by insulin-dependent diabetes mellitus (type I diabetes). |
| 560 | 7955566 | These T cells displayed ADA enzymatic activity and produced interleukin-2 after engagement of their T cell receptor (TCR)/CD3 complex. |
| 561 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 562 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 563 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 564 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 565 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 566 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 567 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 568 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 569 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 570 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 571 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 572 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 573 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 574 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 575 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 576 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 577 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 578 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 579 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 580 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 581 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 582 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 583 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 584 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 585 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 586 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 587 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 588 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 589 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 590 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 591 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 592 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 593 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 594 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 595 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 596 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 597 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 598 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 599 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 600 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 601 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 602 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 603 | 7981575 | Low interleukin-2 receptor levels in serum of patients with insulin-dependent diabetes. |
| 604 | 7981575 | Abnormal serum interleukin-2 receptor levels have been found in young children with type 1 diabetes and "prediabetes." |
| 605 | 7981575 | We measured interleukin-2 receptor levels in 17 patients with newly diagnosed type 1 diabetes, 21 patients with long-standing type 1 diabetes, 19 patients with long-standing type 2 diabetes, 19 islet-cell antibody positive nondiabetic polyendocrine patients, 12 islet-cell antibody-positive first-degree relatives of patients with type 1 diabetes and compared the results to age- and sex-matched normal controls. |
| 606 | 7981575 | We found significantly lower interleukin-2 receptor levels in patients with newly diagnosed and long-standing type 1 diabetes compared to normal controls (87 +/- 11 and 93 +/- 11 vs. 142 +/- 25 and 132 +/- 40 U/ml, P < 0.001 and P < 0.01). |
| 607 | 7981575 | There were no significant differences in interleukin-2 receptor levels between prediabetic groups and normal controls or patients with long-standing type 1 or type 2 diabetes. |
| 608 | 7981575 | There was no correlation between glycosylated hemoglobin, blood glucose levels, and interleukin-2 receptor in the groups with long-standing type 1 or type 2 diabetes. |
| 609 | 7981575 | We conclude that patients with type 1 diabetes have low interleukin-2 receptor serum levels. |
| 610 | 7988786 | Analysis of cytokine mRNA expression in syngeneic islet grafts of NOD mice: interleukin 2 and interferon gamma mRNA expression correlate with graft rejection and interleukin 10 with graft survival. |
| 611 | 7988786 | Interleukin 10 mRNA expression was significantly increased whereas interleukin 2 and interferon gamma mRNA levels were significantly decreased in islet grafts from complete Freund's adjuvant-injected mice compared to control mice. |
| 612 | 7988786 | Levels of mRNA for interleukin 1 beta, interleukin 4, and tumour necrosis factor alpha were not significantly different in islet grafts from complete Freund's adjuvant-injected and control mice. |
| 613 | 7988786 | These findings suggest that a Th1 subset of lymphocytes and their cytokine products, interleukin 2 and interferon gamma, may be involved in the rejection of syngeneic islet grafts and diabetes recurrence in NOD mice, and that the protective effect of complete Freund's adjuvant may result from the induction of interleukin 10 production and consequent down-regulation of Th1 cells and cytokines in the islet graft. |
| 614 | 7988786 | Analysis of cytokine mRNA expression in syngeneic islet grafts of NOD mice: interleukin 2 and interferon gamma mRNA expression correlate with graft rejection and interleukin 10 with graft survival. |
| 615 | 7988786 | Interleukin 10 mRNA expression was significantly increased whereas interleukin 2 and interferon gamma mRNA levels were significantly decreased in islet grafts from complete Freund's adjuvant-injected mice compared to control mice. |
| 616 | 7988786 | Levels of mRNA for interleukin 1 beta, interleukin 4, and tumour necrosis factor alpha were not significantly different in islet grafts from complete Freund's adjuvant-injected and control mice. |
| 617 | 7988786 | These findings suggest that a Th1 subset of lymphocytes and their cytokine products, interleukin 2 and interferon gamma, may be involved in the rejection of syngeneic islet grafts and diabetes recurrence in NOD mice, and that the protective effect of complete Freund's adjuvant may result from the induction of interleukin 10 production and consequent down-regulation of Th1 cells and cytokines in the islet graft. |
| 618 | 7988786 | Analysis of cytokine mRNA expression in syngeneic islet grafts of NOD mice: interleukin 2 and interferon gamma mRNA expression correlate with graft rejection and interleukin 10 with graft survival. |
| 619 | 7988786 | Interleukin 10 mRNA expression was significantly increased whereas interleukin 2 and interferon gamma mRNA levels were significantly decreased in islet grafts from complete Freund's adjuvant-injected mice compared to control mice. |
| 620 | 7988786 | Levels of mRNA for interleukin 1 beta, interleukin 4, and tumour necrosis factor alpha were not significantly different in islet grafts from complete Freund's adjuvant-injected and control mice. |
| 621 | 7988786 | These findings suggest that a Th1 subset of lymphocytes and their cytokine products, interleukin 2 and interferon gamma, may be involved in the rejection of syngeneic islet grafts and diabetes recurrence in NOD mice, and that the protective effect of complete Freund's adjuvant may result from the induction of interleukin 10 production and consequent down-regulation of Th1 cells and cytokines in the islet graft. |
| 622 | 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. |
| 623 | 8019399 | Immunomodulation by interleukin-2 receptor targeted therapy. |
| 624 | 8019399 | The interleukin-2 receptor (IL-2R) is expressed on proliferating T-lymphocytes following antigen stimulation. |
| 625 | 8019399 | Activated IL-2R bearing lymphocytes accumulate as cellular infiltrates in autoimmune thyroiditis, insulin-dependent diabetes mellitus, rheumatoid arthritis and graft rejection. |
| 626 | 8019399 | In open uncontrolled trials, chimeric IL-2R toxin was found to be safe and effective in patients with refractory rheumatoid arthritis, insulin-dependent diabetes mellitus and IL-2R bearing leukaemias and lymphomas. |
| 627 | 8019399 | Immunomodulation by interleukin-2 receptor targeted therapy. |
| 628 | 8019399 | The interleukin-2 receptor (IL-2R) is expressed on proliferating T-lymphocytes following antigen stimulation. |
| 629 | 8019399 | Activated IL-2R bearing lymphocytes accumulate as cellular infiltrates in autoimmune thyroiditis, insulin-dependent diabetes mellitus, rheumatoid arthritis and graft rejection. |
| 630 | 8019399 | In open uncontrolled trials, chimeric IL-2R toxin was found to be safe and effective in patients with refractory rheumatoid arthritis, insulin-dependent diabetes mellitus and IL-2R bearing leukaemias and lymphomas. |
| 631 | 8043899 | The effects of indomethacin on PHA-induced TCGF activity and the effects of adherent cells (macrophages) from group A and group C on TCGF production of normal group-matched non-adherent cells (lymphocytes) were also studied. |
| 632 | 8043899 | Interestingly, a significant inverse correlation was found between TCGF activity and the required dose of insulin only in group A (r = -0.66; P < 0.05). |
| 633 | 8043899 | The effects of indomethacin on PHA-induced TCGF activity and the effects of adherent cells (macrophages) from group A and group C on TCGF production of normal group-matched non-adherent cells (lymphocytes) were also studied. |
| 634 | 8043899 | Interestingly, a significant inverse correlation was found between TCGF activity and the required dose of insulin only in group A (r = -0.66; P < 0.05). |
| 635 | 8050776 | Production and in vivo characterization of a bifunctional antibody (IVA039.1) with specificity for the mouse interleukin-2 receptor and vinca alkaloids. |
| 636 | 8056041 | Protection from experimental autoimmune diabetes in the non-obese diabetic mouse with soluble interleukin-1 receptor. |
| 637 | 8056041 | We have evaluated the effects of a treatment with soluble interleukin-1 receptor (sIL-1R) in the accelerated model of autoimmune diabetes induced by cyclophosphamide (CY) in the non-obese diabetic (NOD) mouse. |
| 638 | 8056041 | In contrast, repeated injections with sIL-1R protected NOD mice from insulin-dependent diabetes mellitus (IDDM) development in a dose-dependent fashion; the incidence of IDDM was 53.3% (8/15) in the mice treated with 0.2 mg/kg and only 6.7% (1/15) in those treated with 2 mg/kg. |
| 639 | 8056041 | Importantly, the anti-diabetogenic property of sIL-1R may not involve major T cell function impairment; accordingly, in parallel experiments, splenic lymphoid cells from NOD mice not challenged with CY, but treated with 2 mg/kg sIL-1R for 5 consecutive days showed a normal distribution of mononuclear cell subsets and maintained their capacity to secrete interferon-gamma and IL-2 and to proliferate in response to polyclonal mitogenic stimulation with concanavalin A. |
| 640 | 8056185 | In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. |
| 641 | 8056185 | On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. |
| 642 | 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. |
| 643 | 8056185 | These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply. |
| 644 | 8056185 | In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. |
| 645 | 8056185 | On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. |
| 646 | 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. |
| 647 | 8056185 | These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply. |
| 648 | 8056185 | In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. |
| 649 | 8056185 | On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. |
| 650 | 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. |
| 651 | 8056185 | These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply. |
| 652 | 8090562 | It also blocks the accumulation of the mRNAs for IL-2, IFN-gamma and GM-CSF. |
| 653 | 8094734 | Diabetes in these lymphopoenic rats was associated with extensive insulitis involving CD4+ and CD8+ T cells and macrophages. |
| 654 | 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-. |
| 655 | 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. |
| 656 | 8095271 | To confirm this hypothesis we investigated the T-cell activation trend, evaluating the surface expression of IL-2 receptor (CD25), transferrin (CD71), HLA class II (DR), and CD69 phenotypes after in vitro stimulation with phytohemagglutinin (PHA; 1 and 10 micrograms/ml) and concanavalin A (12.5 micrograms/ml) in six newly diagnosed Type I diabetics and six islet cell- and insulin autoantibody-positive first-degree relatives. |
| 657 | 8095271 | Using both PHA concentrations, a lower level of CD25, CD71, CD69, and DR antigen expression was found in newly diagnosed patients at all observation times with respect to control cultures (P < 0.001). |
| 658 | 8095271 | Unexpectedly, pre-Type I diabetic subjects, after 1 microgram/ml of PHA, showed a significantly reduced expression of CD69 (P < 0.001) and CD71 (P < 0.001). |
| 659 | 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. |
| 660 | 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. |
| 661 | 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. |
| 662 | 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. |
| 663 | 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. |
| 664 | 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. |
| 665 | 8098881 | Our studies demonstrate for the first time that CD3 antigen-derived signals and CD2 antigen-derived signals are synergistic in inducing the emergence of transcription factors that bind to the NF-AT1, AP-1, and NF-kB sites located in the promoter/enhancer region of the IL-2 gene. |
| 666 | 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. |
| 667 | 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. |
| 668 | 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. |
| 669 | 8116045 | To investigate this new postulate independently of an IL-2-dependent mechanism, we utilized, as probes, two mammalian cell lines, distinguished by their sensitivity to growth inhibition by TGF-beta and resistance to IL-2: CCL-64 mink lung epithelial cells (CCL-64 cells) and A-549 human adenocarcinoma cells (A-549 cells). |
| 670 | 8149968 | Interestingly, addition of either recombinant interleukin (IL)-2 or phorbol 12-myristate 13-acetate to the cell culture was able to completely restore impaired anti-CD3-induced proliferation in diabetic T cells, suggesting the presence of a defect through the TcR/CD3 pathway, located upstream of protein kinase C (PKC) activation and resulting in low IL-2 production and proliferation. |
| 671 | 8168635 | The autoimmune response that leads to destruction of pancreatic islet beta-cells and insulin-dependent diabetes mellitus (IDDM) has a genetic basis; however, environmental factors can exert profound modulating effects on the genetic predisposition to this autoimmune response. |
| 672 | 8168635 | Thus, recent studies in NOD mice suggest that the islet beta-cell-directed autoimmune response may be mediated by a T-helper 1 (Th1) subset of T-cells producing the cytokines interleukin-2 (IL-2) and interferon-gamma. |
| 673 | 8168635 | These studies also suggest that the diabetes-protective effects of administering microbial agents, adjuvants, and a beta-cell autoantigen (GAD65 [glutamic acid decarboxylase]) may result from activation of a Th2 subset of T-cells that produce the cytokines IL-4 and IL-10 and consequently downregulate the Th1-cell-mediated autoimmune response. |
| 674 | 8178347 | We have shown that, although tolerant in vivo, animals bearing long-term cultured islet allografts are donor-reactive in vitro as assessed by (1) CTL precursor frequency, (2) antidonor proliferative and cytotoxic responses, and (3) lymphokine production (IL-2, IL-3, TNF, and IFN-gamma). |
| 675 | 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. |
| 676 | 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. |
| 677 | 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. |
| 678 | 8251150 | Our studies, over the last 10 years, have revealed that a subgroup of schizophrenics have several significant immunological abnormalities, including increased prevalence of autoimmune diseases and of antinuclear antibodies (ANA) and anticytoplasmic antibodies (ACA), decreased lymphocyte interleukin-2 (IL-2) production, increased serum IL-2 receptor concentration, increased serum IL-6 concentration, and an association with HLA antigens. |
| 679 | 8268651 | The nucleotide sequences of the NOD and C57BL/6J alleles of Glut-2, Sod-2, and Il-2 were determined by RT-PCR sequencing. |
| 680 | 8297521 | Mutations have been described in the genes encoding Fc gamma RI, interleukin-2 and natural resistance associated macrophage protein, which are all candidate genes for susceptibility loci associated with autoimmune diabetes in non-obese diabetic mice. |
| 681 | 8299687 | Consistent with the anti-apoptotic function of the Bcl-2 gene product, activated T lymphocytes from NOD mice showed a markedly increased resistance to induction of apoptosis following deprivation of interleukin-2 when compared to those from non-autoimmune strains. |
| 682 | 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. |
| 683 | 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. |
| 684 | 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. |
| 685 | 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. |
| 686 | 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. |
| 687 | 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. |
| 688 | 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. |
| 689 | 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. |
| 690 | 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. |
| 691 | 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. |
| 692 | 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. |
| 693 | 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. |
| 694 | 8324945 | Early clinical studies of IL-2 fusion toxin in patients with severe rheumatoid arthritis and recent onset insulin-dependent diabetes mellitus. |
| 695 | 8324945 | This agent is an interleukin-2 receptor (IL-2R)-targeted cytotoxin which kills activated IL-2R-expressing lymphocytes at 10(-10) M concentrations. |
| 696 | 8324945 | Initial safety, pharmacokinetics and evidence of IL-2R specific cytotoxicity were obtained in patients with IL-2 receptor expressing malignancies; these studies served as a basis for the initiation of an open label phase I/II evaluation of DAB486IL-2 in patients with severe, methotrexate refractory rheumatoid arthritis. |
| 697 | 8324945 | Early clinical studies of IL-2 fusion toxin in patients with severe rheumatoid arthritis and recent onset insulin-dependent diabetes mellitus. |
| 698 | 8324945 | This agent is an interleukin-2 receptor (IL-2R)-targeted cytotoxin which kills activated IL-2R-expressing lymphocytes at 10(-10) M concentrations. |
| 699 | 8324945 | Initial safety, pharmacokinetics and evidence of IL-2R specific cytotoxicity were obtained in patients with IL-2 receptor expressing malignancies; these studies served as a basis for the initiation of an open label phase I/II evaluation of DAB486IL-2 in patients with severe, methotrexate refractory rheumatoid arthritis. |
| 700 | 8324945 | Early clinical studies of IL-2 fusion toxin in patients with severe rheumatoid arthritis and recent onset insulin-dependent diabetes mellitus. |
| 701 | 8324945 | This agent is an interleukin-2 receptor (IL-2R)-targeted cytotoxin which kills activated IL-2R-expressing lymphocytes at 10(-10) M concentrations. |
| 702 | 8324945 | Initial safety, pharmacokinetics and evidence of IL-2R specific cytotoxicity were obtained in patients with IL-2 receptor expressing malignancies; these studies served as a basis for the initiation of an open label phase I/II evaluation of DAB486IL-2 in patients with severe, methotrexate refractory rheumatoid arthritis. |
| 703 | 8336904 | In the present study, we specifically investigated the presence of the main immune cells, namely T helper/inducer lymphocytes, T suppressor/cytotoxic lymphocytes, B lymphocytes and macrophages, for HLA-DR antigen expression and the cytokines IL-1 alpha and IL-2 in epiretinal membranes of proliferative diabetic retinopathy (PDR) using immunohistochemical staining. |
| 704 | 8336904 | The levels of the two cytokines (IL-1 alpha and IL-2) in the vitreous were measured by ELISA. |
| 705 | 8336904 | IL-1 alpha and IL-2 were detected in the epiretinal membranes in 8 out of 13 tested cases (62%). |
| 706 | 8336904 | However, in the vitreous, IL-1 alpha was detected in only 3 out of 13 cases (70, 75 and 80 pg/ml, respectively), while IL-2 was not detected in any of the vitreous samples. |
| 707 | 8336904 | In the present study, we specifically investigated the presence of the main immune cells, namely T helper/inducer lymphocytes, T suppressor/cytotoxic lymphocytes, B lymphocytes and macrophages, for HLA-DR antigen expression and the cytokines IL-1 alpha and IL-2 in epiretinal membranes of proliferative diabetic retinopathy (PDR) using immunohistochemical staining. |
| 708 | 8336904 | The levels of the two cytokines (IL-1 alpha and IL-2) in the vitreous were measured by ELISA. |
| 709 | 8336904 | IL-1 alpha and IL-2 were detected in the epiretinal membranes in 8 out of 13 tested cases (62%). |
| 710 | 8336904 | However, in the vitreous, IL-1 alpha was detected in only 3 out of 13 cases (70, 75 and 80 pg/ml, respectively), while IL-2 was not detected in any of the vitreous samples. |
| 711 | 8336904 | In the present study, we specifically investigated the presence of the main immune cells, namely T helper/inducer lymphocytes, T suppressor/cytotoxic lymphocytes, B lymphocytes and macrophages, for HLA-DR antigen expression and the cytokines IL-1 alpha and IL-2 in epiretinal membranes of proliferative diabetic retinopathy (PDR) using immunohistochemical staining. |
| 712 | 8336904 | The levels of the two cytokines (IL-1 alpha and IL-2) in the vitreous were measured by ELISA. |
| 713 | 8336904 | IL-1 alpha and IL-2 were detected in the epiretinal membranes in 8 out of 13 tested cases (62%). |
| 714 | 8336904 | However, in the vitreous, IL-1 alpha was detected in only 3 out of 13 cases (70, 75 and 80 pg/ml, respectively), while IL-2 was not detected in any of the vitreous samples. |
| 715 | 8336904 | In the present study, we specifically investigated the presence of the main immune cells, namely T helper/inducer lymphocytes, T suppressor/cytotoxic lymphocytes, B lymphocytes and macrophages, for HLA-DR antigen expression and the cytokines IL-1 alpha and IL-2 in epiretinal membranes of proliferative diabetic retinopathy (PDR) using immunohistochemical staining. |
| 716 | 8336904 | The levels of the two cytokines (IL-1 alpha and IL-2) in the vitreous were measured by ELISA. |
| 717 | 8336904 | IL-1 alpha and IL-2 were detected in the epiretinal membranes in 8 out of 13 tested cases (62%). |
| 718 | 8336904 | However, in the vitreous, IL-1 alpha was detected in only 3 out of 13 cases (70, 75 and 80 pg/ml, respectively), while IL-2 was not detected in any of the vitreous samples. |
| 719 | 8340230 | Mononuclear cells obtained from a child at the acute presentation of type I diabetes were stimulated in vitro with human insulin followed by IL-2 and IL-4. |
| 720 | 8405738 | In response to NOD antigen presenting cells, C2 cells secreted interferon-gamma, tumour necrosis factor-alpha and interleukin-6 but no detectable interleukin-2, interleukin-4 or interleukin-10, a pattern of cytokine secretion more characteristic of Th1 CD4 cells. |
| 721 | 8409387 | IL-2-dependent IL-2R alpha expression in PMA blasts and NF-kB induction in resting human T cells were also inhibited by Dex. |
| 722 | 8428390 | Moreover, DSP-treated animals showed reduced signs of pancreatic insulitis, had lower percentages of splenic lymphoid cells (SLC) expressing IL-2 receptors and Ly-6C antigens on their surfaces, and these cells released lower amounts of interferon-gamma (IFN) when stimulated in vitro. |
| 723 | 8461395 | Interleukin-2 receptor-targeted immune therapy. |
| 724 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 725 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 726 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 727 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 728 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 729 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 730 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 731 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 732 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 733 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 734 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 735 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 736 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 737 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 738 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 739 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 740 | 8473495 | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. |
| 741 | 8473495 | Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. |
| 742 | 8473495 | Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. |
| 743 | 8473495 | Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. |
| 744 | 8473495 | In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. |
| 745 | 8473495 | These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. |
| 746 | 8473495 | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. |
| 747 | 8473495 | Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. |
| 748 | 8473495 | Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. |
| 749 | 8473495 | Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. |
| 750 | 8473495 | In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. |
| 751 | 8473495 | These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. |
| 752 | 8473495 | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. |
| 753 | 8473495 | Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. |
| 754 | 8473495 | Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. |
| 755 | 8473495 | Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. |
| 756 | 8473495 | In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. |
| 757 | 8473495 | These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. |
| 758 | 8473495 | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. |
| 759 | 8473495 | Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. |
| 760 | 8473495 | Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. |
| 761 | 8473495 | Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. |
| 762 | 8473495 | In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. |
| 763 | 8473495 | These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. |
| 764 | 8473495 | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. |
| 765 | 8473495 | Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. |
| 766 | 8473495 | Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. |
| 767 | 8473495 | Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. |
| 768 | 8473495 | In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. |
| 769 | 8473495 | These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. |
| 770 | 8473495 | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. |
| 771 | 8473495 | Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. |
| 772 | 8473495 | Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. |
| 773 | 8473495 | Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. |
| 774 | 8473495 | In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. |
| 775 | 8473495 | These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. |
| 776 | 8476255 | Interleukin-2 receptor-directed therapies: antibody-or cytokine-based targeting molecules. |
| 777 | 8476255 | Hence, we wondered whether administration of anti-IL-2 receptor (IL-2R) monoclonal antibody (mAb) or chimeric IL-2 toxins would provide a utilitarian way to achieve immunosuppression aimed directly at activated lymphocytes, or whether this approach could be used to treat IL-2R+ leukemia/lymphoma. |
| 778 | 8476255 | The results of open, uncontrolled studies provide preliminary evidence that a chimeric IL-2 toxin is well tolerated at doses that may induce improvement in patients with IL-2R+ leukemia/lymphoma, as well as in patients with refractory rheumatoid arthritis or new-onset diabetes mellitus. |
| 779 | 8476255 | Interleukin-2 receptor-directed therapies: antibody-or cytokine-based targeting molecules. |
| 780 | 8476255 | Hence, we wondered whether administration of anti-IL-2 receptor (IL-2R) monoclonal antibody (mAb) or chimeric IL-2 toxins would provide a utilitarian way to achieve immunosuppression aimed directly at activated lymphocytes, or whether this approach could be used to treat IL-2R+ leukemia/lymphoma. |
| 781 | 8476255 | The results of open, uncontrolled studies provide preliminary evidence that a chimeric IL-2 toxin is well tolerated at doses that may induce improvement in patients with IL-2R+ leukemia/lymphoma, as well as in patients with refractory rheumatoid arthritis or new-onset diabetes mellitus. |
| 782 | 8476255 | Interleukin-2 receptor-directed therapies: antibody-or cytokine-based targeting molecules. |
| 783 | 8476255 | Hence, we wondered whether administration of anti-IL-2 receptor (IL-2R) monoclonal antibody (mAb) or chimeric IL-2 toxins would provide a utilitarian way to achieve immunosuppression aimed directly at activated lymphocytes, or whether this approach could be used to treat IL-2R+ leukemia/lymphoma. |
| 784 | 8476255 | The results of open, uncontrolled studies provide preliminary evidence that a chimeric IL-2 toxin is well tolerated at doses that may induce improvement in patients with IL-2R+ leukemia/lymphoma, as well as in patients with refractory rheumatoid arthritis or new-onset diabetes mellitus. |
| 785 | 8492414 | CS seems to inhibit the production of cytokines such as IL-2 and IFN-gamma, and it damages the activated suppressor/cytotoxic T cells. |
| 786 | 8558012 | IFN-gamma and IL-12p40 mRNA increase with age in both diabetic and insulin-treated nondiabetic BB rats. |
| 787 | 8558012 | In both DP and RT6-depleted DR rats, IFN-gamma mRNA was present in islets before and during disease onset. |
| 788 | 8558012 | IL-2 and IL-4 mRNAs were minimal or undetectable in infiltrated islets but present in activated peripheral T cells. |
| 789 | 8558012 | Similar cytokine mRNA profiles were observed in the thyroids of RT6-depleted DR rats and in the islets of DP rats treated with prophylactic parenteral insulin to prevent diabetes. |
| 790 | 8558012 | We conclude that IFN-gamma and IL-12 may play a major role in the expression of insulitis and thyroiditis in the BB rat, that Th1 lymphocytes may predominate over Th2 lymphocytes in these inflammatory lesions, and that prevention of diabetes by insulin is not associated with an alteration in the cytokine gene profile of islet infiltrating cells. |
| 791 | 8586407 | We measured the interleukin-2 (IL-2) and soluble interleukin-2 receptor (SIL-2R) in 86 senile patients (aged 71.5 +/- 8.45) with various diseases in order to evaluate the cell immune function in the elderly. |
| 792 | 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. |
| 793 | 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. |
| 794 | 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. |
| 795 | 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. |
| 796 | 8597171 | A simple model system based on the effect of FK 506 on isolated rat pancreatic islets was utilised to study the relationship between inhibition of insulin biosynthesis, inhibition of interleukin 2 (IL-2) activation and FK binding protein (FKBP-12) binding of FK 506 and a number of FK 506 analogues. |
| 797 | 8617981 | We have found that IL-2, IL-4, TNF-alpha, and IFN-gamma are expressed by the time the fourth dose of STZ is given. |
| 798 | 8617981 | However, expression of IFN-gamma, but not IL-4, was limited to intrapancreatic lymphocytes and was not detectable at extrapancreatic lymphoid sites. |
| 799 | 8617981 | Moreover, mAbs against IFN-gamma, but not against IL-4 or IL-2, prevent hyperglycemia and insulitis in MDSDM, suggesting that IFN-gamma regulates development of disease. |
| 800 | 8617981 | Cells in the pancreases of nondiabetic mice treated with anti-IFN-gamma mAb and STZ show enhanced expression of IL-4, but the prevention of disease is due to blockade of the IFN-gamma itself, and not due to secretion of IL-4, because systemic administration of IL-4 does not prevent MDSDM. |
| 801 | 8617981 | We have found that IL-2, IL-4, TNF-alpha, and IFN-gamma are expressed by the time the fourth dose of STZ is given. |
| 802 | 8617981 | However, expression of IFN-gamma, but not IL-4, was limited to intrapancreatic lymphocytes and was not detectable at extrapancreatic lymphoid sites. |
| 803 | 8617981 | Moreover, mAbs against IFN-gamma, but not against IL-4 or IL-2, prevent hyperglycemia and insulitis in MDSDM, suggesting that IFN-gamma regulates development of disease. |
| 804 | 8617981 | Cells in the pancreases of nondiabetic mice treated with anti-IFN-gamma mAb and STZ show enhanced expression of IL-4, but the prevention of disease is due to blockade of the IFN-gamma itself, and not due to secretion of IL-4, because systemic administration of IL-4 does not prevent MDSDM. |
| 805 | 8627174 | Aod2, the locus controlling development of atrophy in neonatal thymectomy-induced autoimmune ovarian dysgenesis, co-localizes with Il2, Fgfb, and Idd3. |
| 806 | 8627174 | We report here the mapping of Aod2, the locus that controls this phenotype, to mouse chromosomes 3 within a region encoding Il2 and Fgfb. |
| 807 | 8627174 | Aod2, the locus controlling development of atrophy in neonatal thymectomy-induced autoimmune ovarian dysgenesis, co-localizes with Il2, Fgfb, and Idd3. |
| 808 | 8627174 | We report here the mapping of Aod2, the locus that controls this phenotype, to mouse chromosomes 3 within a region encoding Il2 and Fgfb. |
| 809 | 8635648 | Tumor necrosis factor-alpha, IL-4, and IL-10 mRNA levels were not significantly different in islet leukocytes from the four groups of rats. |
| 810 | 8635648 | These findings suggest that production of T-helper 1 (Th1)-type cytokines, IFN-gamma and IL-2, by islet-infiltrating cells in BB rats is associated with beta-cell destruction and IDDM development. |
| 811 | 8638283 | Interferon-alpha (IFN-alpha) treatment has now been clearly linked with the exacerbation or the occurrence of several types of autoantibodies or autoimmune diseases (thyroiditis, systemic lupus erythematosus, hematologic disorders, insulin-dependent diabetes mellitus) or diseases involving altered cell-mediated immune functions (inflammatory dermatologic diseases, nephritis, pneumonitis, colitis). |
| 812 | 8638283 | By contrast immunological side-effects of IFN-beta and IFN-gamma have been seldom reported. |
| 813 | 8638283 | Exacerbation of autoimmune thyroiditis was described with granulocyte-macrophage colony-stimulating factor (GM-CSF) only. |
| 814 | 8638283 | The immunogenicity of cytokines is also of great relevance and the occurrence of antibodies binding IFN-alpha and IFN-beta, IL2 and GM-CSF have been reported. |
| 815 | 8638283 | Finally, several isolated reports have recently suggested that IFN-alpha treatment may be associated with several immunosuppressive effects while IL-2 is clinically associated with an increased incidence of infectious complications. |
| 816 | 8638283 | Interferon-alpha (IFN-alpha) treatment has now been clearly linked with the exacerbation or the occurrence of several types of autoantibodies or autoimmune diseases (thyroiditis, systemic lupus erythematosus, hematologic disorders, insulin-dependent diabetes mellitus) or diseases involving altered cell-mediated immune functions (inflammatory dermatologic diseases, nephritis, pneumonitis, colitis). |
| 817 | 8638283 | By contrast immunological side-effects of IFN-beta and IFN-gamma have been seldom reported. |
| 818 | 8638283 | Exacerbation of autoimmune thyroiditis was described with granulocyte-macrophage colony-stimulating factor (GM-CSF) only. |
| 819 | 8638283 | The immunogenicity of cytokines is also of great relevance and the occurrence of antibodies binding IFN-alpha and IFN-beta, IL2 and GM-CSF have been reported. |
| 820 | 8638283 | Finally, several isolated reports have recently suggested that IFN-alpha treatment may be associated with several immunosuppressive effects while IL-2 is clinically associated with an increased incidence of infectious complications. |
| 821 | 8660843 | Prostaglandin E2 inhibits the nuclear transcription of the human interleukin 2, but not the Il-4, gene in human T cells by targeting transcription factors AP-1 and NF-AT. |
| 822 | 8660843 | Using DNA transfection and electrophoretic mobility shift assays (EMSA), we have examined the mechanisms for the transcriptional regulation of human IL-2 and IL-4 genes by PGE2. |
| 823 | 8660843 | Stimulation of Jurkat cells with ionomycin and PMA in the presence of PGE2 inhibited the IL-2- but not the IL-4-promoter activity. |
| 824 | 8660843 | In EMSAs, nuclear extracts from primary human T cells stimulated with ionomycin and phorbol esters in the presence of PGE2 demonstrated decreased binding at the AP-1 and NF-AT sites of the human IL-2 promoter; binding to the OCT-1 and NF-kappa B sites was not affected. |
| 825 | 8660843 | Prostaglandin E2 inhibits the nuclear transcription of the human interleukin 2, but not the Il-4, gene in human T cells by targeting transcription factors AP-1 and NF-AT. |
| 826 | 8660843 | Using DNA transfection and electrophoretic mobility shift assays (EMSA), we have examined the mechanisms for the transcriptional regulation of human IL-2 and IL-4 genes by PGE2. |
| 827 | 8660843 | Stimulation of Jurkat cells with ionomycin and PMA in the presence of PGE2 inhibited the IL-2- but not the IL-4-promoter activity. |
| 828 | 8660843 | In EMSAs, nuclear extracts from primary human T cells stimulated with ionomycin and phorbol esters in the presence of PGE2 demonstrated decreased binding at the AP-1 and NF-AT sites of the human IL-2 promoter; binding to the OCT-1 and NF-kappa B sites was not affected. |
| 829 | 8660843 | Prostaglandin E2 inhibits the nuclear transcription of the human interleukin 2, but not the Il-4, gene in human T cells by targeting transcription factors AP-1 and NF-AT. |
| 830 | 8660843 | Using DNA transfection and electrophoretic mobility shift assays (EMSA), we have examined the mechanisms for the transcriptional regulation of human IL-2 and IL-4 genes by PGE2. |
| 831 | 8660843 | Stimulation of Jurkat cells with ionomycin and PMA in the presence of PGE2 inhibited the IL-2- but not the IL-4-promoter activity. |
| 832 | 8660843 | In EMSAs, nuclear extracts from primary human T cells stimulated with ionomycin and phorbol esters in the presence of PGE2 demonstrated decreased binding at the AP-1 and NF-AT sites of the human IL-2 promoter; binding to the OCT-1 and NF-kappa B sites was not affected. |
| 833 | 8660843 | Prostaglandin E2 inhibits the nuclear transcription of the human interleukin 2, but not the Il-4, gene in human T cells by targeting transcription factors AP-1 and NF-AT. |
| 834 | 8660843 | Using DNA transfection and electrophoretic mobility shift assays (EMSA), we have examined the mechanisms for the transcriptional regulation of human IL-2 and IL-4 genes by PGE2. |
| 835 | 8660843 | Stimulation of Jurkat cells with ionomycin and PMA in the presence of PGE2 inhibited the IL-2- but not the IL-4-promoter activity. |
| 836 | 8660843 | In EMSAs, nuclear extracts from primary human T cells stimulated with ionomycin and phorbol esters in the presence of PGE2 demonstrated decreased binding at the AP-1 and NF-AT sites of the human IL-2 promoter; binding to the OCT-1 and NF-kappa B sites was not affected. |
| 837 | 8664448 | During the early phase of insulitis from 6 to 12 weeks of age, mainly the monokines IL-1 alpha, IL-6, and TNF were detected. |
| 838 | 8664448 | After stimulation, also IFN-gamma and low numbers of IL-10 and GM-CSF producing cells could be observed, but no IL-2 or IL-4 was seen. |
| 839 | 8664448 | During a later phase, between 4 and 6 months, there is a characteristic TH1 cytokine profile with production of IL-2 and IFN-gamma occurring after stimulation, as well as lymphocytes producing TNF, supposedly TNF-beta. |
| 840 | 8664448 | During this period IL-10 was very rarely observed, and no IL-4 production could be found throughout the study. |
| 841 | 8664448 | During the early phase of insulitis from 6 to 12 weeks of age, mainly the monokines IL-1 alpha, IL-6, and TNF were detected. |
| 842 | 8664448 | After stimulation, also IFN-gamma and low numbers of IL-10 and GM-CSF producing cells could be observed, but no IL-2 or IL-4 was seen. |
| 843 | 8664448 | During a later phase, between 4 and 6 months, there is a characteristic TH1 cytokine profile with production of IL-2 and IFN-gamma occurring after stimulation, as well as lymphocytes producing TNF, supposedly TNF-beta. |
| 844 | 8664448 | During this period IL-10 was very rarely observed, and no IL-4 production could be found throughout the study. |
| 845 | 8671656 | Partially purified MLR-IA inhibits IL-2 production in a primary allo-MLR, and decreases IFN-gamma production during secondary allo-MLR and Con A activation, whereas it enhances IL-4 production in both primary and secondary Con A activation. |
| 846 | 8671656 | MLR-IA is not neutralized by combination of antibodies specific for transforming growth factor-beta, IL-10, tumor necrosis factor-alpha/beta or IFN-gamma, suggestive of a novel activity. |
| 847 | 8671656 | Our work suggests that a potentially novel immunoregulatory activity, capable of inhibiting T lymphocyte proliferation and IFN-gamma production, and stimulating IL-4 production, may regulate development of autoimmune diabetes in NOD mice. |
| 848 | 8705860 | Analysis of T cells reacting to the pathogenic portion of the MBP molecule indicated that in the vaccinated mice there was a reduction in the Th1 cytokines interleukin-2 (IL-2) and interferon-gama. |
| 849 | 8706342 | Glutamic acid decarboxylase (GAD) could be a key antigen involved in this disease, and GAD65 peptide 524-543 has been implicated in early T cell response in young NOD mice. |
| 850 | 8706342 | After peptide challenge of splenocytes in vitro, protection against CY-accelerated diabetes was associated with higher peptide-specific production of T helper type 2 (Th2)-associated interleukins 4 and 10, whereas Th1-associated interferon-gamma and IL-2 were proportionally less represented. |
| 851 | 8706342 | It is concluded that immunization of NOD mice with GAD65 peptide 524-543 can counteract CY-accelerated diabetes, possibly through active cellular suppression linked to a shift of Th1/Th2 balance toward the production of Th2 cytokines such as IL-4 and IL-10. |
| 852 | 8720604 | To determine whether cytokines could have a role in the development of insulin-dependent diabetes mellitus (IDDM), we measured serum levels of cytokines derived from T helper 1 (interleukin-2 and interferon-gamma), T helper 2 (interleukin-4 and interleukin-10) lymphocytes and macrophages (tumour necrosis factor-alpha, interleukin-1 alpha and interleukin-1 beta) in patients before and after the onset of IDDM. |
| 853 | 8720604 | Recently diagnosed IDDM patients had significantly higher levels of interleukin-2, interferon-gamma, tumour necrosis factor-alpha and interleukin-1 alpha than patients with either long-standing IDDM, non-insulin-dependent diabetes (NIDDM), Graves' disease, or control subjects (p < 0.05 for all). |
| 854 | 8720604 | Compared with control subjects, patients with long-standing IDDM and those with NIDDM had higher interleukin-2 and tumour necrosis factor-alpha levels (p < 0.01 for all). |
| 855 | 8720604 | Interleukin-4 and interleukin-10 were detectable in sera of patients with Graves' disease only, while interleukin-1 beta was not detectable in the serum of any control or test subject. |
| 856 | 8720604 | To determine whether cytokines could have a role in the development of insulin-dependent diabetes mellitus (IDDM), we measured serum levels of cytokines derived from T helper 1 (interleukin-2 and interferon-gamma), T helper 2 (interleukin-4 and interleukin-10) lymphocytes and macrophages (tumour necrosis factor-alpha, interleukin-1 alpha and interleukin-1 beta) in patients before and after the onset of IDDM. |
| 857 | 8720604 | Recently diagnosed IDDM patients had significantly higher levels of interleukin-2, interferon-gamma, tumour necrosis factor-alpha and interleukin-1 alpha than patients with either long-standing IDDM, non-insulin-dependent diabetes (NIDDM), Graves' disease, or control subjects (p < 0.05 for all). |
| 858 | 8720604 | Compared with control subjects, patients with long-standing IDDM and those with NIDDM had higher interleukin-2 and tumour necrosis factor-alpha levels (p < 0.01 for all). |
| 859 | 8720604 | Interleukin-4 and interleukin-10 were detectable in sera of patients with Graves' disease only, while interleukin-1 beta was not detectable in the serum of any control or test subject. |
| 860 | 8720604 | To determine whether cytokines could have a role in the development of insulin-dependent diabetes mellitus (IDDM), we measured serum levels of cytokines derived from T helper 1 (interleukin-2 and interferon-gamma), T helper 2 (interleukin-4 and interleukin-10) lymphocytes and macrophages (tumour necrosis factor-alpha, interleukin-1 alpha and interleukin-1 beta) in patients before and after the onset of IDDM. |
| 861 | 8720604 | Recently diagnosed IDDM patients had significantly higher levels of interleukin-2, interferon-gamma, tumour necrosis factor-alpha and interleukin-1 alpha than patients with either long-standing IDDM, non-insulin-dependent diabetes (NIDDM), Graves' disease, or control subjects (p < 0.05 for all). |
| 862 | 8720604 | Compared with control subjects, patients with long-standing IDDM and those with NIDDM had higher interleukin-2 and tumour necrosis factor-alpha levels (p < 0.01 for all). |
| 863 | 8720604 | Interleukin-4 and interleukin-10 were detectable in sera of patients with Graves' disease only, while interleukin-1 beta was not detectable in the serum of any control or test subject. |
| 864 | 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. |
| 865 | 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. |
| 866 | 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. |
| 867 | 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. |
| 868 | 8750571 | Surprisingly, the number of CD3+ TL bearing the IL-2 receptor (CD25) and transferrin receptor (CD71) was not increased. |
| 869 | 8760354 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in beta-cell destruction and immune regulation. |
| 870 | 8760354 | A major target of beta-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD). |
| 871 | 8760354 | Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67. |
| 872 | 8760354 | Incubation of islets with interleukin (IL)-1 beta (1 ng/ml, 24 h), tumour necrosis factor alpha (TNF-alpha; 200 units/ml, 24 h) or interferon gamma (IFN-gamma; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content. |
| 873 | 8760354 | Incubation of islets for 24 h in IFN-alpha (1000 units/ml), TNF-beta (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor beta 2 (TGF-beta 2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis. |
| 874 | 8760354 | Inhibition of GAD65 and GAD67 protein synthesis by IL-1 beta, TNF-alpha or IFN-gamma was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA). |
| 875 | 8760354 | Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1 beta and completely restored to baseline levels by NMMA. |
| 876 | 8760354 | Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1 beta, TNF-alpha or IFN-gamma by a NO-mediated mechanism, probably at the level of cytokine gene transcription. |
| 877 | 8760354 | As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of beta-cell destruction in IDDM. |
| 878 | 8808683 | Functional analyses of T cells isolated from CD28-deficient mice demonstrated that the GAD-specific T cells produced enhanced Th1-type cytokines (IL-2 and IFN gamma) and diminished Th2-type cytokine, IL-4. |
| 879 | 8811061 | Administration of recombinant interleukin (IL)-2 was shown to reverse the tolerance induced by feeding low doses of MBP, but not the tolerance induced by feeding high doses of MBP, indicating that deletion had occurred in the high-dose group. |
| 880 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 881 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 882 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 883 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 884 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 885 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 886 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 887 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 888 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 889 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 890 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 891 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 892 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 893 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 894 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 895 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 896 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 897 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 898 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 899 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 900 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 901 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 902 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 903 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 904 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 905 | 8816966 | Th1 cytokines are thought to play a key role in islet inflammation and destruction in insulin-dependent diabetes mellitus (IDDM). |
| 906 | 8816966 | In contrast, expression of message for IL-2 and IL-4 is minimal to undetectable in DP-BB and RT6-depleted DR-BB animals at any age. |
| 907 | 8816966 | Incubation of 10 wk old DP islets for 48 h in the presence of anti-CD3 antibody, followed by an incubation with rIL-2 for an additional 5-7 days, results in an expansion of T lymphocytes, and these cells express high levels of IFN-gamma and IL-10 mRNA. |
| 908 | 8816966 | Our results suggest that autoimmunity in DP-BB and DR-BB rats is mediated by Th1 lymphocytes and that IFN-gamma and IL-12 are likely to play a key role in islet and thyroid inflammation and destruction in IDDM. |
| 909 | 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. |
| 910 | 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. |
| 911 | 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. |
| 912 | 8816971 | Analysis of in vitro production of IFN gamma, IL-2 and IL-4 demonstrated a TH1 and TH0 like functional subset of the individual clones. |
| 913 | 8816972 | Insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse results from a T lymphocyte mediated destruction of the insulin-producing beta cells of the pancreas and serves as a model for human type I diabetes. |
| 914 | 8816972 | It has previously been shown that a T helper 1 (Th1) response to the islet antigen, glutamic acid decarboxylase (GAD65, henceforth GAD) spontaneously develops in NOD mice concurrent with the onset of lymphocytic infiltration into the islets (insulitis). |
| 915 | 8816972 | Each hybridoma displayed a unique cytokine profile when stimulated with peptides 524-538 and 527-541, assaying IL-2, IFN-gamma, and IL-5 production by peptide-stimulated hybridomas. |
| 916 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 917 | 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. |
| 918 | 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. |
| 919 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 920 | 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). |
| 921 | 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. |
| 922 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 923 | 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. |
| 924 | 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. |
| 925 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 926 | 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). |
| 927 | 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. |
| 928 | 8826980 | Antibody cross-linking of RT6 enhanced expression of the alpha subunit of the interleukin-2 (IL-2) receptor and potentiated the proliferation of rat T-cells cultured in the presence of phorbol ester plus recombinant IL-2 (rIL-2) and/or rIL-4. |
| 929 | 8826980 | RT6 was found to coimmunoprecipitate with five tyrosine phosphorylated proteins including p60fyn and p56lck, members of the src tyrosine kinase family. |
| 930 | 8826980 | Pretreatment of T-cells with phorbol ester increased the phosphorylation of proteins that coimmunoprecipitated with RT6, altered the electrophoretic mobility of several of these coimmunoprecipitated phosphoproteins, and increased the amount of p60fyn and p56lck coimmunoprecipitated with RT6. |
| 931 | 8871765 | With a semi-quantitative reverse transcriptase-PCR assay, we examined whether the disease process was reflected in the profiles of TH1 (IL-2, IFN-gamma and IL-12) and TH2 (IL-4, IL-6 and IL-10) cytokine mRNAs expressed in pancreata of NOD mice. |
| 932 | 8900312 | Glucocorticoids modulate CD28 mediated pathways for interleukin 2 production in human T cells: evidence for posttranscriptional regulation. |
| 933 | 8900312 | In these cells costimulation via the CD28 cell surface molecule further increases the transcription of IL-2 and stabilizes its mRNA, resulting in a 20-30 fold induction in IL-2 production. |
| 934 | 8900312 | These results suggest that GC inhibit accessory pathways for IL-2 production via CD28 by predominantly posttranscriptional mechanisms. |
| 935 | 8900312 | Glucocorticoids modulate CD28 mediated pathways for interleukin 2 production in human T cells: evidence for posttranscriptional regulation. |
| 936 | 8900312 | In these cells costimulation via the CD28 cell surface molecule further increases the transcription of IL-2 and stabilizes its mRNA, resulting in a 20-30 fold induction in IL-2 production. |
| 937 | 8900312 | These results suggest that GC inhibit accessory pathways for IL-2 production via CD28 by predominantly posttranscriptional mechanisms. |
| 938 | 8900312 | Glucocorticoids modulate CD28 mediated pathways for interleukin 2 production in human T cells: evidence for posttranscriptional regulation. |
| 939 | 8900312 | In these cells costimulation via the CD28 cell surface molecule further increases the transcription of IL-2 and stabilizes its mRNA, resulting in a 20-30 fold induction in IL-2 production. |
| 940 | 8900312 | These results suggest that GC inhibit accessory pathways for IL-2 production via CD28 by predominantly posttranscriptional mechanisms. |
| 941 | 8917637 | A patient with advanced colorectal cancer, treated with 1.5 x 10(6) international units of IL-2 daily, developed insulin-requiring diabetes during therapy. |
| 942 | 8933279 | Differential expression of ICAM-1 and LFA-1 versus L-selectin and VCAM-1 in autoimmune insulitis of NOD mice and association with both Th1- and Th2-type infiltrates. |
| 943 | 8933279 | NOD mouse islets did not show the expression of ICAM-1, LFA-1, L-selectin and VCAM-1 prior to infiltration by mononuclear cells. |
| 944 | 8933279 | ICAM-1 and LFA-1 were first demonstrable in islets with strong periinsular infiltrates (insulitis grade 2) while L-selectin and VCAM-1 were only seen in islets with mild or strong intraislet infiltration (grade 3-4). |
| 945 | 8933279 | Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.). |
| 946 | 8933279 | ICAM-1 and LFA-1 expression is seen prior to L-selectin and VCAM-1. |
| 947 | 8933280 | Interferon-gamma (IFN-gamma) is implicated as a mediator of islet beta-cell destruction in autoimmune, insulin-dependent diabetes mellitus (IDDM). |
| 948 | 8933280 | Because interleukin 12 (IL-12) is a potent inducer of IFN-gamma production, we sought evidence implicating IL-12 in IDDM development. |
| 949 | 8933280 | Expression of mRNA encoding the p40 chain of IL-12 (IL-12 p40) in mono-nuclear leukocytes isolated from islets of female NOD mice increased progressively from age 5 weeks to diabetes onset (> 13 weeks). |
| 950 | 8933280 | By contrast, IL-12 p40 mRNA levels were significantly decreased in islet mononuclear leukocytes, but not spleens, from female NOD mice protected from diabetes by administration of complete Freund's adjuvant (CFA) in early life. |
| 951 | 8933280 | In addition, mRNA levels of IL-12 p40, IFN-gamma and IL-2 were significantly decreased in syngeneic islet grafts, but not spleens, from female NOD mice protected from diabetes recurrence by CFA administration at the time of islet transplantation. |
| 952 | 8933280 | These findings show that IL-12 gene expression in the insulitis lesion correlates with both primary and recurrent diabetes development in NOD mice, possibly via induction of T helper (Th) 1-type cytokines, IL-2 and IFN-gamma. |
| 953 | 8933280 | Interferon-gamma (IFN-gamma) is implicated as a mediator of islet beta-cell destruction in autoimmune, insulin-dependent diabetes mellitus (IDDM). |
| 954 | 8933280 | Because interleukin 12 (IL-12) is a potent inducer of IFN-gamma production, we sought evidence implicating IL-12 in IDDM development. |
| 955 | 8933280 | Expression of mRNA encoding the p40 chain of IL-12 (IL-12 p40) in mono-nuclear leukocytes isolated from islets of female NOD mice increased progressively from age 5 weeks to diabetes onset (> 13 weeks). |
| 956 | 8933280 | By contrast, IL-12 p40 mRNA levels were significantly decreased in islet mononuclear leukocytes, but not spleens, from female NOD mice protected from diabetes by administration of complete Freund's adjuvant (CFA) in early life. |
| 957 | 8933280 | In addition, mRNA levels of IL-12 p40, IFN-gamma and IL-2 were significantly decreased in syngeneic islet grafts, but not spleens, from female NOD mice protected from diabetes recurrence by CFA administration at the time of islet transplantation. |
| 958 | 8933280 | These findings show that IL-12 gene expression in the insulitis lesion correlates with both primary and recurrent diabetes development in NOD mice, possibly via induction of T helper (Th) 1-type cytokines, IL-2 and IFN-gamma. |
| 959 | 8940385 | Under ex vivo conditions, sIFNgammaR exhibited a more powerful modulatory effect than XMG 1.2 mAb on cytokine secretion from splenic lymphoid cells, which resulted in a significant reduction of Concanavalin A-induced IL-2 secretion and an augmented release of both unstimulated and lipopolysaccharide-induced IL-6. |
| 960 | 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. |
| 961 | 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. |
| 962 | 8953520 | Evaluation of T-splenocytes indicated a 2:1 ratio of CD4 to CD8 T-lymphocytes in the spleen. |
| 963 | 8953520 | Pancreatic immunocompetent cell subsets expressed lower percentages of IL-2R, PRLR and Hi-PRLR compared to splenocytes. |
| 964 | 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. |
| 965 | 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. |
| 966 | 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. |
| 967 | 8953520 | Evaluation of T-splenocytes indicated a 2:1 ratio of CD4 to CD8 T-lymphocytes in the spleen. |
| 968 | 8953520 | Pancreatic immunocompetent cell subsets expressed lower percentages of IL-2R, PRLR and Hi-PRLR compared to splenocytes. |
| 969 | 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. |
| 970 | 8961238 | These shared symptoms include elevated tumour necrosis factor-alpha, down-regulated interleukin-2 and interleukin-4 and depletion of lean body mass. |
| 971 | 8961238 | Furthermore, the following neuropeptides are dysregulated in both anorexia nervosa and cancer cachexia: vasoactive intestinal peptide, cholecystokinin, corticotropin-releasing factor, neuropeptide Y, peptide YY and beta-endorphin. |
| 972 | 8977415 | The role of endogenous interferon-gamma (IFN gamma) in the development of insulin-dependent diabetes mellitus (IDDM) in diabetes-prone BB rats was evaluated. |
| 973 | 8977415 | At histoimmunological analyses, the BB rats treated with 200 micrograms/ week anti-IFN gamma Abs from 30-80 days of age exhibited a milder insulitic process along with diminished spleen frequency of activated lymphoid cells (MHC class II and interleukin-2 receptor positive). |
| 974 | 8977415 | Taken together, these results provide further in vivo evidence for the central pathogenic role of IFN gamma in BB rat IDDM and anticipate the usefulness of specific IFN gamma inhibitors in the prevention of the disease in the clinical setting. |
| 975 | 9012538 | Cytokine-inducers prevent insulin-dependent diabetes mellitus (IDDM) in animal models. |
| 976 | 9012538 | We extend this therapy to non-insulin-dependent diabetes mellitus (NIDDM), because it was reported that diabetes of KK-Ay mice, a model for NIDDM, was recovered by allogenic bone-marrow transplantation that also prevented IDDM in animal models. |
| 977 | 9012538 | Among various cytokines possibly induced by OK-432 and BCG, IL-1 alpha, TNF alpha and lymphotoxin significantly improved FBG and GTT in KK-Ay mice, whereas IL-2 and IFN gamma did not. |
| 978 | 9032395 | The Rep proteins of adeno-associated virus type 2 (AAV) are known to bind to Rep recognition sequences (RRSs) in the AAV inverted terminal repeats (ITRs), the AAV p5 promoter, and the preferred AAV integration site in human chromosome 19, called AAVS1. |
| 979 | 9032395 | We used the 16-mer core sequences of the RRSs in the AAV ITRs and AAVS1 separately as query sequences and identified 18 new RRSs in or flanking the genes coding for the following: tyrosine kinase activator protein 1 (TKA-1); colony stimulating factor-1; insulin-like growth factor binding protein 2 (IGFBP-2); histone H2B.1; basement membrane heparan sulfate proteoglycan, also known as perlecan; the AF-9 gene product, which is involved in the chromosomal translocation t (9:11)(p22:q23); the betaB subunit of the hormone known as inhibin; interleukin-2 enhancer binding factor; an endoplasmic reticulum-Golgi intermediate compartment resident protein called p63; a global transcription activator (hSNF2L); the beta-actin repair domain; a retinoic acid-inducible factor, also known as midkine; a breast tumor autoantigen; a growth-arrest- and DNA-damage-inducible protein called gadd45; the cyclin-dependent kinase inhibitor called KIP2, which inhibits several G1 cyclin-cyclin-dependent kinase complexes; and the hereditary breast and ovarian cancer gene (BRCA1). |
| 980 | 9047096 | Increased soluble interleukin-2 receptor concentrations in patients with insulin-dependent diabetes mellitus. |
| 981 | 9048875 | Using lipopolysaccharide (LPS)-stimulated cells, sulphatide increased the IL-2 production (163 +/- 17% of controls without sulphatide, p = 0.02), and gal-cer increased the IL-1 alpha production (145 +/- 13%, p = 0.006), whereas neither gal-cer nor sulphatide had an effect on the production of IL-6, IL-10 or TNF alpha. |
| 982 | 9048875 | When stimulating cells with phytohaemagglutinin (PHA), sulphatide decreased the production of IL-6 (88 +/- 5%, p = 0.009), IL-10 (66 +/- 3%, p = 0.000003), and TNF alpha (75 +/- 9% p = 0.02). |
| 983 | 9048875 | Gal-cer, however, increased the production of IL-6 (188 +/- 13% p = 0.000006), and decreased the production of TNF beta (80 +/- 6%, p = 0.007). |
| 984 | 9048875 | Neither gal-cer nor sulphatide had an effect on the production of IL-2 or IFN gamma from PHA-stimulated cells. |
| 985 | 9048875 | Using lipopolysaccharide (LPS)-stimulated cells, sulphatide increased the IL-2 production (163 +/- 17% of controls without sulphatide, p = 0.02), and gal-cer increased the IL-1 alpha production (145 +/- 13%, p = 0.006), whereas neither gal-cer nor sulphatide had an effect on the production of IL-6, IL-10 or TNF alpha. |
| 986 | 9048875 | When stimulating cells with phytohaemagglutinin (PHA), sulphatide decreased the production of IL-6 (88 +/- 5%, p = 0.009), IL-10 (66 +/- 3%, p = 0.000003), and TNF alpha (75 +/- 9% p = 0.02). |
| 987 | 9048875 | Gal-cer, however, increased the production of IL-6 (188 +/- 13% p = 0.000006), and decreased the production of TNF beta (80 +/- 6%, p = 0.007). |
| 988 | 9048875 | Neither gal-cer nor sulphatide had an effect on the production of IL-2 or IFN gamma from PHA-stimulated cells. |
| 989 | 9058834 | The tolerogenic properties of 145 2C11 did not depend on its mitogenic capacity, since nonmitogenic F(ab')2 fragments also appeared potent at inducing durable remission in overtly diabetic NOD, although nonmitogenic CD3 F(ab')2 fragments could mediate T cell signaling, as evidenced by cytokine gene transcription (IL-2, IFN-gamma, IL-4, and IL-10) assessed by PCR on splenocytes from treated mice. |
| 990 | 9123210 | IL-2 and IL-4 double knock-out mice reject islet allografts: a role for novel T-cell growth factors? |
| 991 | 9127018 | Immunohistochemistry studies show that IL-10/Fc treatment inhibits expression of TNF-alpha, proinflammatory cytokine, as well as Th1-type cytokines, IL-2 and IFN-gamma, but promotes expression of IL-4 and IL-10, Th2-type cytokines, by islet-infiltrating leukocytes. |
| 992 | 9185876 | The cell recruitment phase, between 6 and 12 weeks of age, is predominated by production of the monokines IL-1alpha, IL-6, and TNF After stimulation IFN-gamma and occasional IL-10 and GM-CSF producing cells could also be observed. |
| 993 | 9185876 | During the effector phase, between 4 and 6 months, there is a characteristic Th1 cytokine profile with lymphocytes producing IL-2, IFN-gamma and TNF, supposedly TNF-beta. |
| 994 | 9185876 | No IL-4 production could be detected and IL-10 was very rarely found, indicating the absence of a Th2 response. |
| 995 | 9193658 | The percentage of RT6 positive cells was increased by in vitro stimulation of isolated NK cells with high concentrations of recombinant rat IL-2 indicating that RT6 expression may be associated with an activated state in NK cells. |
| 996 | 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. |
| 997 | 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. |
| 998 | 9207862 | At doses approximating those achieved in vivo (0.4 and 2 micrograms/ml), dapsone was found to inhibit murine splenocyte IL-2 and IL-4 secretion in response to concanavalin A. |
| 999 | 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. |
| 1000 | 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. |
| 1001 | 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. |
| 1002 | 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. |
| 1003 | 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. |
| 1004 | 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). |
| 1005 | 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. |
| 1006 | 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. |
| 1007 | 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. |
| 1008 | 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. |
| 1009 | 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. |
| 1010 | 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. |
| 1011 | 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. |
| 1012 | 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. |
| 1013 | 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). |
| 1014 | 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. |
| 1015 | 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. |
| 1016 | 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. |
| 1017 | 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. |
| 1018 | 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. |
| 1019 | 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. |
| 1020 | 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. |
| 1021 | 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. |
| 1022 | 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). |
| 1023 | 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. |
| 1024 | 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. |
| 1025 | 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. |
| 1026 | 9267984 | Potentiation of the effect of oral insulin by the adjuvant was associated with upregulation of interleukin (IL)-4 Th2 cells in infiltrated islets and sustained local IL-2 gene expression. |
| 1027 | 9267984 | RT PCR analyses of cytokine expression in the gut showed a clear deviation to Th2 type reactivity and downregulation of inducible nitric oxide (NO) synthase (iNOS) expression by the bacterial adjuvant but not by oral insulin alone. |
| 1028 | 9279510 | Cytokine production, especially that of interferon-gamma and interleukin 2, was also inhibited in the oral LC-treated group. |
| 1029 | 9298104 | Analysis of cytokine production revealed lower interferon-gamma production in the LC-treated group compared to the control group, while the interleukin (IL)-2 production was higher. |
| 1030 | 9298104 | The levels of IL-4, IL-5, IL-6 and IL-10 in the LC-treated group were somewhat higher than in the control group. |
| 1031 | 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. |
| 1032 | 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. |
| 1033 | 9366391 | IL-4 prevents insulitis and insulin-dependent diabetes mellitus in nonobese diabetic mice by potentiation of regulatory T helper-2 cell function. |
| 1034 | 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. |
| 1035 | 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). |
| 1036 | 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. |
| 1037 | 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. |
| 1038 | 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. |
| 1039 | 9379064 | CD40 ligand-CD40 interactions are necessary for the initiation of insulitis and diabetes in nonobese diabetic mice. |
| 1040 | 9379064 | Here, we investigate the role of CD40 ligand (CD40L)-CD40 costimulation in the initiation and progression of this disease. |
| 1041 | 9379064 | Cytokine analysis revealed a dramatic decrease in IFN-gamma and IL-2 release without a concomitant increase in IL-4 production by T cells from anti-CD40L-treated mice. |
| 1042 | 9416430 | The ability of splenocytes to proliferate, respond to, or secrete interleukin-2 and interleukin-4 was explored in young, pre-diabetic or old non-diabetic female NOD mice. |
| 1043 | 9416430 | These results suggest that diabetes induction is preceded by V beta + subset-specific functional changes in the ability of various T cells to respond to or secrete interleukin-2 and interleukin-4, indicating a functional imbalance of the T-cell repertoire expanded by the autoimmune process. |
| 1044 | 9416430 | The ability of splenocytes to proliferate, respond to, or secrete interleukin-2 and interleukin-4 was explored in young, pre-diabetic or old non-diabetic female NOD mice. |
| 1045 | 9416430 | These results suggest that diabetes induction is preceded by V beta + subset-specific functional changes in the ability of various T cells to respond to or secrete interleukin-2 and interleukin-4, indicating a functional imbalance of the T-cell repertoire expanded by the autoimmune process. |
| 1046 | 9421371 | Previous studies have shown that anti-gamma-interferon (IFN-gamma) antibody reduces the frequency of autoimmune IDDM in the DP-BB rat. |
| 1047 | 9421371 | Unexpectedly, IFN-gamma markedly reduced the incidence of IDDM as compared with control rats when administered six times per week at a dosage of 280,000 U between ages 30-35 to 105 days or ages 60-64 to 105 days. |
| 1048 | 9421371 | However, long-lasting protection against IDDM development over the 1-year study period was achieved only by the highest dosage of IFN-gamma administered from age 30 to 105 days. |
| 1049 | 9421371 | Ex vivo production of tumor necrosis factor-alpha from splenic lymphoid cells (SLCs) and peritoneal macrophages of the rats treated with IFN-gamma was comparable with that of controls; however, SLCs from the IFN-gamma-treated animals secreted lower amounts of IFN-gamma after stimulation with concanavalin A. |
| 1050 | 9421371 | IFN-gamma treatment also markedly reduced the frequency of phenotypically activated SLC-expressing class II antigens and interleukin-2 receptor. |
| 1051 | 9421371 | Finally, in agreement with the observed antidiabetogenic effects, exogenously administered IFN-gamma induced neither insulitis nor IDDM development in DR-BB rats, a subline of DP-BB rats in which autoimmune diabetes rarely occurs spontaneously but can be induced by administration of polyinosinic-polycytidilic acid. |
| 1052 | 9473384 | By measuring the cytokine production of splenic T cells after stimulation, it was shown that CD45RBlowCD4+ T cells predominantly produced IL-4 and IL-10 but produced less IL-2 and interferon-gamma (IFN-gamma). |
| 1053 | 9473384 | A semiquantitative reverse-transcriptase polymerase chain reaction assay revealed a higher expression of IL-4 and IL-10 mRNA and an apparent decrease in IFN-gamma mRNA in the islets of NOD mice which were administered rIL-4. |
| 1054 | 9480724 | Insulin-dependent diabetes mellitus (IDDM) results from chronic, T-cell dependent, autoimmune destruction of the insulin-producing beta-cells in the Langerhans' islets of the pancreas. |
| 1055 | 9480724 | However, DAP.3Ag7 cells are able to process and present antigen, as indicated by I-Ag7-dependent IL-2 production by a GAD67-specific NDO T-cell hybridoma after stimulation with GAD and live, but not fixed, DAP.3Ag7 cells. |
| 1056 | 9480724 | The IL-2 response to GAD when presented by DAP.3Ag7 was significantly higher than the response to GAD presented by NOD splenocytes. |
| 1057 | 9480724 | Insulin-dependent diabetes mellitus (IDDM) results from chronic, T-cell dependent, autoimmune destruction of the insulin-producing beta-cells in the Langerhans' islets of the pancreas. |
| 1058 | 9480724 | However, DAP.3Ag7 cells are able to process and present antigen, as indicated by I-Ag7-dependent IL-2 production by a GAD67-specific NDO T-cell hybridoma after stimulation with GAD and live, but not fixed, DAP.3Ag7 cells. |
| 1059 | 9480724 | The IL-2 response to GAD when presented by DAP.3Ag7 was significantly higher than the response to GAD presented by NOD splenocytes. |
| 1060 | 9498651 | Moreover, in both NOD and B6 mice, CD4+ T cells were more resistant to PCD induced by IL-2 deprivation than CD8+ cells. |
| 1061 | 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. |
| 1062 | 9498651 | Moreover, in both NOD and B6 mice, CD4+ T cells were more resistant to PCD induced by IL-2 deprivation than CD8+ cells. |
| 1063 | 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. |
| 1064 | 9541176 | Healthy family members of patients with insulin-dependent diabetes mellitus (IDDM) are known to share a number of immunological abnormalities with their affected relatives. |
| 1065 | 9541176 | We report that circulating tumour necrosis factor-alpha (TNF-alpha) and soluble interleukin-2 (sIL-2) receptor were present in increased amounts in non-diabetic family members at levels similar to those found in the diabetic children (duration of disease 3 months-5 years). |
| 1066 | 9550282 | Whereas we and others have observed a delay in the onset of diabetes in NOD mice that have been fed with insulin from early life, we report here for the first time that feedings with porcine GAD65 alone (p = 0.226) or in combination with insulin (p = 0.011), have anti-diabetic effects in a prolonged study period (>400 days). |
| 1067 | 9550282 | IFN-gamma mRNA levels were downregulated in the islet infiltrates following oral antigen treatments while IL-2 and TNF-beta were expressed in all instances. |
| 1068 | 9550282 | We also observed that I.V. human recombinant GAD65, and porcine GAD given at weaning, delayed diabetes onset (p = 0.004) while similar treatments with a variety of inactive insulin preparations were generally ineffective. |
| 1069 | 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. |
| 1070 | 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. |
| 1071 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 1072 | 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. |
| 1073 | 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. |
| 1074 | 9576014 | When cytokine profiles were examined, feeding led to a predominance of IL-10 and TGF-beta production. |
| 1075 | 9576014 | Furthermore, feeding SEA in combination with insulin B-chain augmented the level of IL-10 production to insulin. |
| 1076 | 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. |
| 1077 | 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. |
| 1078 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 1079 | 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. |
| 1080 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 1081 | 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. |
| 1082 | 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. |
| 1083 | 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. |
| 1084 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 1085 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 1086 | 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. |
| 1087 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 1088 | 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. |
| 1089 | 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. |
| 1090 | 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. |
| 1091 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 1092 | 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. |
| 1093 | 9626161 | Increased CD69 and human leukocyte antigen-DR expression on T lymphocytes in insulin-dependent diabetes mellitus of long standing. |
| 1094 | 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. |
| 1095 | 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. |
| 1096 | 9626161 | CD69 expression did not differ between IDDM and HS, but differed between DML (CD4+, CD8+, and CD45RA- CD4+) and DM only. |
| 1097 | 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. |
| 1098 | 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). |
| 1099 | 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. |
| 1100 | 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). |
| 1101 | 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. |
| 1102 | 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. |
| 1103 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 1104 | 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. |
| 1105 | 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. |
| 1106 | 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). |
| 1107 | 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. |
| 1108 | 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). |
| 1109 | 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. |
| 1110 | 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. |
| 1111 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 1112 | 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. |
| 1113 | 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. |
| 1114 | 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). |
| 1115 | 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. |
| 1116 | 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). |
| 1117 | 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. |
| 1118 | 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. |
| 1119 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 1120 | 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. |
| 1121 | 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. |
| 1122 | 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). |
| 1123 | 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. |
| 1124 | 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). |
| 1125 | 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. |
| 1126 | 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. |
| 1127 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 1128 | 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. |
| 1129 | 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. |
| 1130 | 9712353 | Pancreatic islet beta cell destruction leading to insulin-dependent diabetes mellitus (IDDM) is believed to be mediated by a T-helper 1 (T(H)1) lymphocyte response to islet antigens. |
| 1131 | 9712353 | In the mouse, T(H)1 (IL-2, IFN-gamma) and T(H)2 (IL-4, -5, -6, -10) responses are associated with the generation of IgG2a and IgG1 subclasses, respectively. |
| 1132 | 9712353 | Because the IgG subclass response to an antigen may be a potentially useful marker of T(H)1/T(H)2 immune balance we measured IgG subclass antibodies to glutamic acid decarboxylase (GAD), a major islet autoantigen in IDDM, in 34 newly-diagnosed IDDM patients and in 28 at-risk, first-degree relatives of people with IDDM. |
| 1133 | 9713328 | Islets cultured with 10 ng/ml IL-12 showed a decrease in medium insulin accumulation both in mouse and rat. |
| 1134 | 9713328 | Glucose-stimulated insulin release was lowered in rat islets exposed to 10 ng/ml IL-12, but not affected in NMRI islets. |
| 1135 | 9713328 | Islets were isolated from female NOD mice (age 5, 12, 20 and 26 weeks) and examined either immediately or cultured for 7 days with 10 ng/ml IL-12 alone or in combination with 4 ng/ml of the T-cell stimulating cytokine interleukin-2 (IL-2). |
| 1136 | 9713328 | IL-2 + IL-12 addition induced a small decrease in glucose-stimulated insulin release in islets from 12-week-old animals. |
| 1137 | 9713328 | The suppressed insulin release in NOD mouse islets treated with IL-2 + IL-12 suggests, however, that the accelerating effect might partly be attributed to stimulation of immune cells present in the insulitic lesion. |
| 1138 | 9713328 | Islets cultured with 10 ng/ml IL-12 showed a decrease in medium insulin accumulation both in mouse and rat. |
| 1139 | 9713328 | Glucose-stimulated insulin release was lowered in rat islets exposed to 10 ng/ml IL-12, but not affected in NMRI islets. |
| 1140 | 9713328 | Islets were isolated from female NOD mice (age 5, 12, 20 and 26 weeks) and examined either immediately or cultured for 7 days with 10 ng/ml IL-12 alone or in combination with 4 ng/ml of the T-cell stimulating cytokine interleukin-2 (IL-2). |
| 1141 | 9713328 | IL-2 + IL-12 addition induced a small decrease in glucose-stimulated insulin release in islets from 12-week-old animals. |
| 1142 | 9713328 | The suppressed insulin release in NOD mouse islets treated with IL-2 + IL-12 suggests, however, that the accelerating effect might partly be attributed to stimulation of immune cells present in the insulitic lesion. |
| 1143 | 9713328 | Islets cultured with 10 ng/ml IL-12 showed a decrease in medium insulin accumulation both in mouse and rat. |
| 1144 | 9713328 | Glucose-stimulated insulin release was lowered in rat islets exposed to 10 ng/ml IL-12, but not affected in NMRI islets. |
| 1145 | 9713328 | Islets were isolated from female NOD mice (age 5, 12, 20 and 26 weeks) and examined either immediately or cultured for 7 days with 10 ng/ml IL-12 alone or in combination with 4 ng/ml of the T-cell stimulating cytokine interleukin-2 (IL-2). |
| 1146 | 9713328 | IL-2 + IL-12 addition induced a small decrease in glucose-stimulated insulin release in islets from 12-week-old animals. |
| 1147 | 9713328 | The suppressed insulin release in NOD mouse islets treated with IL-2 + IL-12 suggests, however, that the accelerating effect might partly be attributed to stimulation of immune cells present in the insulitic lesion. |
| 1148 | 9716913 | It was found that strain-related susceptibility to diabetes induction correlated with a higher level of IL-2, IFN-gamma, and TNF-alpha production, whereas such differences were not observed when IL-1 and NO production by macrophages were analyzed; elimination of immunoregulatory RT6+T cells that increases IFN-gamma production, enhances susceptibility to MLD-STZ-induced diabetes; mercury-induced Th-2 cells down-regulated the disease; IFN-gamma-mediated macrophage activation to produce proinflammatory cytokines rather than NO is an important event in early diabetogenic effects of invading macrophages; inhibition of IL-1 activity downregulates diabetes induction; and generation of NO in beta cells appears to be important for diabetogenic effects. |
| 1149 | 9719467 | Insulin-dependent diabetes mellitus (IDDM) is a disease that results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans. |
| 1150 | 9719467 | Type 1 cytokines--interleukin 2 (IL-2), interferon gamma (IFNgamma), and tumor necrosis factor beta (TNFbeta), dominate over an immunoregulatory (suppressor) Th2 subset of T cells and their cytokine products, i.e. |
| 1151 | 9719467 | Type 2 cytokines--IL-4 and IL-10. |
| 1152 | 9719467 | Type 1 cytokines activate (1) cytotoxic T cells that interact specifically with beta-cells and destroy them, and (2) macrophages to produce proinflammatory cytokines (IL-1 and TNFalpha), and oxygen and nitrogen free radicals that are highly toxic to islet beta-cells. |
| 1153 | 9719467 | Furthermore, the cytokines IL-1, TNFalpha, and IFNgamma are cytotoxic to beta-cells, in large part by inducing the formation of oxygen free radicals, nitric oxide, and peroxynitrite in the beta-cells themselves. |
| 1154 | 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. |
| 1155 | 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. |
| 1156 | 9761385 | Decreased in vitro IL-4 [corrected] and IL-10 production by peripheral blood in first degree relatives at high risk of diabetes type-I. |
| 1157 | 9761385 | The aim of the present study was the estimation of in vitro production of Th1 (INF-gamma, IL-2) and Th2-derived (IL-4, IL-10) cytokines by peripheral blood in ICA and GADA positive first degree relatives of Type-I diabetes patients, since they could represent primary events triggering an immune-mediated islets destruction. |
| 1158 | 9761385 | In subjects at increased risk of Type-I diabetes, levels of IL-4 positively correlated with those of IL-10. |
| 1159 | 9761385 | In conclusion our study has shown decreased IL-4 and IL-10 production, but normal secretion of Th1-derived cytokines by peripheral blood of prediabetic humans. |
| 1160 | 9790722 | We have further found that normal splenic T cells from the NOD mouse proliferate poorly to IL-2 in vitro, yet secrete IFN-gamma in response to IL-2 stimulation. |
| 1161 | 9878085 | Therefore, we examined the peak levels, secretory pattern and total cytokine production (calculated as the area under the curve, AUC) of the Th1 cytokines, IL-2 and IFN-gamma, and Th2 cytokines, IL-4 and IL-10, from stimulated peripheral blood mononuclear cells, from 17 IDDM patients and 24 normal controls. |
| 1162 | 9878085 | This resulted in significant differences in secretory patterns of IFN-gammaIL-2, IL-4 and IL-10 between the two groups; P<0.001, P<0.005, P<0.005 and P<0.001, respectively. |
| 1163 | 9878085 | No correlation was found in the diabetic patients between any profiles of the cytokines and their various clinical parameters, including age, gender, disease duration, insulin requirements or glycated hemoglobin levels. |
| 1164 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 1165 | 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. |
| 1166 | 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. |
| 1167 | 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. |
| 1168 | 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. |
| 1169 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 1170 | 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. |
| 1171 | 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. |
| 1172 | 10066341 | Secretion of IL-4 was dramatically reduced; however, secretion of IL-2 or IFN-gamma was not significantly inhibited. |
| 1173 | 10066341 | Levels of mRNA encoding IFN-gamma were similar, but the appearance was delayed in thymocytes derived from STZ-treated mice, implying differential regulation of IL-4 and IFN-gamma. |
| 1174 | 10066341 | Defective thymocyte proliferation was partially restored by exposure to IL-2 in vitro; however, IL-4 completely reversed the STZ-induced defect. |
| 1175 | 10066341 | Secretion of IL-4 was dramatically reduced; however, secretion of IL-2 or IFN-gamma was not significantly inhibited. |
| 1176 | 10066341 | Levels of mRNA encoding IFN-gamma were similar, but the appearance was delayed in thymocytes derived from STZ-treated mice, implying differential regulation of IL-4 and IFN-gamma. |
| 1177 | 10066341 | Defective thymocyte proliferation was partially restored by exposure to IL-2 in vitro; however, IL-4 completely reversed the STZ-induced defect. |
| 1178 | 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. |
| 1179 | 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. |
| 1180 | 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. |
| 1181 | 10096786 | During proliferation in response to islet cells, interleukin-10 increased 43-fold (p<0.01) but interferon-gamma increased only slightly. |
| 1182 | 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. |
| 1183 | 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. |
| 1184 | 10201899 | p38 mitogen-activated protein kinase mediates signal integration of TCR/CD28 costimulation in primary murine T cells. |
| 1185 | 10201899 | In contrast to that reported for human Jurkat T cells, we found that p38 MAPK, but not Jun NH2-terminal kinase (JNK), is weakly activated upon stimulation with either anti-CD3 or anti-CD28 in murine thymocytes and splenic T cells. |
| 1186 | 10201899 | However, p38 MAPK is activated strongly and synergistically by either CD3/CD28 coligation or PMA/Ca2+ ionophore stimulation, which mimics TCR-CD3/CD28-mediated signaling. |
| 1187 | 10201899 | Activation of p38 MAPK correlates closely with the stimulation of T cell proliferation. |
| 1188 | 10201899 | T cell proliferation and production of IL-2, IL-4, and IFN-gamma induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580. |
| 1189 | 10201899 | Our findings demonstrate that p38 MAPK 1) plays an important role in signal integration during costimulation of primary mouse T cells, 2) may be involved in the induction of c-Jun activation and augmentation of AP-1 transcriptional activity, and 3) regulates whether T cells enter a state of functional unresponsiveness. |
| 1190 | 10323367 | Type I (insulin-dependent) diabetes mellitus (IDDM) is an autoimmune disease that results from the destruction of insulin-secreting pancreatic islet beta-cells by autoreactive cells and their mediators. |
| 1191 | 10323367 | Th1 cytokines, including interleukin-2 and interferon-gamma, induced islet beta-cell destruction directly by accelerating activation-induced cell death (apoptosis) and by up-regulating the expression of select adhesion molecules, Th1 cytokines facilitated the pancreatic homing of autoreactive leukocytes, hence enhancing beta-cell destruction. |
| 1192 | 10330296 | Regulatory Th2-type T cell lines against insulin and GAD peptides derived from orally- and nasally-treated NOD mice suppress diabetes. |
| 1193 | 10330296 | Ourselves and others have previously shown that oral and nasal administration of insulin or glutamic acid decarboxylase (GAD) suppresses development of diabetes in the NOD mouse and that this suppression appears secondary to the generation of regulatory T cells that act by secreting anti-inflammatory cytokines such as IL-4 and TGF-beta. |
| 1194 | 10330296 | In the present study, we analysed cytokine patterns associated with mucosal administration of insulin B-chain, B-chain peptide 10-24 and GAD peptide 524-543 and derived lines and clones from mucosally-treated animals. |
| 1195 | 10330296 | There was significantly less IFN-gamma production in mucosally-treated mice associated with increased production of IL-10 and TGF-beta. |
| 1196 | 10330296 | T cell clones, established from draining lymph nodes of fed or nasally-treated animals, secreted IL-4, IL-10 and TGF-beta whereas those from non-fed mice secreted IL-2 and IFN-gamma. |
| 1197 | 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. |
| 1198 | 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. |
| 1199 | 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. |
| 1200 | 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. |
| 1201 | 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. |
| 1202 | 10357884 | These T cells can be rescued from apoptosis if they are provided with costimulation supplied, for example, by engaging the CD28 co-receptor with an anti-CD28 monoclonal antibody or by adding an exogenous source of interleukin-2. |
| 1203 | 10357884 | This was not due to the inability of BB-DP T cells to upregulate CD28 and the IL-2 receptor in response to TCR crosslinking. |
| 1204 | 10357884 | These T cells can be rescued from apoptosis if they are provided with costimulation supplied, for example, by engaging the CD28 co-receptor with an anti-CD28 monoclonal antibody or by adding an exogenous source of interleukin-2. |
| 1205 | 10357884 | This was not due to the inability of BB-DP T cells to upregulate CD28 and the IL-2 receptor in response to TCR crosslinking. |
| 1206 | 10377954 | We propose that the increase in lymphocyte suppressive activity caused by cerebrocrast administration may prevent the development of IDDM and NIDDM in patients with pre-diabetes, but in patients with early and overt diabetes mellitus the drug administration may prevent the overexpression of insulin antibodies and other antibodies. |
| 1207 | 10377954 | The effect of cerebrocrast on the de novo production of insulin and IL-2 receptors may be beneficial for IDDM and NIDDM patients. |
| 1208 | 10377955 | In the present work we studied the effect of some 1, 4-dihydropyridines (DHP) such as nimodipine, nicardipine, nifedipine, niludipine, cerebrocrast, etaftoron, as well as metabolites of cerebrocrast: compounds 7 and 8, (four of the last were synthesized in the Latvian Institute of Organic Synthesis) on rat spleen isolated lymphocyte activation and proliferation in vitro following stimulation with the mitogens concanavalin A (Con A) and recombinant interleukin-2 (IL-2), insulin and insulin antibodies. |
| 1209 | 10377955 | Cerebrocrast among all the studied DHP Ca antagonists was the most potent in studies of activation of the lymphocytes in the presence of Con A, IL-2 and insulin, which indicates the number of suppressor and helper lymphocytes and formation of insulin and interleukin receptors on their membrane surface. |
| 1210 | 10377955 | In the present work we studied the effect of some 1, 4-dihydropyridines (DHP) such as nimodipine, nicardipine, nifedipine, niludipine, cerebrocrast, etaftoron, as well as metabolites of cerebrocrast: compounds 7 and 8, (four of the last were synthesized in the Latvian Institute of Organic Synthesis) on rat spleen isolated lymphocyte activation and proliferation in vitro following stimulation with the mitogens concanavalin A (Con A) and recombinant interleukin-2 (IL-2), insulin and insulin antibodies. |
| 1211 | 10377955 | Cerebrocrast among all the studied DHP Ca antagonists was the most potent in studies of activation of the lymphocytes in the presence of Con A, IL-2 and insulin, which indicates the number of suppressor and helper lymphocytes and formation of insulin and interleukin receptors on their membrane surface. |
| 1212 | 10400828 | Although we saw no difference in type 1 cytokine production (IL-2 and IFN-gamma) in either dialysis group, there was a clear increase in the percentage of T cells spontaneously producing the type 02 cytokines in the PD group (IL-4, r = 0.558, P < 0.05; IL-10, r = 0.527, p < 0.05). |
| 1213 | 10400828 | As expected there was no increase in the spontaneous production of either IL-4 or IL-10 in either disease group with patients undergoing HD treatment. |
| 1214 | 10400828 | However, there was a clear correlation with the frequency of T cells producing IL-4 (r = 0.755, P < 0.05) and IL-10 (r = 0.725, P < 0.05) and time on dialysis in the PD patients with DN, but not those with GN. |
| 1215 | 10404814 | Whereas no relation of PBMC reactivity with insulin autoantibodies was found, there was a positive correlation with the presence of at least one of the four autoantibodies tested and with IA-2 antibody. |
| 1216 | 10404814 | Furthermore, interleukin-4 (IL-4) production was lower in type 1 diabetic patients who proliferated to insulin than in those who did not (23+/-15 vs. 64+/-47 pg/mL; P = 0.04), but interferon-gamma, IL-2, and IL-10 productions were similar. |
| 1217 | 10415614 | Treatment of Balb/c male mice for two weeks resulted in the increase of IL-4, and the decrease of TNF-alpha, IFN-gamma, and IL-2 release from stimulated splenocytes, suggesting that UK-114 modulates the Th1/Th2 cytokine profile toward Th2. |
| 1218 | 10449443 | In this report, we demonstrate aberrant constitutive expression of the normally inducible cyclooxygenase PG synthase 2 (PGS(2)/ COX-2) in nonactivated monocytes of humans with insulin-dependent diabetes mellitus (IDDM) and those with islet autoantibodies at increased risk of developing this disease. |
| 1219 | 10449443 | Constitutive PGS(2) appears to characterize a high risk for diabetes as it correlates with and predicts a low first-phase insulin response in autoantibody-positive subjects. |
| 1220 | 10449443 | Abnormal PGS(2) expression in at-risk subjects affected immune response in vitro, as the presence of a specific PGS(2) inhibitor, NS398, significantly increased IL-2 receptor alpha-chain (CD25) expression on phytohemagglutinin-stimulated T cells. |
| 1221 | 10449443 | The effect of PGS(2) on CD25 expression was most profound in subjects expressing both DR04 and DQbeta0302 high-risk alleles, suggesting that this cyclooxygenase interacts with diabetes-associated MHC class II antigens to limit T-cell activation. |
| 1222 | 10449443 | These results indicate that constitutive PGS(2) expression in monocytes defines an antigen-presenting cell defect affecting immune response, and that this expression is a novel cell-associated risk marker for IDDM. |
| 1223 | 10464178 | Furthermore, NOD mice which spontaneously develop diabetes are susceptible to EAE induction with myelin oligodendrocyte glycoprotein (MOG) 35-55, whereas a MHC congenic strain, III, which also expresses I-A(g7) MHC haplotype does not develop diabetes and is also resistant to EAE induction. |
| 1224 | 10464178 | In the susceptible strains (SJL and NOD) in vitro, there are high levels of IFN-gamma production, whereas the resistant strains (B10.S or III) secreted primarily IL-4/IL-10 and transforming growth factor (TGF)-beta, and had decreased levels of IFN-gamma. |
| 1225 | 10464178 | When brains from susceptible and resistant mice were examined by immunohistochemical methods for cytokine expression, the brains from resistant mice showed fewer infiltrates which predominantly expressed IL-4 and IL-10 and/or TGF-beta. |
| 1226 | 10464178 | Brains from NOD and SJL with EAE showed mainly IL-2 and IFN-gamma positive cells. |
| 1227 | 10473808 | A total of 72 patients, who were treated with a regimen consisting of IL-2 (18 MIU m(-2) day(-1) by continuous infusion), interferon alpha (IFNalpha; 5 MIU m(-2) day(-1), intramuscularly) and lymphokine-activated killer (LAK) lymphocytes, were analysed. |
| 1228 | 10479531 | Messenger RNA expression of several inflammatory cytokines, including interleukin-1beta (IL-1beta), IL-2, IL-10, interferon-gamma, and tumor necrosis factor-alpha was detected in the submandibular glands of both NOD and BALB/c mice by the reverse transcription polymerase chain reaction. |
| 1229 | 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. |
| 1230 | 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. |
| 1231 | 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. |
| 1232 | 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. |
| 1233 | 10512062 | A review of interleukin-2 receptor antagonists in solid organ transplantation. |
| 1234 | 10586096 | Most (78-91%) patient and sib responses to glutamate decarboxylase of 65 kDa (GAD65), islet cell cytoplasmic autoantibody (ICA) 69, diabetes-associated T cell epitopes in ICA69 (Tep69), and heat shock protein (Hsp) 60 involved anergic T cells that required exogenous IL-2 to proliferate. |
| 1235 | 10586096 | Responses to proinsulin, IA-2 (and tetanus toxoid) required no IL-2 and generated sufficient cytokine to rescue anergic T cell responses. |
| 1236 | 10586096 | Most (78-91%) patient and sib responses to glutamate decarboxylase of 65 kDa (GAD65), islet cell cytoplasmic autoantibody (ICA) 69, diabetes-associated T cell epitopes in ICA69 (Tep69), and heat shock protein (Hsp) 60 involved anergic T cells that required exogenous IL-2 to proliferate. |
| 1237 | 10586096 | Responses to proinsulin, IA-2 (and tetanus toxoid) required no IL-2 and generated sufficient cytokine to rescue anergic T cell responses. |
| 1238 | 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. |
| 1239 | 10605017 | Consistently, the inhibition of diabetes transfer was not mediated by IL-4 and IL-10. |
| 1240 | 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. |
| 1241 | 10684857 | CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. |
| 1242 | 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. |
| 1243 | 10684857 | To investigate potential mechanisms of CD40L-induced allograft acceptance, we coimmobilized hu5C8 with suboptimal amounts of anti-CD3 to stimulate CD4(+) T cells. |
| 1244 | 10684857 | We now report that anti-CD3/CD40L costimulation results in CD28-independent activation and subsequent deletion of resting T cells. |
| 1245 | 10684857 | Coligation of CD3 and CD40L increased expression of CD69, CD25, and CD54 on CD4(+) T cells. |
| 1246 | 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. |
| 1247 | 10684857 | Consistent with that observation, anti-CD3/CD40L did not enhance the antiapoptotic proteins Bcl-2 and Bcl-xL. |
| 1248 | 10684857 | Further, the addition of CD28 at 24 h failed to rescue those cells induced to die after costimulation with anti-CD3/CD40L. |
| 1249 | 10707936 | Neither the pancreata of normal BALB/c mice nor NOD mice at 2-16 weeks of age contained tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), IL-4, or IL-12. |
| 1250 | 10707936 | At 8 weeks of age, a few IL-2+ cells were found in the pancreas of one of three NOD mice. |
| 1251 | 10707937 | Sections from the pancreata of these injected mice were stained for cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], CD1d, interleukin 2 [IL-2], IL-4, IL-6, IL-10, and IL-12). |
| 1252 | 10707937 | The expression of IL-2 and IL-12 was very scarce. |
| 1253 | 10707937 | Sections from the pancreata of these injected mice were stained for cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], CD1d, interleukin 2 [IL-2], IL-4, IL-6, IL-10, and IL-12). |
| 1254 | 10707937 | The expression of IL-2 and IL-12 was very scarce. |
| 1255 | 10741564 | An islet-specific CD8+ T cell hybridoma generated from non-obese diabetic mice recognizes insulin as an autoantigen. |
| 1256 | 10741564 | Although CD8+ T cells play a major role in beta cell destruction in insulin-dependent diabetes in the non-obese diabetic mouse, the T cell autoantigen(s) recognized by such cells remains to be identified. |
| 1257 | 10741564 | In the presence of islets, none of the 12 CD3+ CD8+ T cell hybridomas isolated secreted IL-2/IL-4 or IFNgamma but three were islet specific, as shown by activation induced cell death. |
| 1258 | 10769431 | At a cellular and molecular level, the hormone preferentially targets helper T cell activity (Th1) by inhibiting the secretion of both IL-2 and IFN-gamma by Th1 and by suppressing the secretion pro-Th1 cytokine IL-12 by antigen-presenting cells. |
| 1259 | 10773364 | The popliteal lymph node response to streptozotocin is under type 1, MHC class-I restricted, CD8(+) T-cell control. |
| 1260 | 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. |
| 1261 | 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). |
| 1262 | 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. |
| 1263 | 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. |
| 1264 | 10773364 | No effects on IL-4, IL-5 and IL-10 mRNAs synthesis were noted. |
| 1265 | 10773364 | In CD8(+) T-cell deficient mice, there was no production of IFN-gamma or IL-6 mRNAs. |
| 1266 | 10773364 | These results suggest that PLN responses to STZ are under the control of type 1, MHC class-I-restricted, CD8(+) T-cells. |
| 1267 | 10773364 | The popliteal lymph node response to streptozotocin is under type 1, MHC class-I restricted, CD8(+) T-cell control. |
| 1268 | 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. |
| 1269 | 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). |
| 1270 | 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. |
| 1271 | 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. |
| 1272 | 10773364 | No effects on IL-4, IL-5 and IL-10 mRNAs synthesis were noted. |
| 1273 | 10773364 | In CD8(+) T-cell deficient mice, there was no production of IFN-gamma or IL-6 mRNAs. |
| 1274 | 10773364 | These results suggest that PLN responses to STZ are under the control of type 1, MHC class-I-restricted, CD8(+) T-cells. |
| 1275 | 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. |
| 1276 | 10857762 | The insulin-dependent diabetes (Idd) gene, Idd3, has been localised to a 0.35 cM region of chromosome 3 containing the structural gene for the cytokine interleukin 2 (IL-2). |
| 1277 | 10893848 | To determine whether fasting glucose/insulin (FG/I) ratio and insulin levels 2 h after 75-g oral load of glucose (IL-2 h PG) are predictors for type 2 diabetes mellitus, a comparative 2 year follow-up study was conducted. |
| 1278 | 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. |
| 1279 | 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. |
| 1280 | 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). |
| 1281 | 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. |
| 1282 | 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. |
| 1283 | 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. |
| 1284 | 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). |
| 1285 | 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. |
| 1286 | 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. |
| 1287 | 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. |
| 1288 | 11090238 | On day 14 after SZ, fusidin markedly altered the circulating cytokine profile induced in vivo by ConA, reducing the levels of IFN-gamma, IL-2 and TNF-alpha and augmenting the level of IL-6. |
| 1289 | 11090238 | In fact, the disease was prevented by a neutralizing monoclonal antibody (mAb) against IFN-gamma, but not by anti-IL-2 receptor mAb, a soluble form of TNF-receptor type 1 or recombinant human IL-6. |
| 1290 | 11090238 | On day 14 after SZ, fusidin markedly altered the circulating cytokine profile induced in vivo by ConA, reducing the levels of IFN-gamma, IL-2 and TNF-alpha and augmenting the level of IL-6. |
| 1291 | 11090238 | In fact, the disease was prevented by a neutralizing monoclonal antibody (mAb) against IFN-gamma, but not by anti-IL-2 receptor mAb, a soluble form of TNF-receptor type 1 or recombinant human IL-6. |
| 1292 | 11106928 | In addition, the T cell activation markers HLA-DR, IL-2 receptor and transferrin receptor) were not upregulated. |
| 1293 | 11106928 | Anti-glutamate decarboxylase (GAD65) and anti-IA-2 antibodies remained persistently high. |
| 1294 | 11131295 | Autoimmunity is unregulated hyperimmunity to organ-specific proteins, inducing rapid turnover of antigen-specific T cells of the acquired immune system with ultimate exhaustion and loss of acquired immunity IL-2 and IFN-gamma production and proliferative decline, conforming to the limited capacity of clonal division (Hayflick phenonmenon). |
| 1295 | 11133172 | N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. |
| 1296 | 11133172 | Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1beta, IL-6 and IL-18. |
| 1297 | 11170619 | TPS treatment was beneficial not only for the subsequent production of interleukin (IL) 2 in spleen cells of adjuvant arthritis (AA) rats but also because it prohibited the body from producing too much IL-1 in AA rats. |
| 1298 | 11222507 | CD28 co-stimulation restores T cell responsiveness in NOD mice by overcoming deficiencies in Rac-1/p38 mitogen-activated protein kinase signaling and IL-2 and IL-4 gene transcription. |
| 1299 | 11222507 | Neonatal CD28 co-stimulation reverses T cell hyporesponsiveness and protects NOD mice from diabetes by an IL-4-mediated mechanism, indicating that a deficiency in TCR signaling may be overcome by CD28/B7-2 co-stimulation in NOD T cells. |
| 1300 | 11222507 | To investigate which co-stimulation-induced signaling events mediate this protection, we analyzed the activity of Ras, Rac-1, mitogen-activated protein kinases (MAPK) and several transcription factors in TCR-activated NOD T cells in the presence or absence of CD28 co-stimulation. |
| 1301 | 11222507 | We show that CD28 co-stimulation restores normal TCR-induced activation of Rac-1 and p38 MAPK in NOD T cells. |
| 1302 | 11222507 | Deficiencies in TCR-induced nuclear expression of activating protein (AP)-1 binding proteins as well as activation of AP-1 and NF-AT in the IL-2 and IL-4 P1 promoters are also corrected by CD28 co-stimulation. |
| 1303 | 11222507 | Thus, CD28 co-stimulation reverses NOD T cell hyporesponsiveness by restoring TCR signaling leading to the activation of AP-1 and NF-AT during IL-2 and IL-4 gene transcription. |
| 1304 | 11222507 | CD28 co-stimulation restores T cell responsiveness in NOD mice by overcoming deficiencies in Rac-1/p38 mitogen-activated protein kinase signaling and IL-2 and IL-4 gene transcription. |
| 1305 | 11222507 | Neonatal CD28 co-stimulation reverses T cell hyporesponsiveness and protects NOD mice from diabetes by an IL-4-mediated mechanism, indicating that a deficiency in TCR signaling may be overcome by CD28/B7-2 co-stimulation in NOD T cells. |
| 1306 | 11222507 | To investigate which co-stimulation-induced signaling events mediate this protection, we analyzed the activity of Ras, Rac-1, mitogen-activated protein kinases (MAPK) and several transcription factors in TCR-activated NOD T cells in the presence or absence of CD28 co-stimulation. |
| 1307 | 11222507 | We show that CD28 co-stimulation restores normal TCR-induced activation of Rac-1 and p38 MAPK in NOD T cells. |
| 1308 | 11222507 | Deficiencies in TCR-induced nuclear expression of activating protein (AP)-1 binding proteins as well as activation of AP-1 and NF-AT in the IL-2 and IL-4 P1 promoters are also corrected by CD28 co-stimulation. |
| 1309 | 11222507 | Thus, CD28 co-stimulation reverses NOD T cell hyporesponsiveness by restoring TCR signaling leading to the activation of AP-1 and NF-AT during IL-2 and IL-4 gene transcription. |
| 1310 | 11222507 | CD28 co-stimulation restores T cell responsiveness in NOD mice by overcoming deficiencies in Rac-1/p38 mitogen-activated protein kinase signaling and IL-2 and IL-4 gene transcription. |
| 1311 | 11222507 | Neonatal CD28 co-stimulation reverses T cell hyporesponsiveness and protects NOD mice from diabetes by an IL-4-mediated mechanism, indicating that a deficiency in TCR signaling may be overcome by CD28/B7-2 co-stimulation in NOD T cells. |
| 1312 | 11222507 | To investigate which co-stimulation-induced signaling events mediate this protection, we analyzed the activity of Ras, Rac-1, mitogen-activated protein kinases (MAPK) and several transcription factors in TCR-activated NOD T cells in the presence or absence of CD28 co-stimulation. |
| 1313 | 11222507 | We show that CD28 co-stimulation restores normal TCR-induced activation of Rac-1 and p38 MAPK in NOD T cells. |
| 1314 | 11222507 | Deficiencies in TCR-induced nuclear expression of activating protein (AP)-1 binding proteins as well as activation of AP-1 and NF-AT in the IL-2 and IL-4 P1 promoters are also corrected by CD28 co-stimulation. |
| 1315 | 11222507 | Thus, CD28 co-stimulation reverses NOD T cell hyporesponsiveness by restoring TCR signaling leading to the activation of AP-1 and NF-AT during IL-2 and IL-4 gene transcription. |
| 1316 | 11238667 | Chronic inflammatory autoimmune diseases such as diabetes, experimental autoimmune encephalomyelitis, and collagen-induced arthritis (CIA) are associated with type 1 (Th1, Tc1) T cell-dependent responses against autoantigens. |
| 1317 | 11238667 | In response to IL-2 binding, this chimeric receptor transduces IL-4-specific signals and dramatically enhances type 2 responses. |
| 1318 | 11238667 | The aggravated disease in transgenic mice was associated with an increase in type 2 cytokines (IL-4, IL-5, IL-10) and an increase in collagen-specific IgG1 levels. |
| 1319 | 11269889 | In this study, we focused on the cytotoxic activity of peripheral lymphocytes in patients with type 1 DM against the peptides of glutamic acid decarboxylase (GAD) and insulin, which can bind MHC class 1 A24. |
| 1320 | 11269889 | The effector cells were cultured with peptides, IL-2 and IL-7, restimulated weekly by autologous antigen presenting cells, which were cultured with IL-4 and GM-CSF. |
| 1321 | 11269889 | The results showed that cytotoxicity against insulin peptide binding to MHC class I A24 was observed in lymphocytes of four out of ten patients with type 1 DM. |
| 1322 | 11269889 | Cytotoxicity against GAD peptide which bind MHC class I A24 was not observed in seven patients. |
| 1323 | 11269889 | None of healthy controls showed cytotoxicity against GAD or insulin peptides was observed. |
| 1324 | 11269889 | This is the first report describing the cytotoxic activity of CD8+ T lymphocytes against insulin in type 1 DM. |
| 1325 | 11369711 | Treatment of (PL/J x SJL)F(1) mice with low-dose oral myelin basic protein (MBP) (0.5 mg) and simultaneous oral IL-10 given 3 times reduced the severity and incidence of experimental autoimmune encephalomyelitis (EAE), whereas administration of oral IL-10 alone or MBP alone given in these doses had no effect. |
| 1326 | 11369711 | Lymphocytes from mice treated orally with MBP and IL-10 proliferated less, and produced decreased amounts of IFN-gamma and IL-2 and increased amounts of IL-10 and transforming growth factor-beta upon in vitro stimulation with MBP. |
| 1327 | 11369711 | Nasal administration of antigen and IL-10 reduced proliferative responses and IFN-gamma production, increased IL-10 production, and enhanced protection from EAE. |
| 1328 | 11369711 | In addition, oral IL-10 combined with oral myelin oligodendrocyte glycoprotein (MOG) 35-55 reduced relapses in MOG-induced EAE in the NOD mouse, as well as enhanced the protective effect of oral insulin in the NOD model of diabetes. |
| 1329 | 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. |
| 1330 | 11498153 | Induction immunosuppression with interleukin-2 receptor antibodies (basiliximab and daclizumab) in renal transplant recipients. |
| 1331 | 11533853 | This holds true for the tumor necrosis factor(TNF)-system, the interleukin(IL)-2-system, IL-6, and granulocyte colony-stimulating factor (G-CSF). |
| 1332 | 11544341 | IL-15 is a powerful T cell growth factor (TCGF) with particular importance for the maintenance of CD8(+) T cells. |
| 1333 | 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. |
| 1334 | 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. |
| 1335 | 11544341 | The IL-15-related fusion protein was used as monotherapy or in combination with CTLA4/Fc in murine islet allograft models. |
| 1336 | 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. |
| 1337 | 11544341 | The analysis revealed that the IL-15 mutant/Fc treatment confers partial protection from both CD4(+) and CD8(+) T cell graft infiltration. |
| 1338 | 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. |
| 1339 | 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. |
| 1340 | 11592833 | Combined administration of plasmids encoding IL-4 and IL-10 prevents the development of autoimmune diabetes in nonobese diabetic mice. |
| 1341 | 11592833 | Studies of animals with spontaneous autoimmune diabetes have revealed that autoreactive T cells that mediate islet beta-cell destruction belong to the Th1 subset (producing IL-2 and IFN-gamma), whereas regulatory T cells are Th2 type (producing IL-4 and IL-10). |
| 1342 | 11592833 | Here, we evaluate the effect of combined delivery of plasmid DNA encoding IL-4 and IL-10 using a degradable, cationic polymeric carrier, poly[gamma-(4-aminobutyl)-L-glycolic acid] (PAGA), in nonobese diabetic (NOD) mice. |
| 1343 | 11592833 | In the liver of NOD mice, we detected mouse Il4 and Il10 mRNA 5 days after intravenous injection of both PAGA-Il4 and PAGA-Il10 plasmid complexes. |
| 1344 | 11592833 | Thus, combined administration of mouse Il4 and Il10 plasmids prevents the development of autoimmune diabetes in NOD mice. |
| 1345 | 11602650 | Although PDG does not block interleukin (IL)-2 production, it efficiently inhibits interleukin-2 receptor alpha-chain (IL-2Ralpha) expression, and this results in a disruption of the IL-2/IL-2R signaling pathway, on which a great part of the regulation of T cell activation depends. |
| 1346 | 11602650 | PDG blocks T cell differentiation into effector helper T cells secreting interferon-gamma and IL-4 as well as into effector cytotoxic T lymphocytes expressing perforin, which is at least in part resulting from inhibition of the IL-2/IL-2R signaling. |
| 1347 | 11602650 | In conclusion, our results demonstrate that PDG has a unique mode of action, namely, that it blocks T cell activation by inhibiting primarily IL-2Ralpha expression in the IL-2/IL-2R signaling, and show that this compound represents a promising immunosuppressant candidate for the treatment of autoimmune diseases. |
| 1348 | 11602650 | Although PDG does not block interleukin (IL)-2 production, it efficiently inhibits interleukin-2 receptor alpha-chain (IL-2Ralpha) expression, and this results in a disruption of the IL-2/IL-2R signaling pathway, on which a great part of the regulation of T cell activation depends. |
| 1349 | 11602650 | PDG blocks T cell differentiation into effector helper T cells secreting interferon-gamma and IL-4 as well as into effector cytotoxic T lymphocytes expressing perforin, which is at least in part resulting from inhibition of the IL-2/IL-2R signaling. |
| 1350 | 11602650 | In conclusion, our results demonstrate that PDG has a unique mode of action, namely, that it blocks T cell activation by inhibiting primarily IL-2Ralpha expression in the IL-2/IL-2R signaling, and show that this compound represents a promising immunosuppressant candidate for the treatment of autoimmune diseases. |
| 1351 | 11602650 | Although PDG does not block interleukin (IL)-2 production, it efficiently inhibits interleukin-2 receptor alpha-chain (IL-2Ralpha) expression, and this results in a disruption of the IL-2/IL-2R signaling pathway, on which a great part of the regulation of T cell activation depends. |
| 1352 | 11602650 | PDG blocks T cell differentiation into effector helper T cells secreting interferon-gamma and IL-4 as well as into effector cytotoxic T lymphocytes expressing perforin, which is at least in part resulting from inhibition of the IL-2/IL-2R signaling. |
| 1353 | 11602650 | In conclusion, our results demonstrate that PDG has a unique mode of action, namely, that it blocks T cell activation by inhibiting primarily IL-2Ralpha expression in the IL-2/IL-2R signaling, and show that this compound represents a promising immunosuppressant candidate for the treatment of autoimmune diseases. |
| 1354 | 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. |
| 1355 | 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. |
| 1356 | 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. |
| 1357 | 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. |
| 1358 | 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. |
| 1359 | 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. |
| 1360 | 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. |
| 1361 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1362 | 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. |
| 1363 | 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. |
| 1364 | 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. |
| 1365 | 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. |
| 1366 | 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. |
| 1367 | 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. |
| 1368 | 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. |
| 1369 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1370 | 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. |
| 1371 | 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. |
| 1372 | 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. |
| 1373 | 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. |
| 1374 | 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. |
| 1375 | 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. |
| 1376 | 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. |
| 1377 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1378 | 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. |
| 1379 | 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. |
| 1380 | 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. |
| 1381 | 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. |
| 1382 | 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. |
| 1383 | 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. |
| 1384 | 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. |
| 1385 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1386 | 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. |
| 1387 | 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. |
| 1388 | 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. |
| 1389 | 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. |
| 1390 | 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. |
| 1391 | 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. |
| 1392 | 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. |
| 1393 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1394 | 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. |
| 1395 | 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. |
| 1396 | 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. |
| 1397 | 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. |
| 1398 | 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. |
| 1399 | 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. |
| 1400 | 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. |
| 1401 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1402 | 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. |
| 1403 | 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. |
| 1404 | 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. |
| 1405 | 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. |
| 1406 | 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. |
| 1407 | 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. |
| 1408 | 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. |
| 1409 | 11729828 | The present study suggests the involvement of IL-2 in the pathogenesis of IDDM. |
| 1410 | 11755473 | Although the cytokine TGF-beta is secreted from regulatory T-cells (Th3), and is related to oral tolerance, the interleukin-2 (IL-2, Th1)/IL-4 (Th2) ratio in the patient group was significantly elevated (P<0.001), which might indicate that the oral tolerance is impaired in patients. |
| 1411 | 11756326 | Previous studies using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) have demonstrated that islet xenograft rejection in mice is dominated by Th2-associated cytokines, i.e., interleukin (IL)-4 and IL-10. |
| 1412 | 11756326 | By day 1, mRNA expression levels of IL-1 beta, IL-2, IL-12p40, interferon-gamma, and tumor necrosis factor-alpha were already induced in the lymph nodes. |
| 1413 | 11826762 | It shares many of these functions with other cytokines such as IL-15, which complicates the interpretation of the IL-2-deficient phenotype. |
| 1414 | 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. |
| 1415 | 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. |
| 1416 | 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. |
| 1417 | 11826762 | It shares many of these functions with other cytokines such as IL-15, which complicates the interpretation of the IL-2-deficient phenotype. |
| 1418 | 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. |
| 1419 | 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. |
| 1420 | 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. |
| 1421 | 11826762 | It shares many of these functions with other cytokines such as IL-15, which complicates the interpretation of the IL-2-deficient phenotype. |
| 1422 | 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. |
| 1423 | 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. |
| 1424 | 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. |
| 1425 | 11872661 | In addition, Th1-type cells (gamma-interferon-positive and IL-2(+)) were decreased the most, and Th2-type cells (IL-4(+) and IL-10(+)) and Th3-type cells (transforming growth factor-beta1(+)) were increased the most in islet grafts of sirolimus and IL-2-treated mice. |
| 1426 | 11985511 | Cytokine mRNA analysis of the grafts 6 days after transplantation revealed a significant decrease in IL-2, IFN-gamma and IL-12 messages in both IFN-beta plus TX 527- and CsA plus TX 527-treated mice, while only in the IFN-beta with TX 527 group were higher levels of IL-10 transcripts observed. |
| 1427 | 12021108 | Cytokine secretion (TNF-alpha, IFN-gamma, IL-2, IL-4, IL-5, and IL-10) was measured in the supernatants of the cultures stimulated with 21 overlapping preproinsulin peptides as well as proinsulin and insulin. |
| 1428 | 12021108 | In Ab+ individuals our results reveal higher IL-4 levels in CD45RO+ memory cells and higher IL-5 levels in CD45RA+ naive/resting cells, while higher IL-2 production was found in PBMCs. |
| 1429 | 12021108 | In contrast, in PBMCs of T1D patients higher IFN-gamma and IL-10 secretion was found. |
| 1430 | 12021108 | Cytokine secretion (TNF-alpha, IFN-gamma, IL-2, IL-4, IL-5, and IL-10) was measured in the supernatants of the cultures stimulated with 21 overlapping preproinsulin peptides as well as proinsulin and insulin. |
| 1431 | 12021108 | In Ab+ individuals our results reveal higher IL-4 levels in CD45RO+ memory cells and higher IL-5 levels in CD45RA+ naive/resting cells, while higher IL-2 production was found in PBMCs. |
| 1432 | 12021108 | In contrast, in PBMCs of T1D patients higher IFN-gamma and IL-10 secretion was found. |
| 1433 | 12047753 | In this study a series of fusions was constructed between the genes encoding CTB and the B-chain of human insulin (InsB). |
| 1434 | 12047753 | In vitro assays showed that the CI fusion protein was 300-fold more potent than native insulin at inducing interleukin-2 (IL-2) production by an insulin-specific T-cell hybridoma. |
| 1435 | 12118901 | To address that question, we studied the inheritance patterns for polymorphisms in several cytokine genes (IL-2, IL-6, IL-10, TNF-alpha, TGF-beta, and IFN-gamma) within an ethnically diverse study population comprised of 216 Whites, 58 Blacks, 25 Hispanics, and 31 Asians. |
| 1436 | 12118901 | Blacks, Hispanics and Asians demonstrated marked differences in the inheritance of IL-6 alleles and IL-10 genotypes that result in high expression when compared with Whites. |
| 1437 | 12142560 | Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. |
| 1438 | 12142560 | A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. |
| 1439 | 12142560 | Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. |
| 1440 | 12142560 | Acetylcholine receptor antibody levels were normal before starting IL-2. |
| 1441 | 12142560 | After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. |
| 1442 | 12142560 | These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. |
| 1443 | 12142560 | Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. |
| 1444 | 12142560 | A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. |
| 1445 | 12142560 | Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. |
| 1446 | 12142560 | Acetylcholine receptor antibody levels were normal before starting IL-2. |
| 1447 | 12142560 | After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. |
| 1448 | 12142560 | These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. |
| 1449 | 12142560 | Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. |
| 1450 | 12142560 | A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. |
| 1451 | 12142560 | Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. |
| 1452 | 12142560 | Acetylcholine receptor antibody levels were normal before starting IL-2. |
| 1453 | 12142560 | After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. |
| 1454 | 12142560 | These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. |
| 1455 | 12142560 | Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. |
| 1456 | 12142560 | A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. |
| 1457 | 12142560 | Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. |
| 1458 | 12142560 | Acetylcholine receptor antibody levels were normal before starting IL-2. |
| 1459 | 12142560 | After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. |
| 1460 | 12142560 | These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. |
| 1461 | 12142560 | Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. |
| 1462 | 12142560 | A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. |
| 1463 | 12142560 | Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. |
| 1464 | 12142560 | Acetylcholine receptor antibody levels were normal before starting IL-2. |
| 1465 | 12142560 | After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. |
| 1466 | 12142560 | These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. |
| 1467 | 12142560 | Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. |
| 1468 | 12142560 | A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. |
| 1469 | 12142560 | Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. |
| 1470 | 12142560 | Acetylcholine receptor antibody levels were normal before starting IL-2. |
| 1471 | 12142560 | After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. |
| 1472 | 12142560 | These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. |
| 1473 | 12153522 | Interleukin-2 (IL-2) basally and IL-2 and interferon-gamma (IFN-gamma) in response to GAD, were detected more frequently and at higher levels in diabetic compared to non-diabetic twins. |
| 1474 | 12153522 | OAS activity was increased in diabetic compared to non-diabetic twins and showed a correlation with basal IL-2 and GAD-stimulated IFN-gamma and IL-10. |
| 1475 | 12153522 | Interleukin-2 (IL-2) basally and IL-2 and interferon-gamma (IFN-gamma) in response to GAD, were detected more frequently and at higher levels in diabetic compared to non-diabetic twins. |
| 1476 | 12153522 | OAS activity was increased in diabetic compared to non-diabetic twins and showed a correlation with basal IL-2 and GAD-stimulated IFN-gamma and IL-10. |
| 1477 | 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. |
| 1478 | 12186840 | CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. |
| 1479 | 12186840 | These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. |
| 1480 | 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. |
| 1481 | 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. |
| 1482 | 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. |
| 1483 | 12202150 | Baseline and PHA-stimulated IL-2 production were also similar among control and CTLA-4 clones expressing both alleles. |
| 1484 | 12202150 | After anti-CTLA-4 engagement, IL-2 production was markedly inhibited in a dose- and time-dependent manner but this also appeared to be similar in the A and G allele expressing cells (95.7+/-1.2% inhibition and 94.9+/-1.1% inhibition, respectively). |
| 1485 | 12202150 | Baseline and PHA-stimulated IL-2 production were also similar among control and CTLA-4 clones expressing both alleles. |
| 1486 | 12202150 | After anti-CTLA-4 engagement, IL-2 production was markedly inhibited in a dose- and time-dependent manner but this also appeared to be similar in the A and G allele expressing cells (95.7+/-1.2% inhibition and 94.9+/-1.1% inhibition, respectively). |
| 1487 | 12218168 | In addition, proliferation and ex vivo IFN-gamma production of HCV-tetramer+ cells, but not influenza-virus-specific T cells, were defective in chronically infected patients and could not be restored by in vitro stimulation with peptide and IL-2. |
| 1488 | 12235920 | Serum interleukin 2 levels in patients with rheumatoid arthritis and correlation with insulin sensitivity. |
| 1489 | 12235920 | Interleukin 2 (IL-2), a Th1 lymphocyte-derived cytokine, is thought to play an important role in the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). |
| 1490 | 12235920 | The aim of our study was to evaluate changes in serum IL-2 levels and their correlation with glucose metabolism abnormalities, such as insulin resistance, in patients with RA. |
| 1491 | 12235920 | After a 12-h overnight fast, fasting insulin levels, homeostatic model assessment-insulin resistance (HOMA-IR) estimated insulin sensitivity, and serum IL-2 levels were significantly higher in all patients with RA than in the control individuals. |
| 1492 | 12235920 | Fasting insulin, HOMA-IR scores and IL-2 levels were correlated in the RA group. |
| 1493 | 12235920 | This study showed that patients with RA have altered IL-2 regulation, and that there was a significant correlation between serum IL-2 levels and insulin sensitivity. |
| 1494 | 12235920 | Serum interleukin 2 levels in patients with rheumatoid arthritis and correlation with insulin sensitivity. |
| 1495 | 12235920 | Interleukin 2 (IL-2), a Th1 lymphocyte-derived cytokine, is thought to play an important role in the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). |
| 1496 | 12235920 | The aim of our study was to evaluate changes in serum IL-2 levels and their correlation with glucose metabolism abnormalities, such as insulin resistance, in patients with RA. |
| 1497 | 12235920 | After a 12-h overnight fast, fasting insulin levels, homeostatic model assessment-insulin resistance (HOMA-IR) estimated insulin sensitivity, and serum IL-2 levels were significantly higher in all patients with RA than in the control individuals. |
| 1498 | 12235920 | Fasting insulin, HOMA-IR scores and IL-2 levels were correlated in the RA group. |
| 1499 | 12235920 | This study showed that patients with RA have altered IL-2 regulation, and that there was a significant correlation between serum IL-2 levels and insulin sensitivity. |
| 1500 | 12235920 | Serum interleukin 2 levels in patients with rheumatoid arthritis and correlation with insulin sensitivity. |
| 1501 | 12235920 | Interleukin 2 (IL-2), a Th1 lymphocyte-derived cytokine, is thought to play an important role in the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). |
| 1502 | 12235920 | The aim of our study was to evaluate changes in serum IL-2 levels and their correlation with glucose metabolism abnormalities, such as insulin resistance, in patients with RA. |
| 1503 | 12235920 | After a 12-h overnight fast, fasting insulin levels, homeostatic model assessment-insulin resistance (HOMA-IR) estimated insulin sensitivity, and serum IL-2 levels were significantly higher in all patients with RA than in the control individuals. |
| 1504 | 12235920 | Fasting insulin, HOMA-IR scores and IL-2 levels were correlated in the RA group. |
| 1505 | 12235920 | This study showed that patients with RA have altered IL-2 regulation, and that there was a significant correlation between serum IL-2 levels and insulin sensitivity. |
| 1506 | 12235920 | Serum interleukin 2 levels in patients with rheumatoid arthritis and correlation with insulin sensitivity. |
| 1507 | 12235920 | Interleukin 2 (IL-2), a Th1 lymphocyte-derived cytokine, is thought to play an important role in the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). |
| 1508 | 12235920 | The aim of our study was to evaluate changes in serum IL-2 levels and their correlation with glucose metabolism abnormalities, such as insulin resistance, in patients with RA. |
| 1509 | 12235920 | After a 12-h overnight fast, fasting insulin levels, homeostatic model assessment-insulin resistance (HOMA-IR) estimated insulin sensitivity, and serum IL-2 levels were significantly higher in all patients with RA than in the control individuals. |
| 1510 | 12235920 | Fasting insulin, HOMA-IR scores and IL-2 levels were correlated in the RA group. |
| 1511 | 12235920 | This study showed that patients with RA have altered IL-2 regulation, and that there was a significant correlation between serum IL-2 levels and insulin sensitivity. |
| 1512 | 12235920 | Serum interleukin 2 levels in patients with rheumatoid arthritis and correlation with insulin sensitivity. |
| 1513 | 12235920 | Interleukin 2 (IL-2), a Th1 lymphocyte-derived cytokine, is thought to play an important role in the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). |
| 1514 | 12235920 | The aim of our study was to evaluate changes in serum IL-2 levels and their correlation with glucose metabolism abnormalities, such as insulin resistance, in patients with RA. |
| 1515 | 12235920 | After a 12-h overnight fast, fasting insulin levels, homeostatic model assessment-insulin resistance (HOMA-IR) estimated insulin sensitivity, and serum IL-2 levels were significantly higher in all patients with RA than in the control individuals. |
| 1516 | 12235920 | Fasting insulin, HOMA-IR scores and IL-2 levels were correlated in the RA group. |
| 1517 | 12235920 | This study showed that patients with RA have altered IL-2 regulation, and that there was a significant correlation between serum IL-2 levels and insulin sensitivity. |
| 1518 | 12235920 | Serum interleukin 2 levels in patients with rheumatoid arthritis and correlation with insulin sensitivity. |
| 1519 | 12235920 | Interleukin 2 (IL-2), a Th1 lymphocyte-derived cytokine, is thought to play an important role in the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). |
| 1520 | 12235920 | The aim of our study was to evaluate changes in serum IL-2 levels and their correlation with glucose metabolism abnormalities, such as insulin resistance, in patients with RA. |
| 1521 | 12235920 | After a 12-h overnight fast, fasting insulin levels, homeostatic model assessment-insulin resistance (HOMA-IR) estimated insulin sensitivity, and serum IL-2 levels were significantly higher in all patients with RA than in the control individuals. |
| 1522 | 12235920 | Fasting insulin, HOMA-IR scores and IL-2 levels were correlated in the RA group. |
| 1523 | 12235920 | This study showed that patients with RA have altered IL-2 regulation, and that there was a significant correlation between serum IL-2 levels and insulin sensitivity. |
| 1524 | 12239095 | Effect of proinflammatory cytokines on gene expression of the diabetes-associated autoantigen IA-2 in INS-1 cells. |
| 1525 | 12239095 | Inhibition of insulin expression has been described, but their effects on other major target autoantigens, such as the tyrosine phosphatase-like protein IA-2, is not known. |
| 1526 | 12239095 | In the present study, we established sensitive real-time RT-PCR to measure IA-2, insulin, and inducible nitric oxide (NO) synthase (iNOS) mRNA expression. |
| 1527 | 12239095 | Rat insulinoma INS-1 cells were stimulated with IL-1beta, TNF-alpha, interferon (IFN)-gamma, and IL-2 as well as with two combinations of these cytokines (C1: IL-1beta + TNF-alpha + IFN-gamma; C2: TNF-alpha + IFN-gamma). |
| 1528 | 12239095 | Treatment with IL-1beta, TNF-alpha, or IFN-gamma alone caused a significant down-regulation of IA-2 and insulin mRNA levels in a time and dose-dependent manner, whereas IL-2 had no effect. |
| 1529 | 12239095 | The hypothesis that the formation of NO is involved in IA-2 regulation was confirmed by the finding that the coincubation of C1 with 4 mM L-N(G)-monomethyL-L-arginine, an inhibitor of the iNOS, partly reversed the down-regulation of IA-2. |
| 1530 | 12239095 | In conclusion, we have demonstrated for the first time that IL-1beta, TNF-alpha, and IFN-gamma exert a strong inhibitory effect on expression of the diabetes autoantigen IA-2. |
| 1531 | 12239095 | Effect of proinflammatory cytokines on gene expression of the diabetes-associated autoantigen IA-2 in INS-1 cells. |
| 1532 | 12239095 | Inhibition of insulin expression has been described, but their effects on other major target autoantigens, such as the tyrosine phosphatase-like protein IA-2, is not known. |
| 1533 | 12239095 | In the present study, we established sensitive real-time RT-PCR to measure IA-2, insulin, and inducible nitric oxide (NO) synthase (iNOS) mRNA expression. |
| 1534 | 12239095 | Rat insulinoma INS-1 cells were stimulated with IL-1beta, TNF-alpha, interferon (IFN)-gamma, and IL-2 as well as with two combinations of these cytokines (C1: IL-1beta + TNF-alpha + IFN-gamma; C2: TNF-alpha + IFN-gamma). |
| 1535 | 12239095 | Treatment with IL-1beta, TNF-alpha, or IFN-gamma alone caused a significant down-regulation of IA-2 and insulin mRNA levels in a time and dose-dependent manner, whereas IL-2 had no effect. |
| 1536 | 12239095 | The hypothesis that the formation of NO is involved in IA-2 regulation was confirmed by the finding that the coincubation of C1 with 4 mM L-N(G)-monomethyL-L-arginine, an inhibitor of the iNOS, partly reversed the down-regulation of IA-2. |
| 1537 | 12239095 | In conclusion, we have demonstrated for the first time that IL-1beta, TNF-alpha, and IFN-gamma exert a strong inhibitory effect on expression of the diabetes autoantigen IA-2. |
| 1538 | 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. |
| 1539 | 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. |
| 1540 | 12369724 | Current evidence indicates that islet beta cell-specific autoreactive T cells belong to a T helper 1 (Th1) subset, and these Th1 cells and their characteristic cytokine products, IFNgamma and IL-2, are believed to cause islet inflammation (insulitis) and beta cell destruction. |
| 1541 | 12369724 | Approaches that attempt to correct underlying immunoregulatory defects in autoimmune diabetes include interventions aimed at i) deleting beta cell autoreactive Th1 cells and cytokines (IFNgamma and IL-2) and/or ii) increasing regulatory Th2 cells and/or Th3 cells and their cytokine products (IL-4, IL-10 and TGFbeta1). |
| 1542 | 12369724 | Current evidence indicates that islet beta cell-specific autoreactive T cells belong to a T helper 1 (Th1) subset, and these Th1 cells and their characteristic cytokine products, IFNgamma and IL-2, are believed to cause islet inflammation (insulitis) and beta cell destruction. |
| 1543 | 12369724 | Approaches that attempt to correct underlying immunoregulatory defects in autoimmune diabetes include interventions aimed at i) deleting beta cell autoreactive Th1 cells and cytokines (IFNgamma and IL-2) and/or ii) increasing regulatory Th2 cells and/or Th3 cells and their cytokine products (IL-4, IL-10 and TGFbeta1). |
| 1544 | 12393479 | HDAC-i furthermore inhibited activation-induced CD25 and CD154 expression on CD4 cells, without affecting induction of CD69. |
| 1545 | 12393479 | HDAC-i thus inhibited interleukin 2 (IL-2)-induced CD154 expression on effector T cells and constitutively expressed CD154 on various tumor cells, events that were not affected by cyclosporine. |
| 1546 | 12393479 | Additional studies showed that HDAC-i treatment inhibited c-Myc expression, which was further shown to be important for CD154 gene activation. |
| 1547 | 12419283 | The expressions of the co-stimulatory molecules B7-2 and ICAM-1 were significantly increased in spleen cells of rIFN-gamma treated mice while the expression of MHC class I was decreased. |
| 1548 | 12419283 | In vitro studies demonstrated that NOD mouse mononuclear spleen cells preincubated with rIFN-gamma and subsequently cocultured with responder cells, potently inhibited responder T-cell proliferative responses. rIFN-gamma administration decreased IL-12 and IL-2 mRNA expression in spleen cells while increasing IL-1 expression. |
| 1549 | 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. |
| 1550 | 12486207 | In a phase I open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual beta-cell function in recent onset patients. |
| 1551 | 12486207 | In a second phase I trial, treatment of rheumatoid arthritis with ingested IFN-alpha reduced the secretion of interleukin (IL)-1, a pro-inflammatory cytokine. |
| 1552 | 12486207 | In a third phase I trial in multiple sclerosis, there was a significant decrease in peripheral blood mononuclear cell IL-2 and IFN-gamma production after ingesting IFN-alpha. |
| 1553 | 12486207 | In a phase II randomized, placebo-controlled, double-blind trial in multiple sclerosis, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. |
| 1554 | 12486207 | Tumor necrosis factor-alpha and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. |
| 1555 | 12486207 | Ingested IFN-alpha was not toxic in any of these clinical trials. |
| 1556 | 12486207 | These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity. |
| 1557 | 12517935 | Either IL-2 or IL-12 is sufficient to direct Th1 differentiation by nonobese diabetic T cells. |
| 1558 | 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. |
| 1559 | 12517935 | Instead, IL-2 was necessary and sufficient to direct T cell differentiation to the Th1 lineage by nonobese diabetic CD4(+) T cells. |
| 1560 | 12517935 | Either IL-2 or IL-12 is sufficient to direct Th1 differentiation by nonobese diabetic T cells. |
| 1561 | 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. |
| 1562 | 12517935 | Instead, IL-2 was necessary and sufficient to direct T cell differentiation to the Th1 lineage by nonobese diabetic CD4(+) T cells. |
| 1563 | 12581487 | In a phase I open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual beta cell function in recent onset patients. |
| 1564 | 12581487 | In a second phase I trial, treatment of rheumatoid arthritis (RA) with ingested IFN-alpha reduced the secretion of interleukin-1 (IL-1), a proinflammatory cytokine. |
| 1565 | 12581487 | In a third phase I trial in MS, there was a significant decrease in peripheral blood mononuclear cell (PBMC) IL-2 and IFN-gamma production after ingesting IFN-alpha. |
| 1566 | 12581487 | In a phase II randomized, placebo-controlled, double-blind trial in MS, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. |
| 1567 | 12581487 | Tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. |
| 1568 | 12581487 | Ingested IFN-alpha was not toxic in any of these clinical trials. |
| 1569 | 12581487 | These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity. |
| 1570 | 12653847 | Anti-cytokine autoantibodies in autoimmunity: preponderance of neutralizing autoantibodies against interferon-alpha, interferon-omega and interleukin-12 in patients with thymoma and/or myasthenia gravis. |
| 1571 | 12653847 | We tested for both binding and neutralizing autoantibodies to a range of human cytokines, including interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, interferon-alpha2 (IFN-alpha2), IFN-omega, IFN-beta, IFN-gamma, tumour necrosis factor alpha (TNF-alpha), transforming growth factor beta-1 (TGF-beta1) and granulocyte-macrophage colony stimulating factor (GM-CSF), in plasmas or sera. |
| 1572 | 12653847 | With two notable exceptions described below, we found only occasional, mostly low-titre, non-neutralizing antibodies, mainly to GM-CSF; also to IL-10 in pemphigoid. |
| 1573 | 12653847 | Strikingly, however, high-titre, mainly IgG, autoantibodies to IFN-alpha2, IFN-omega and IL-12 were common at diagnosis in patients with late-onset myasthenia gravis (LOMG+), thymoma (T) but no MG (TMG-) and especially with both thymoma and MG together (TMG+). |
| 1574 | 12653847 | The antibodies recognized other closely related type I IFN-alpha subtypes, but rarely the distantly related type I IFN-beta, and never (detectably) the unrelated type II IFN-gamma. |
| 1575 | 12653847 | Antibodies to IL-12 showed a similar distribution to those against IFN-alpha2, although prevalences were slightly lower; correlations between individual titres against each were so modest that they appear to be entirely different specificities. |
| 1576 | 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. |
| 1577 | 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. |
| 1578 | 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. |
| 1579 | 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. |
| 1580 | 12711326 | The expression of the ligand LFA-1 on CD4(+) and CD8(+) T-cells was comparable to that of placebo- and untreated controls. |
| 1581 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 1582 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 1583 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 1584 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 1585 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 1586 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 1587 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 1588 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 1589 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 1590 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 1591 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 1592 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 1593 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 1594 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 1595 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 1596 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 1597 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 1598 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 1599 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 1600 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 1601 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 1602 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 1603 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 1604 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 1605 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 1606 | 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. |
| 1607 | 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). |
| 1608 | 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. |
| 1609 | 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. |
| 1610 | 12759426 | Surprisingly, IL-12-induced IFN-gamma hinders pancreatic B cell infiltration and inhibits the capacity of APCs to activate T cells. |
| 1611 | 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. |
| 1612 | 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. |
| 1613 | 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. |
| 1614 | 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. |
| 1615 | 12761441 | [Anti interleukin-2 receptor alpha antibodies (daclizumab) application for the treatment of kidney recipients]. |
| 1616 | 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). |
| 1617 | 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. |
| 1618 | 12866664 | Our studies show that patients with diabetic ketoacidosis and hyperglycemia have increased proinflammatory cytokines and activated CD4+ and CD8+ T lymphocytes. |
| 1619 | 12866664 | The mechanisms underlying insulin action, in general, or in the CD4+ and CD8+ T-lymphocytes, in particular, have not been clearly elucidated. |
| 1620 | 12882912 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is expressed in different tissues and cells, including pancreas and lymphocytes, and can induce apoptosis in various tumor cells but not in most normal cells. |
| 1621 | 12882912 | Here we show by cDNA array analyses that TRAIL gene expression is upregulated in pancreatic islets during the development of autoimmune type 1 diabetes in nonobese diabetic (NOD) mice and in Min6 islet beta-cells activated by TNF-alpha + interferon-gamma. |
| 1622 | 12882912 | TRAIL inhibits the proliferation of NOD diabetogenic T-cells by suppressing interleukin (IL)-2 production and cell cycle progression, and this inhibition can be rescued in the presence of exogenous IL-2. cDNA array and Western blot analyses indicate that TRAIL upregulates the expression of the cdk inhibitor p27(kip1). |
| 1623 | 12882913 | T-cells from pancreatic lymph nodes of NF-kappaB ODN DC-treated animals exhibited hyporesponsiveness to islet antigens with low production of interferon-gamma and IL-2. |
| 1624 | 12941768 | In addition, the densities of IL-1 alpha- and IL-4-positive cells detected by immunohistochemistry and IL-4 mRNA-expressing cells evaluated by in situ hybridization were increased in the lamina propria in patients with type 1 diabetes and normal mucosa. |
| 1625 | 12941768 | Instead, the densities of IL-2, gamma-interferon (IFN-gamma), and tumor necrosis factor alpha-positive cells, the density of IFN-gamma mRNA positive cells, and the amounts of IFN-gamma mRNA detected by RT-PCR correlated with the degree of celiac disease in patients with type 1 diabetes. |
| 1626 | 14499240 | Plasma IL-10, IL-1beta, TNF-alpha, IL-6, IL-8 and IL-2 cytokine levels were assayed by ELISA at each of the time points. |
| 1627 | 14499240 | Treatment of DKA resulted in a significant decrease of IL-10 at 6-8 h (p = 0.0062), and further increases in the inflammatory cytokines at 6-8 h and/or 24 h vs 120 h (baseline): IL-1beta (p =.0048); TNF-alpha (p =.0188) and IL-8 (p =.0048). |
| 1628 | 14500627 | Cutting edge: CD28 controls peripheral homeostasis of CD4+CD25+ regulatory T cells. |
| 1629 | 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). |
| 1630 | 14500627 | CD28 engagement promotes survival by regulating IL-2 production by conventional T cells and CD25 expression on Tregs. |
| 1631 | 14500690 | Islet allograft rejection in nonobese diabetic mice involves the common gamma-chain and CD28/CD154-dependent and -independent mechanisms. |
| 1632 | 14500690 | In the present study we tested the hypothesis that islet allograft survival in the diabetic NOD mouse is determined by the interplay of diverse islet-specific T cell subsets whose activation is regulated by CD28/CD154 costimulatory signals and the common gamma-chain (gammac; a shared signaling element by receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21). |
| 1633 | 14500690 | We found that common gammac blockade is remarkably effective in blocking the onset and the ongoing autoimmune diabetes, whereas CD28/CD154 blockade has no effect in suppressing the ongoing diabetes. |
| 1634 | 14500690 | However, CD28/CD154 blockade completely blocks the alloimmune-mediated islet rejection. |
| 1635 | 14500690 | Also, a subset of memory-like T cells in the NOD mice is resistant to CD28/CD154 blockade, but is sensitive to the common gammac blockade. |
| 1636 | 14500690 | Nonetheless, neither common gammac blockade nor CD28/CD154 blockade can prevent islet allograft rejection in diabetic NOD mice. |
| 1637 | 14500690 | Treatment of diabetic NOD recipients with CD28/CD154 blockade plus gammac blockade markedly prolongs islet allograft survival compared with the controls. |
| 1638 | 14500690 | We concluded that the effector mechanisms in diabetic NOD hosts are inherently complex, and rejection in this model involves CD28/CD154/gammac-dependent and -independent mechanisms. |
| 1639 | 14510627 | The anti-interleukin-2 receptor (anti-IL-2R) antibody therapy is an exciting approach to the prevention of acute rejection after renal allograft transplantation whereby immunosuppression is exerted by a selective and competitive inhibition of IL-2-induced T cell proliferation, a critical pathway of allorecognition. |
| 1640 | 14567106 | The pathogenesis is related to metabolic alterations of the adipocytes with cellular insulin resistance and enhanced apoptosis of these cells caused by adipocytic cytokines such as adiponectin, leptin, TNF-alpha and interleukin 2. |
| 1641 | 14571458 | Significant reduction of anti-acetylcholine receptor antibody titers and interleukin 2 production were observed at the end of this study. |
| 1642 | 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. |
| 1643 | 14610290 | In addition, the drug induces a population of CD4+IL-10+ CCR4+ cells in vivo. |
| 1644 | 14679041 | Both TCR transgenics respond to their cognate peptide/MHC (GAD65 206-220 and 286-300) and produce IL-2, IFN-gamma, and small amounts of IL-10. |
| 1645 | 14679041 | Thus, GAD65 specific TCR transgenic T cells (1) must express a second a chain to survive negative selection, (2) produce IL-2 and IFN-gamma, and (3) have a mildly protective effect on transfer of diabetes with diabetogenic spleen cells. |
| 1646 | 14679041 | Both TCR transgenics respond to their cognate peptide/MHC (GAD65 206-220 and 286-300) and produce IL-2, IFN-gamma, and small amounts of IL-10. |
| 1647 | 14679041 | Thus, GAD65 specific TCR transgenic T cells (1) must express a second a chain to survive negative selection, (2) produce IL-2 and IFN-gamma, and (3) have a mildly protective effect on transfer of diabetes with diabetogenic spleen cells. |
| 1648 | 14679059 | IIS-Idd3 congenic mice, which share the same alleles at both Il2 and Il21 as the NOD mouse, were indistinguishable from the NOD parental strain, indicating that both Il2 and Il21 are candidates for Idd3. |
| 1649 | 14681852 | De novo emergence of growth factor receptors in activated human CD4+ and CD8+ T lymphocytes. |
| 1650 | 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. |
| 1651 | 14681852 | These events, which are actinomycin- and cycloheximide-sensitive, occur only in activated, but not nonactivated, CD4(+) and CD8(+) lymphocytes. |
| 1652 | 14688055 | Broadly impaired NK cell function in non-obese diabetic mice is partially restored by NK cell activation in vivo and by IL-12/IL-18 in vitro. |
| 1653 | 14688055 | In addition, killing of some tumor targets was restored in vitro after activation of NK cells with IL-12 plus IL-18 or with IFN-alpha/beta, but not with IL-2. |
| 1654 | 14735147 | Genetic association with type 1 diabetes (T1D) has been established for two chromosomal regions: HLA DQ/DR (IDDM1) and INS VNTR (IDDM2). |
| 1655 | 14735147 | Functional genetic polymorphisms of proinflammatory (T-helper-1: IL-2, IL-12 and IFN-gamma), anti-inflammatory (T-helper-2: IL-4, IL-6 and IL-10) and metabolic (IGF-I, VDR and INS) genes were determined in 206 Dutch simplex families with juvenile onset T1D and the results were analysed using the transmission disequilibrium test. |
| 1656 | 14735147 | Significantly increased transmission to T1D probands was observed for the loci IDDM1, IDDM2 and the vitamin D receptor. |
| 1657 | 14735147 | Although none of the other individual polymorphisms was associated with disease individually, the combination of T-helper-2 and metabolic/growth alleles IL-10(*)R2, IL-4(*)C, VDR(*)C and IGF-I(*)wt was found to be transmitted more frequently than expected (67%, P(c)=0.015). |
| 1658 | 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. |
| 1659 | 14981264 | The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity. |
| 1660 | 14981264 | Channel inhibition improves experimental autoimmune encephalitis, in part by reducing IL-2 and tumor necrosis factor production by peripheral T lymphocytes. |
| 1661 | 14981264 | Interestingly, although Kv1.3-/- mice on the high-calorie diet gain weight, they remain euglycemic, with low blood insulin levels. |
| 1662 | 14981264 | This observation prompted us to examine the effect of Kv1.3 gene inactivation and inhibition on peripheral glucose homeostasis and insulin sensitivity. |
| 1663 | 14981264 | Here we show that Kv1.3 gene deletion and channel inhibition increase peripheral insulin sensitivity in vivo. |
| 1664 | 14981264 | Baseline and insulin-stimulated glucose uptake are increased in adipose tissue and skeletal muscle of Kv1.3-/- mice. |
| 1665 | 14981264 | Inhibition of Kv1.3 activity facilitates the translocation of the glucose transporter, GLUT4, to the plasma membrane. |
| 1666 | 14981264 | It also suppresses c-JUN terminal kinase activity in fat and skeletal muscle and decreases IL-6 and tumor necrosis factor secretion by adipose tissue. |
| 1667 | 14981264 | We conclude that Kv1.3 inhibition improves insulin sensitivity by increasing the amount of GLUT4 at the plasma membrane. |
| 1668 | 15024185 | The expression of cytokine genes in the peritoneal macrophages and splenic CD4- and CD8-positive lymphocytes of the nonobese diabetic mice. |
| 1669 | 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. |
| 1670 | 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. |
| 1671 | 15024185 | The expression of IL-4 and IL-10 decreased in splenic CD4-positive lymphocytes. |
| 1672 | 15024185 | Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred. |
| 1673 | 15037212 | Type 1, or cellular, immune response is characterized by overproduction of TNF-alpha, IFN-gamma, IL-1, IL-2 and IL-8 and is the underlying immune mechanism of psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis (EAU). |
| 1674 | 15037212 | Cetirizine, supposed to inhibit DNA binding activity of NF-kappa B, inhibits the expression of adhesion molecules on immunocytes and endothelial cells and the production of IL-8 and LTB4, two potent chemoattractants, by immune cells. |
| 1675 | 15037212 | Tryptase is a chemoattractant, generates kinins from kininogen, activates mast cells, triggers maturation of dendritic cells and stimulates the release of IL-8 from endothelial cells and the production of Th1 lymphokines by mononuclear immunocytes. |
| 1676 | 15037212 | Allopurinol is a free radical scavenger, suppresses the production of TNF-alpha and downregulates the expression of ICAM-1 and P2X(7) receptors on monocyte/macrophages. |
| 1677 | 15037212 | ICAM-1 serves as a ligand for LFA-1 (on T lymphocytes), allowing proper antigen presentation. |
| 1678 | 15037212 | P2X(7) receptors are thought to be involved in IL-1beta release, mitogenic stimulation of T lymphocytes and the probable cytoplasmic communication between macrophages and lymphocytes at inflammation sites. |
| 1679 | 15041039 | STAT4 mediates IL-12 signaling and regulates T helper 1 (Th1) cell differentiation. |
| 1680 | 15041039 | In Stat4-/- NOD mice, serum levels of both IFN-gamma and IL-2 were significantly reduced as compared to the controls. |
| 1681 | 15096540 | T-bet controls autoaggressive CD8 lymphocyte responses in type 1 diabetes. |
| 1682 | 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. |
| 1683 | 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. |
| 1684 | 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. |
| 1685 | 15096540 | Further analysis showed that T-bet intrinsically controls the generation, but not apoptosis, maintenance, or secondary expansion of antiviral effector/memory CD8 lymphocytes. |
| 1686 | 15115315 | Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. |
| 1687 | 15115315 | Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. |
| 1688 | 15115315 | PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. |
| 1689 | 15115315 | Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. |
| 1690 | 15115315 | Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. |
| 1691 | 15115315 | PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. |
| 1692 | 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. |
| 1693 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 1694 | 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. |
| 1695 | 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. |
| 1696 | 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. |
| 1697 | 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. |
| 1698 | 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. |
| 1699 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 1700 | 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. |
| 1701 | 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. |
| 1702 | 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. |
| 1703 | 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. |
| 1704 | 15162466 | Interleukin-2 receptor antibody (basiliximab) for immunosuppressive induction therapy after liver transplantation: a protocol with early elimination of steroids and reduction of tacrolimus dosage. |
| 1705 | 15162466 | A prospective evaluation was performed to study the potential benefits of the use of interleukin-2 receptor antibody (IL-2Rab) in the induction therapy with early elimination of steroid and reduction of tacrolimus dosage in liver transplant recipients among whom 94% had chronic hepatitis B infection. |
| 1706 | 15162466 | Interleukin-2 receptor antibody (basiliximab) for immunosuppressive induction therapy after liver transplantation: a protocol with early elimination of steroids and reduction of tacrolimus dosage. |
| 1707 | 15162466 | A prospective evaluation was performed to study the potential benefits of the use of interleukin-2 receptor antibody (IL-2Rab) in the induction therapy with early elimination of steroid and reduction of tacrolimus dosage in liver transplant recipients among whom 94% had chronic hepatitis B infection. |
| 1708 | 15179321 | JAK3, a member of JAK kinase family of four (JAK1, JAK2, JAK3 and TYK2), is abundantly expressed in lymphoid cells. |
| 1709 | 15179321 | JAK3 has been found to initiate signaling of interleukin (IL)-2, IL-4, IL-7, IL-9, IL-13 and IL-15. |
| 1710 | 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. |
| 1711 | 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. |
| 1712 | 15251379 | In a densitometric study of RT-PCR products, the Th2 cytokine (IL-10) was significantly up-regulated in BD (2.91 +/- 0.26 vs 1.76 +/- 0.40), but a Th1 cytokine (IL-2) showed minimal change. |
| 1713 | 15296648 | Intracellular IFN-gamma production and IL-12 serum levels in latent autoimmune diabetes of adults (LADA) and in type 2 diabetes. |
| 1714 | 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. |
| 1715 | 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. |
| 1716 | 15296648 | In all study groups, IFN-gamma content of CD4(+) and CD8(+) lymphocytes was significantly upregulated by stimulation. |
| 1717 | 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. |
| 1718 | 15296648 | However, the percentages of CD4(+)/IFN-gamma(+) and CD8(+)/IFN-gamma(+) cells from type 2 diabetics were significantly higher compared with controls. |
| 1719 | 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. |
| 1720 | 15382512 | [Plasma levels of interleukin-1beta, interleukin-2 and interleukin-4 in recently diagnosed type 1 diabetic children and their association with beta-pancreatic autoantibodies]. |
| 1721 | 15474483 | Transcriptome and proteome expression in activated human CD4 and CD8 T-lymphocytes. |
| 1722 | 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. |
| 1723 | 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. |
| 1724 | 15474483 | Genes for IL-2, insulin, and IGF-1 receptors were increased at least 2-fold in activated vs non-activated T-cells. |
| 1725 | 15474483 | Among activated ontologies were signal transduction pathways such as IRS-1, IRS-2, Akt, and glycolytic pathways. |
| 1726 | 15474483 | Transcriptome and proteome expression in activated human CD4 and CD8 T-lymphocytes. |
| 1727 | 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. |
| 1728 | 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. |
| 1729 | 15474483 | Genes for IL-2, insulin, and IGF-1 receptors were increased at least 2-fold in activated vs non-activated T-cells. |
| 1730 | 15474483 | Among activated ontologies were signal transduction pathways such as IRS-1, IRS-2, Akt, and glycolytic pathways. |
| 1731 | 15543094 | The elevated levels of immunoglobulins, about 20% more muscle in the pulmonary arteries, increased airway smooth muscle cells, and increased fetal hemoglobin and erythropoietin are evidence of chronic hypoxia before death. |
| 1732 | 15543094 | These proinflammatory cytokines down-regulate gene expression of major cytochrome P-450 and/or other enzymes with the specific effects on mRNA levels, protein expression, and enzyme activity, thus affecting metabolism of several endogenous lipophilic substances, such as steroids, lipid-soluble vitamins, prostaglandins, leukotrienes, thromboxanes, and exogenous substances. |
| 1733 | 15543094 | PEPCK deficit found in SIDS infants (caused also by vitamin A deficiency) and eventually enhanced by PACAP lipolysis of adipocyte triglycerides resulted in an increased FA level in blood because of their impaired reesterification to triacylglycerol in adipocytes. |
| 1734 | 15543094 | Pulmonary edema and petechial hemorrhages often present in SIDS victims may be the result of the vascular leak syndrome caused by IL-2 and IFN-alpha. |
| 1735 | 15543094 | Chronic hypoxia with the release of proinflammatory mediators IL-1alpha, IL-1beta and IL-6, and overloading of the cardiovascular and respiratory systems due to the narrowing airways and small pulmonary arteries of these children could also contribute to the development of these abnormalities. |
| 1736 | 15543094 | Moreover, chronic hypoxia of SIDS infants induced also production of hypoxia-inducible factor 1alpha (HIF-1alpha), which stimulated synthesis and release of different growth factors by vascular endothelial cells and intensified subclinical inflammatory reactions in the central nervous system, perhaps potentiated also by PACAP and VIP gene mutations. |
| 1737 | 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. |
| 1738 | 15557171 | The N221(+) T cells produced IFN-gamma and IL-10, but very little IL-4, in response to p221 stimulation. |
| 1739 | 15557171 | This suppressive activity was cell contact-independent and was abrogated by Abs to IL-10 or IL-10R. |
| 1740 | 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. |
| 1741 | 15563987 | To test whether a combination of the NOD MHC with the NOD allele of Il2 is sufficient for type 1 diabetes, B6.NOD-H-2 mice were crossed with C3H mice, which possess the NOD allele at Il2, and F2 mice homozygous for NOD alleles at both the MHC and Il2 were produced. |
| 1742 | 15563987 | None of the F2 mice developed type 1 diabetes, suggesting that NOD alleles at MHC (Idd1) and Il2 (Idd3) are not sufficient for type 1 diabetes in the NOD mouse. |
| 1743 | 15563987 | To test whether a combination of the NOD MHC with the NOD allele of Il2 is sufficient for type 1 diabetes, B6.NOD-H-2 mice were crossed with C3H mice, which possess the NOD allele at Il2, and F2 mice homozygous for NOD alleles at both the MHC and Il2 were produced. |
| 1744 | 15563987 | None of the F2 mice developed type 1 diabetes, suggesting that NOD alleles at MHC (Idd1) and Il2 (Idd3) are not sufficient for type 1 diabetes in the NOD mouse. |
| 1745 | 15578334 | Recently however a second form of GnRH (GnRH-II) has been described in the human. |
| 1746 | 15578334 | The present study investigates GnRH-I and GnRH-II expression in human peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), as well as their action in regulating B-LCL proliferation in the presence and absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a normal control. |
| 1747 | 15578334 | Co-incubation of IL-2 and IL-2 + GnRH 10 (-5) M with a GnRH antagonist (Cetrorelix; 10 (-6) M) significantly attenuated the proliferation in normal B-LCLs. |
| 1748 | 15578334 | GnRH-II did not affect proliferation of normal B-LCLs alone, and did not alter the proliferative response to IL-2. |
| 1749 | 15578334 | Recently however a second form of GnRH (GnRH-II) has been described in the human. |
| 1750 | 15578334 | The present study investigates GnRH-I and GnRH-II expression in human peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), as well as their action in regulating B-LCL proliferation in the presence and absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a normal control. |
| 1751 | 15578334 | Co-incubation of IL-2 and IL-2 + GnRH 10 (-5) M with a GnRH antagonist (Cetrorelix; 10 (-6) M) significantly attenuated the proliferation in normal B-LCLs. |
| 1752 | 15578334 | GnRH-II did not affect proliferation of normal B-LCLs alone, and did not alter the proliferative response to IL-2. |
| 1753 | 15578334 | Recently however a second form of GnRH (GnRH-II) has been described in the human. |
| 1754 | 15578334 | The present study investigates GnRH-I and GnRH-II expression in human peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), as well as their action in regulating B-LCL proliferation in the presence and absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a normal control. |
| 1755 | 15578334 | Co-incubation of IL-2 and IL-2 + GnRH 10 (-5) M with a GnRH antagonist (Cetrorelix; 10 (-6) M) significantly attenuated the proliferation in normal B-LCLs. |
| 1756 | 15578334 | GnRH-II did not affect proliferation of normal B-LCLs alone, and did not alter the proliferative response to IL-2. |
| 1757 | 15578335 | Normal human lymphocytes and Jurkat T lymphoma cells were transfected with luciferase reporter constructs under the control of the interleukin-2 (IL-2) and the leukemia inhibitory factor (LIF) promoter, respectively. |
| 1758 | 15578335 | Similar results were obtained at the protein level (IL-2- and LIF-specific ELISAs). |
| 1759 | 15578335 | Normal human lymphocytes and Jurkat T lymphoma cells were transfected with luciferase reporter constructs under the control of the interleukin-2 (IL-2) and the leukemia inhibitory factor (LIF) promoter, respectively. |
| 1760 | 15578335 | Similar results were obtained at the protein level (IL-2- and LIF-specific ELISAs). |
| 1761 | 15616624 | The evidence that human insulin-dependent diabetes mellitus (IDDM) is a T cell-mediated disease is well substantiated, and the use of transgenic technology to understand the Th1/Th2 paradigm will provide keys to attenuating pathogenic autoimmunity. |
| 1762 | 15616624 | Insofar as the role of Th1 cytokines in IDDM is concerned, interferon gamma is considered a critical player in the etiology, a proinflammatory role has been determined for IDDM, interleukin-2 is considered an "amplification" factor, and tumor necrosis factor-alpha presents dichotomous effects. |
| 1763 | 15616624 | Regarding the role of Th2 cytokines in IDDM, interleukin-4 is essential for immunoprotection and counterregulation of IDDM, and interleukin-10 plays immunoprotective and destructive roles. |
| 1764 | 15616624 | Of all the cytokines examined, IL-4 seems to be the likely candidate for preventing IDDM. |
| 1765 | 15662595 | To examine this hypothesis, changes in blood glucose concentrations in healthy men were compared following administration of interleukin-2 (IL-2) and IL-6 representing, respectively, major mediators of the adaptive and the early innate immune response to bacterial infection. |
| 1766 | 15662595 | Doses of 10 000 IU/kg IL-2 and 0.5 microg/kg IL-6 (vs. placebo) were administered subcutaneously in two groups of men (n = 18 and 16) at 1900 h before a period of nocturnal rest allowing an assessment of changes under basal conditions. |
| 1767 | 15662595 | The hypoglycemic response to IL-2 was not accompanied by changes in serum insulin, C-peptide or cortisol. |
| 1768 | 15662595 | In contrast to IL-2, IL-6 led to an increase in cortisol, followed by a pronounced increase in blood glucose again peaking about 8 hours after injection (p < 0.001). |
| 1769 | 15662595 | Contrasting with the hyperglycemic effects of the acute phase regulator IL-6, the T-cell cytokine IL-2 seems to support glucose uptake and utilization by immune cells. |
| 1770 | 15662595 | To examine this hypothesis, changes in blood glucose concentrations in healthy men were compared following administration of interleukin-2 (IL-2) and IL-6 representing, respectively, major mediators of the adaptive and the early innate immune response to bacterial infection. |
| 1771 | 15662595 | Doses of 10 000 IU/kg IL-2 and 0.5 microg/kg IL-6 (vs. placebo) were administered subcutaneously in two groups of men (n = 18 and 16) at 1900 h before a period of nocturnal rest allowing an assessment of changes under basal conditions. |
| 1772 | 15662595 | The hypoglycemic response to IL-2 was not accompanied by changes in serum insulin, C-peptide or cortisol. |
| 1773 | 15662595 | In contrast to IL-2, IL-6 led to an increase in cortisol, followed by a pronounced increase in blood glucose again peaking about 8 hours after injection (p < 0.001). |
| 1774 | 15662595 | Contrasting with the hyperglycemic effects of the acute phase regulator IL-6, the T-cell cytokine IL-2 seems to support glucose uptake and utilization by immune cells. |
| 1775 | 15662595 | To examine this hypothesis, changes in blood glucose concentrations in healthy men were compared following administration of interleukin-2 (IL-2) and IL-6 representing, respectively, major mediators of the adaptive and the early innate immune response to bacterial infection. |
| 1776 | 15662595 | Doses of 10 000 IU/kg IL-2 and 0.5 microg/kg IL-6 (vs. placebo) were administered subcutaneously in two groups of men (n = 18 and 16) at 1900 h before a period of nocturnal rest allowing an assessment of changes under basal conditions. |
| 1777 | 15662595 | The hypoglycemic response to IL-2 was not accompanied by changes in serum insulin, C-peptide or cortisol. |
| 1778 | 15662595 | In contrast to IL-2, IL-6 led to an increase in cortisol, followed by a pronounced increase in blood glucose again peaking about 8 hours after injection (p < 0.001). |
| 1779 | 15662595 | Contrasting with the hyperglycemic effects of the acute phase regulator IL-6, the T-cell cytokine IL-2 seems to support glucose uptake and utilization by immune cells. |
| 1780 | 15662595 | To examine this hypothesis, changes in blood glucose concentrations in healthy men were compared following administration of interleukin-2 (IL-2) and IL-6 representing, respectively, major mediators of the adaptive and the early innate immune response to bacterial infection. |
| 1781 | 15662595 | Doses of 10 000 IU/kg IL-2 and 0.5 microg/kg IL-6 (vs. placebo) were administered subcutaneously in two groups of men (n = 18 and 16) at 1900 h before a period of nocturnal rest allowing an assessment of changes under basal conditions. |
| 1782 | 15662595 | The hypoglycemic response to IL-2 was not accompanied by changes in serum insulin, C-peptide or cortisol. |
| 1783 | 15662595 | In contrast to IL-2, IL-6 led to an increase in cortisol, followed by a pronounced increase in blood glucose again peaking about 8 hours after injection (p < 0.001). |
| 1784 | 15662595 | Contrasting with the hyperglycemic effects of the acute phase regulator IL-6, the T-cell cytokine IL-2 seems to support glucose uptake and utilization by immune cells. |
| 1785 | 15662595 | To examine this hypothesis, changes in blood glucose concentrations in healthy men were compared following administration of interleukin-2 (IL-2) and IL-6 representing, respectively, major mediators of the adaptive and the early innate immune response to bacterial infection. |
| 1786 | 15662595 | Doses of 10 000 IU/kg IL-2 and 0.5 microg/kg IL-6 (vs. placebo) were administered subcutaneously in two groups of men (n = 18 and 16) at 1900 h before a period of nocturnal rest allowing an assessment of changes under basal conditions. |
| 1787 | 15662595 | The hypoglycemic response to IL-2 was not accompanied by changes in serum insulin, C-peptide or cortisol. |
| 1788 | 15662595 | In contrast to IL-2, IL-6 led to an increase in cortisol, followed by a pronounced increase in blood glucose again peaking about 8 hours after injection (p < 0.001). |
| 1789 | 15662595 | Contrasting with the hyperglycemic effects of the acute phase regulator IL-6, the T-cell cytokine IL-2 seems to support glucose uptake and utilization by immune cells. |
| 1790 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 1791 | 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. |
| 1792 | 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. |
| 1793 | 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. |
| 1794 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 1795 | 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. |
| 1796 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 1797 | 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. |
| 1798 | 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. |
| 1799 | 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. |
| 1800 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 1801 | 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. |
| 1802 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 1803 | 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. |
| 1804 | 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. |
| 1805 | 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. |
| 1806 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 1807 | 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. |
| 1808 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 1809 | 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. |
| 1810 | 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. |
| 1811 | 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. |
| 1812 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 1813 | 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. |
| 1814 | 15753206 | Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. |
| 1815 | 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. |
| 1816 | 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. |
| 1817 | 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. |
| 1818 | 15753206 | IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). |
| 1819 | 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. |
| 1820 | 15776395 | As part of an ongoing search for genes associated with type 1 diabetes (T1D), a common autoimmune disease, we tested the biological candidate gene IL2RA (CD25), which encodes a subunit (IL-2R alpha) of the high-affinity interleukin-2 (IL-2) receptor complex. |
| 1821 | 15823702 | Oxidative stress and inflammatory cytokines such as monocyte chemoattractant protein 1 (MCP-1), TGF-beta, and IL-2 are supposed to play crucial roles in the pathogenesis of insulin resistance (IR). |
| 1822 | 15823702 | Tranilast is an anti-allergic drug which exerts anti-inflammatory and anti-angiogenesis effects through inhibition of expression of MCP-1, TGF-beta, and antigen-induced IL-2 lymphocyte responsiveness. |
| 1823 | 15823702 | Oxidative stress and inflammatory cytokines such as monocyte chemoattractant protein 1 (MCP-1), TGF-beta, and IL-2 are supposed to play crucial roles in the pathogenesis of insulin resistance (IR). |
| 1824 | 15823702 | Tranilast is an anti-allergic drug which exerts anti-inflammatory and anti-angiogenesis effects through inhibition of expression of MCP-1, TGF-beta, and antigen-induced IL-2 lymphocyte responsiveness. |
| 1825 | 15833265 | Most NKT cells express both an invariant T cell antigen receptor and the NK cell receptor NK1.1, and are referred to as invariant NKT cells. |
| 1826 | 15833265 | This invariant T cell receptor is restricted to interactions with glycolipids presented by the non-classical MHC, CD1d. |
| 1827 | 15833265 | These NKT cells rapidly produce high levels of interleukin (IL)-2, IFN-gamma, TNF-alpha, and IL-4 upon stimulation through their TCR. |
| 1828 | 15847799 | Media supplemented with IL-2+IL-4 supported growth of the largest number of antigen-specific clones. |
| 1829 | 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. |
| 1830 | 15847799 | Media supplemented with IL-2+IL-4 supported growth of the largest number of antigen-specific clones. |
| 1831 | 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. |
| 1832 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 1833 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 1834 | 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. |
| 1835 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 1836 | 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. |
| 1837 | 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. |
| 1838 | 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. |
| 1839 | 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. |
| 1840 | 15870014 | In vitro expanded human CD4+CD25+ regulatory T cells suppress effector T cell proliferation. |
| 1841 | 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. |
| 1842 | 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. |
| 1843 | 15882444 | Chimeric molecules of phogrin transmembrane and cytosolic sequences with the interleukin-2 receptor alpha chain (Tac) were sorted to DCVs through the action of an extended tyrosine-based motif Y(654)QELCRQRMA located in a 27aa sequence adjacent to the membrane-spanning domain. |
| 1844 | 15927845 | We characterized the peak levels, secretory pattern and total cytokine production of the Th1 cytokines (IL-2 and IFN gamma) and Th2 cytokines (IL-4 and IL-10), by stimulated peripheral blood mononuclear cells of twenty six first-degree relatives of T1DM patients, and eleven matched controls. |
| 1845 | 15927845 | At enrollment, first degree relatives demonstrated a significant increase in peak and overall secretion of IL-2; P<0.01 and P<0.005 respectively and IL-4 cytokine; P<0.05 and P<0.01 respectively, as compared to normal controls. |
| 1846 | 15927845 | Their mean IFN gamma secretion increased significantly, P<0.05, after one year while their higher IL-2 and IL-4 secretion remained unchanged. |
| 1847 | 15927845 | Four relatives all Ab positive, developed diabetes: Peak IL-4 levels were low in three and markedly decreased within one year in one of these relatives, while peak IL-2 and IFN gamma levels were elevated in all of them. |
| 1848 | 15927845 | The presence of low IL-4 and elevated IL-2 and IFN gamma levels in autoAb positive relatives is associated with progression to overt disease. |
| 1849 | 15927845 | We characterized the peak levels, secretory pattern and total cytokine production of the Th1 cytokines (IL-2 and IFN gamma) and Th2 cytokines (IL-4 and IL-10), by stimulated peripheral blood mononuclear cells of twenty six first-degree relatives of T1DM patients, and eleven matched controls. |
| 1850 | 15927845 | At enrollment, first degree relatives demonstrated a significant increase in peak and overall secretion of IL-2; P<0.01 and P<0.005 respectively and IL-4 cytokine; P<0.05 and P<0.01 respectively, as compared to normal controls. |
| 1851 | 15927845 | Their mean IFN gamma secretion increased significantly, P<0.05, after one year while their higher IL-2 and IL-4 secretion remained unchanged. |
| 1852 | 15927845 | Four relatives all Ab positive, developed diabetes: Peak IL-4 levels were low in three and markedly decreased within one year in one of these relatives, while peak IL-2 and IFN gamma levels were elevated in all of them. |
| 1853 | 15927845 | The presence of low IL-4 and elevated IL-2 and IFN gamma levels in autoAb positive relatives is associated with progression to overt disease. |
| 1854 | 15927845 | We characterized the peak levels, secretory pattern and total cytokine production of the Th1 cytokines (IL-2 and IFN gamma) and Th2 cytokines (IL-4 and IL-10), by stimulated peripheral blood mononuclear cells of twenty six first-degree relatives of T1DM patients, and eleven matched controls. |
| 1855 | 15927845 | At enrollment, first degree relatives demonstrated a significant increase in peak and overall secretion of IL-2; P<0.01 and P<0.005 respectively and IL-4 cytokine; P<0.05 and P<0.01 respectively, as compared to normal controls. |
| 1856 | 15927845 | Their mean IFN gamma secretion increased significantly, P<0.05, after one year while their higher IL-2 and IL-4 secretion remained unchanged. |
| 1857 | 15927845 | Four relatives all Ab positive, developed diabetes: Peak IL-4 levels were low in three and markedly decreased within one year in one of these relatives, while peak IL-2 and IFN gamma levels were elevated in all of them. |
| 1858 | 15927845 | The presence of low IL-4 and elevated IL-2 and IFN gamma levels in autoAb positive relatives is associated with progression to overt disease. |
| 1859 | 15927845 | We characterized the peak levels, secretory pattern and total cytokine production of the Th1 cytokines (IL-2 and IFN gamma) and Th2 cytokines (IL-4 and IL-10), by stimulated peripheral blood mononuclear cells of twenty six first-degree relatives of T1DM patients, and eleven matched controls. |
| 1860 | 15927845 | At enrollment, first degree relatives demonstrated a significant increase in peak and overall secretion of IL-2; P<0.01 and P<0.005 respectively and IL-4 cytokine; P<0.05 and P<0.01 respectively, as compared to normal controls. |
| 1861 | 15927845 | Their mean IFN gamma secretion increased significantly, P<0.05, after one year while their higher IL-2 and IL-4 secretion remained unchanged. |
| 1862 | 15927845 | Four relatives all Ab positive, developed diabetes: Peak IL-4 levels were low in three and markedly decreased within one year in one of these relatives, while peak IL-2 and IFN gamma levels were elevated in all of them. |
| 1863 | 15927845 | The presence of low IL-4 and elevated IL-2 and IFN gamma levels in autoAb positive relatives is associated with progression to overt disease. |
| 1864 | 15927845 | We characterized the peak levels, secretory pattern and total cytokine production of the Th1 cytokines (IL-2 and IFN gamma) and Th2 cytokines (IL-4 and IL-10), by stimulated peripheral blood mononuclear cells of twenty six first-degree relatives of T1DM patients, and eleven matched controls. |
| 1865 | 15927845 | At enrollment, first degree relatives demonstrated a significant increase in peak and overall secretion of IL-2; P<0.01 and P<0.005 respectively and IL-4 cytokine; P<0.05 and P<0.01 respectively, as compared to normal controls. |
| 1866 | 15927845 | Their mean IFN gamma secretion increased significantly, P<0.05, after one year while their higher IL-2 and IL-4 secretion remained unchanged. |
| 1867 | 15927845 | Four relatives all Ab positive, developed diabetes: Peak IL-4 levels were low in three and markedly decreased within one year in one of these relatives, while peak IL-2 and IFN gamma levels were elevated in all of them. |
| 1868 | 15927845 | The presence of low IL-4 and elevated IL-2 and IFN gamma levels in autoAb positive relatives is associated with progression to overt disease. |
| 1869 | 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). |
| 1870 | 15979891 | Insulin-treated GDM mothers had lower CD4 and CD4/CD8 ratios, and higher CD8 and IL-5 than diet-treated GDM or controls. |
| 1871 | 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. |
| 1872 | 15979891 | GDM newborn had higher CD8 gamma/delta and lower CD16 than NGT babies. |
| 1873 | 15998581 | In the current report we reduce the size of the Idd9.3 interval to 1.2Mb containing 15 genes, including one encoding the immune signaling molecule, 4-1BB, which shows amino acid variation between diabetes sensitive and resistant strains. 4-1BB, a member of the TNF receptor superfamily expressed by a variety of immune cells, mediates growth and survival signals for T cells. |
| 1874 | 15998581 | Functional analyses demonstrate that purified T cells from NOD congenic mice with the C57BL/10 (B10) allele at Idd9.3 produce more IL-2 and proliferate more vigorously in response to anti-CD3 plus immobilized 4-1BB ligand than T cells from NOD mice with the NOD allele at Idd9.3. |
| 1875 | 16048606 | Therefore, a sirolimus-based regimen that is combined with both an interleukin-2 receptor antibody and a calcineurin inhibitor may be excessive immunosuppression for pediatric renal transplant recipients. |
| 1876 | 16054858 | In this study, we measured the production of MMP-9 and its natural tissue inhibitor (TIMP)-1 by leukocytes isolated from human type I diabetic patients. |
| 1877 | 16054858 | TIMP-1 production was also enhanced in leukocytes from diabetics, but substantially less than MMP-9, with the MMP-9/TIMP-1 ratio being 1.6-fold higher in neutrophils and 3-fold higher in monocytes than controls. |
| 1878 | 16054858 | Interleukin (IL)-2 or lipopolysaccharide (LPS) treatment increased MMP-9 production in leukocytes from both diabetics and normal controls, whereas insulin decreased MMP-9 expression. |
| 1879 | 16084832 | Upon activation by phytohemagglutine (PHA), T-lymphocytes (T-cells) express receptors for growth factors, insulin, IGF-1 and IL2 and become insulin sensitive. |
| 1880 | 16084832 | The activation was also associated with incremental changes in GLUT 4, IRS-1, proinflammatory cytokines, and oxidative stress components. |
| 1881 | 16098919 | IL-15 is a 14-15 kD cytokine produced by monocytes/macrophages and shares some biological actions with IL-2. |
| 1882 | 16257508 | Gene variants for the interacting molecules IL2 and CD25, members of a pathway that is essential for immune homeostasis, are present in mice and humans, respectively. |
| 1883 | 16257508 | Variation of two molecules that negatively regulate T cells, CTLA-4 and the tyrosine phosphatase LYP/PEP, are associated with susceptibility to human and NOD T1D. |
| 1884 | 16271309 | Soluble interleukin-2 receptor as a marker for progression of coronary artery calcification in type 1 diabetes. |
| 1885 | 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. |
| 1886 | 16280652 | These activated TH1 CD4+ T cells and CD8+ cytotoxic T cells are involved in the destruction of beta cells. |
| 1887 | 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. |
| 1888 | 16329191 | Specific antiviral (self) CD8 T cells are mandatory for disease, but CD4 T cells are not. |
| 1889 | 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. |
| 1890 | 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. |
| 1891 | 16367949 | Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb). |
| 1892 | 16367949 | The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens. |
| 1893 | 16367949 | During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens. |
| 1894 | 16367949 | The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs. |
| 1895 | 16367949 | IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens. |
| 1896 | 16367949 | In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB. |
| 1897 | 16367949 | IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death. |
| 1898 | 16367949 | Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb). |
| 1899 | 16367949 | The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens. |
| 1900 | 16367949 | During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens. |
| 1901 | 16367949 | The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs. |
| 1902 | 16367949 | IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens. |
| 1903 | 16367949 | In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB. |
| 1904 | 16367949 | IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death. |
| 1905 | 16411065 | In these diseases PRL increases the syntesis of IFNgamma and IL-2 by Th1 lymphocytes. |
| 1906 | 16425035 | The Idd9.3 interval contains the candidate molecule cluster of differentiation (CD)137, which is a member of the tumor necrosis factor (TNF) receptor superfamily, functions as an inducible costimulator of T cells, and controls T-B interactions. |
| 1907 | 16425035 | The NOD and B10 CD137 alleles have sequence polymorphisms and different functional effects on T cells; the NOD CD137 allele mediates weaker T cell proliferative responses and decreased interleukin (IL)-2 production after CD137-mediated costimulation. |
| 1908 | 16443792 | Defective induction of CTLA-4 in the NOD mouse is controlled by the NOD allele of Idd3/IL-2 and a novel locus (Ctex) telomeric on chromosome 1. |
| 1909 | 16443792 | Using a genetic approach we here demonstrate that a novel locus (Ctex) telomeric on chromosome 1 together with the Idd3 (Il-2) gene confers optimal CTLA-4 expression upon CD3 activation of T-cells. |
| 1910 | 16443792 | Based on these data, we provide a model for how gene interaction between Idd3 (IL-2), Ctex, and Idd5.1 (Ctla-4) could confer susceptibility to autoimmune diabetes in the NOD mouse. |
| 1911 | 16443792 | Defective induction of CTLA-4 in the NOD mouse is controlled by the NOD allele of Idd3/IL-2 and a novel locus (Ctex) telomeric on chromosome 1. |
| 1912 | 16443792 | Using a genetic approach we here demonstrate that a novel locus (Ctex) telomeric on chromosome 1 together with the Idd3 (Il-2) gene confers optimal CTLA-4 expression upon CD3 activation of T-cells. |
| 1913 | 16443792 | Based on these data, we provide a model for how gene interaction between Idd3 (IL-2), Ctex, and Idd5.1 (Ctla-4) could confer susceptibility to autoimmune diabetes in the NOD mouse. |
| 1914 | 16443792 | Defective induction of CTLA-4 in the NOD mouse is controlled by the NOD allele of Idd3/IL-2 and a novel locus (Ctex) telomeric on chromosome 1. |
| 1915 | 16443792 | Using a genetic approach we here demonstrate that a novel locus (Ctex) telomeric on chromosome 1 together with the Idd3 (Il-2) gene confers optimal CTLA-4 expression upon CD3 activation of T-cells. |
| 1916 | 16443792 | Based on these data, we provide a model for how gene interaction between Idd3 (IL-2), Ctex, and Idd5.1 (Ctla-4) could confer susceptibility to autoimmune diabetes in the NOD mouse. |
| 1917 | 16478885 | Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C. |
| 1918 | 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. |
| 1919 | 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. |
| 1920 | 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. |
| 1921 | 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. |
| 1922 | 16478885 | This result suggests that HCV infection alters the population of Foxp3(+)CD4(+)CD25(+) T(Reg) cells. |
| 1923 | 16533984 | Diabetic mice showed significantly higher levels of C-reactive protein, fibrinogen, fibronectin and von Willebrand factor than nondiabetic mice (P<0.05), and MRSA infection further elevated the plasma levels of these inflammatory and endothelial markers (P<0.05). |
| 1924 | 16533984 | Before infection, diabetic mice had significantly higher plasminogen activator inhibitor-1 (PAI-1) activity, lower antithrombin III (AT-III) and protein C activities (P<0.05), and MRSA infection significantly increased PAI-1 activity further and reduced the activity of AT-III and protein C (P<0.05). |
| 1925 | 16533984 | MRSA infection increased the production of three Th1 cytokines, interleukin 2 (IL-2), tumour necrosis factor alpha and gamma interferon, in diabetic mice (P<0.05); however, three Th2 cytokines, IL-4, IL-6, IL-10, were elevated at 2 and 4 days p.i., and then dropped gradually. |
| 1926 | 16585566 | We show that effectors generated from murine islet-specific CD4 cells by TCR stimulation with IL-2 and TGF-beta1 have potent suppressive activity. |
| 1927 | 16585566 | However, the adaptive population does acquire the X-linked forkhead/winged helix transcription factor, FoxP3, which is associated with regulatory T cell function and maintains expression in vivo. |
| 1928 | 16585566 | In vivo, they eliminate Th1 cells in lymphoid tissues, where Fas/FasL interactions potentially play a role because Th1 cells persist when this pathway is blocked. |
| 1929 | 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. |
| 1930 | 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. |
| 1931 | 16606670 | PD-L1 and PD-L2 have overlapping functions in inhibiting interleukin-2 and interferon-gamma production during T cell activation. |
| 1932 | 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. |
| 1933 | 16606670 | PD-L1 inhibits pathogenic self-reactive CD4+ T cell-mediated tissue destruction and effector cytokine production. |
| 1934 | 16713180 | The mRNAs of IL-2 and IFN-gamma (Th1 cytokines) and IL-4 (Th2 cytokine) were downregulated in the pancreas and spleen of diabetic pregnant rats. |
| 1935 | 16713180 | Feeding an n-3 PUFA diet to rats with DP upregulated IL-10 mRNA in the pancreas and IL-4 and IL-10 mRNA in the spleen. |
| 1936 | 16713180 | In MAC offspring, high expression of IL-2 and IFN-gamma mRNA, but not of Th2 cytokines, was observed. |
| 1937 | 16713180 | The n-3 PUFA diet diminished Th1 mRNA quantities and increased the levels of IL-4, but not of IL-10, mRNA in MAC offspring. |
| 1938 | 16713180 | The mRNAs of IL-2 and IFN-gamma (Th1 cytokines) and IL-4 (Th2 cytokine) were downregulated in the pancreas and spleen of diabetic pregnant rats. |
| 1939 | 16713180 | Feeding an n-3 PUFA diet to rats with DP upregulated IL-10 mRNA in the pancreas and IL-4 and IL-10 mRNA in the spleen. |
| 1940 | 16713180 | In MAC offspring, high expression of IL-2 and IFN-gamma mRNA, but not of Th2 cytokines, was observed. |
| 1941 | 16713180 | The n-3 PUFA diet diminished Th1 mRNA quantities and increased the levels of IL-4, but not of IL-10, mRNA in MAC offspring. |
| 1942 | 16720206 | Modulation of cytokine release through humanized monoclonal antibodies was moderate and selective: anti-CD25 led to increased release of IL-2 and reduced production of TNFalpha, whereas anti-CD3 decreased release of interferon-y and IL-5 and increased secretion of IL-10. |
| 1943 | 16864902 | This study compared the results of tumour necrosis factor alpha (TNF-alpha), interleukin-2 soluble receptor (sIL-2R), nitric oxide metabolites (NO(x)), C-reactive protein (CRP), and lipids (total cholesterol, high-density lipoprotein (HDL-cholesterol), low-density lipoprotein (LDL-cholesterol), and triglycerides) between control group (nondiabetic subjects) and overweight type 2 DM subjects. |
| 1944 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 1945 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 1946 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 1947 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 1948 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 1949 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 1950 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 1951 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 1952 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 1953 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 1954 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 1955 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 1956 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 1957 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 1958 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 1959 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 1960 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 1961 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 1962 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 1963 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 1964 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 1965 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 1966 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 1967 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 1968 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 1969 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 1970 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 1971 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 1972 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 1973 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 1974 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 1975 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 1976 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 1977 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 1978 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 1979 | 17073617 | In addition, decreased IL-18 production from PBMC was significantly correlated with low production of IL-2. |
| 1980 | 17073617 | During the early stage of HIV-1 infection there is a decreased production of gamma interferon (IFN), IL-12 and IL-2 as well as not activation of IL-18 production and this leads to inhibition of Th1 immune response, whereas in the advanced stage of the disease, strong activation of IL-18 production along with persistent decreased production of gamma IFN, IL-12 and IL-2 may promote a Th2 immune response, which leads to persistent viral replication. |
| 1981 | 17073617 | Several studies have shown increased levels of IL-18 in HIV-seronegative subjects with obesity, insulin resistance and type II diabetes. |
| 1982 | 17073617 | In addition, decreased IL-18 production from PBMC was significantly correlated with low production of IL-2. |
| 1983 | 17073617 | During the early stage of HIV-1 infection there is a decreased production of gamma interferon (IFN), IL-12 and IL-2 as well as not activation of IL-18 production and this leads to inhibition of Th1 immune response, whereas in the advanced stage of the disease, strong activation of IL-18 production along with persistent decreased production of gamma IFN, IL-12 and IL-2 may promote a Th2 immune response, which leads to persistent viral replication. |
| 1984 | 17073617 | Several studies have shown increased levels of IL-18 in HIV-seronegative subjects with obesity, insulin resistance and type II diabetes. |
| 1985 | 17125935 | There is even more evidence that implicates the presence of autoimmune mechanisms in the proliferative stage of this disease: elevated levels of tumor necrosis factor-alpha, interleukin-8 and soluble interleukin-2 receptor in the serum of diabetic patients, increased vitreous concentration of the interleukin-6 and interleukin-8 in patients with proliferative retinopathy. |
| 1986 | 17130491 | Natural CD4(+)CD25(high) regulatory T-cells are derived from thymus, and accordingly human insulin-specific regulatory T-cells should exist. |
| 1987 | 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. |
| 1988 | 17130491 | The secretion of IFN-gamma, IL-2, IL-4, IL-5, and IL-10 was also studied. |
| 1989 | 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. |
| 1990 | 17130491 | The insulin-induced Foxp3 protein expression in CD4(+)CD25(high) cells was detectable in flow cytometry. |
| 1991 | 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. |
| 1992 | 17130555 | Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis. |
| 1993 | 17130555 | Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance. |
| 1994 | 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. |
| 1995 | 17130555 | Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg. |
| 1996 | 17130555 | In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions. |
| 1997 | 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. |
| 1998 | 17130555 | Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis. |
| 1999 | 17130555 | Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance. |
| 2000 | 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. |
| 2001 | 17130555 | Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg. |
| 2002 | 17130555 | In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions. |
| 2003 | 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. |
| 2004 | 17130555 | Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis. |
| 2005 | 17130555 | Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance. |
| 2006 | 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. |
| 2007 | 17130555 | Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg. |
| 2008 | 17130555 | In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions. |
| 2009 | 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. |
| 2010 | 17130555 | Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis. |
| 2011 | 17130555 | Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance. |
| 2012 | 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. |
| 2013 | 17130555 | Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg. |
| 2014 | 17130555 | In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions. |
| 2015 | 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. |
| 2016 | 17142723 | Cutting Edge: Programmed death (PD) ligand-1/PD-1 interaction is required for CD8+ T cell tolerance to tissue antigens. |
| 2017 | 17142723 | In this study we show that programmed death (PD)-1, an inhibitory receptor of the CD28 family, is required for tolerance induction of autoreactive CD8+ T cells. |
| 2018 | 17142723 | An antagonistic Ab against PD-1 provoked destructive autoimmune diabetes in RIP-mOVA mice expressing chicken OVA in the pancreatic islet cells, which received naive OVA-specific CD8+ OT-I cells. |
| 2019 | 17142723 | This effect was mediated by the PD ligand (PD-L) PD-L1 but not by PD-L2. |
| 2020 | 17142723 | An increased number of effector OT-I cells recovered from the pancreatic lymph nodes of anti-PD-L1-treated mice showed down-regulation of PD-1. |
| 2021 | 17142723 | Furthermore, the blockade of PD-1/PD-L1 interaction during the priming phase did not significantly affect OT-I cell division but enhanced its granzyme B, IFN-gamma, and IL-2 production. |
| 2022 | 17142723 | Thus, during the presentation of tissue Ags to CD8+ T cells, PD-1/PD-L1 interaction crucially controls the effector differentiation of autoreactive T cells to maintain self-tolerance. |
| 2023 | 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. |
| 2024 | 17161871 | Additionally, CB-SC also suppressed the proliferation of IL-2-stimulated CD4+CD25+ regulatory T cells. |
| 2025 | 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. |
| 2026 | 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. |
| 2027 | 17161871 | Additionally, CB-SC also suppressed the proliferation of IL-2-stimulated CD4+CD25+ regulatory T cells. |
| 2028 | 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. |
| 2029 | 17210729 | Dendritic cell-expanded, islet-specific CD4+ CD25+ CD62L+ regulatory T cells restore normoglycemia in diabetic NOD mice. |
| 2030 | 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. |
| 2031 | 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. |
| 2032 | 17211725 | Curcumin can also downregulate the expression of various proinflammatory cytokines including TNF, IL-1, IL-2, IL-6, IL-8, IL-12, and chemokines, most likely through inactivation of the transcription factor NF-kappaB. |
| 2033 | 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. |
| 2034 | 17327427 | Previous characterizations of Tregs in type 1 diabetes have used antibodies against CD4 and alpha-chain of the interleukin-2 receptor complex (CD25). |
| 2035 | 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(-)). |
| 2036 | 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. |
| 2037 | 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. |
| 2038 | 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. |
| 2039 | 17332083 | Humanized NOD/LtSz-scid IL2 receptor common gamma chain knockout mice in diabetes research. |
| 2040 | 17371467 | Association of the interleukin-2 receptor alpha (IL-2Ralpha)/CD25 gene region with Graves' disease using a multilocus test and tag SNPs. |
| 2041 | 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. |
| 2042 | 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. |
| 2043 | 17372610 | The absence of IL-2 results in the expansion of low-avidity Foxp3(-) islet-reactive CD4 T cells. |
| 2044 | 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. |
| 2045 | 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. |
| 2046 | 17372610 | The absence of IL-2 results in the expansion of low-avidity Foxp3(-) islet-reactive CD4 T cells. |
| 2047 | 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. |
| 2048 | 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. |
| 2049 | 17372610 | The absence of IL-2 results in the expansion of low-avidity Foxp3(-) islet-reactive CD4 T cells. |
| 2050 | 17390149 | In multivariate adjusted models, the strongest associations observed were between higher European ancestry and interleukin-6 soluble receptor (IL-6 SR), C-reactive protein (CRP), and adiponectin levels, with interleukin-2 soluble receptor (IL-2 SR) and soluble tumor necrosis factor receptor II (TNF-alpha SR II) also showing more modest but significant associations. |
| 2051 | 17390149 | These novel findings suggest that admixture mapping may identify genetic factors influencing the levels of IL-6 SR, CRP, IL-2 SR, and adiponectin. |
| 2052 | 17390149 | In multivariate adjusted models, the strongest associations observed were between higher European ancestry and interleukin-6 soluble receptor (IL-6 SR), C-reactive protein (CRP), and adiponectin levels, with interleukin-2 soluble receptor (IL-2 SR) and soluble tumor necrosis factor receptor II (TNF-alpha SR II) also showing more modest but significant associations. |
| 2053 | 17390149 | These novel findings suggest that admixture mapping may identify genetic factors influencing the levels of IL-6 SR, CRP, IL-2 SR, and adiponectin. |
| 2054 | 17395754 | A novel type 1 diabetes locus was mapped to the interleukin-2 receptor alpha gene (IL2RA) on chromosome 10p15.1, encoding an important modulator of immunity. |
| 2055 | 17459076 | A more selective alternative is daclizumab, a monoclonal antibody directed against the interleukin-2 receptor (CD25) on activated lymphocytes. |
| 2056 | 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. |
| 2057 | 17611256 | It results in insulin deficiency as a consequence of autoimmune destruction of islet beta-cells in the pancreas and is believed to be mediated by Th1 cytokines (IFNgamma, TNFalpha, and IL-2). |
| 2058 | 17611256 | A number of genes have been associated with type 1 diabetes in humans, including the human leukocyte antigen region, the insulin variable number tandem repeat, PTPN22, CTLA4, IL-4, and IL-13. |
| 2059 | 17611256 | In this study, 483 cases of canine diabetes and 869 controls of known breed were analyzed for association with IFNgamma, IGF2, IL-10, IL-12beta, IL-6, insulin, PTPN22, RANTES, IL-4, IL-1alpha and TNFalpha. |
| 2060 | 17611256 | Some associations were with increased susceptibility to the disease (IFNgamma, IL-10, IL-12beta, IL-6, insulin, PTPN22, IL-4, and TNFalpha), whereas others were protective (IL-4, PTPN22, IL-6, insulin, IGF2, TNFalpha). |
| 2061 | 17670937 | In nonobese diabetic (NOD) mice with overt new-onset type 1 diabetes mellitus (T1DM), short-term treatment with a "triple-therapy" regimen [rapamycin plus agonist IL-2-related and antagonist-type, mutant IL-15-related Ig fusion proteins (IL-2.Ig and mutIL-15.Ig)] halts autoimmune destruction of insulin-producing beta cells and restores both euglycemia and immune tolerance to beta cells. |
| 2062 | 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). |
| 2063 | 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. |
| 2064 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 2065 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 2066 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 2067 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 2068 | 17709885 | Type 1 diabetes (T1D) results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans by autoreactive T helper 1 (Th1) cells characterized by their cytokine secretory products, interleukin-2 (IL-2) and interferon gamma (IFNgamma). |
| 2069 | 17709885 | Th1-type cytokines (IL-2 and IFNgamma) correlate with T1D, whereas Th2 (IL-4 and IL-10), Th3 (transforming growth factor beta [TGFbeta]), and T regulatory cell-type cytokines (IL-10 and TGFbeta) correlate with protection from T1D. |
| 2070 | 17709885 | Paradoxically, however, administrations of Th1-type cytokines (IL-2 and IFNgamma) and immunotherapies that induce Th1-type cytokine responses actually prevent T1D, at least in animal models. |
| 2071 | 17709885 | Type 1 diabetes (T1D) results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans by autoreactive T helper 1 (Th1) cells characterized by their cytokine secretory products, interleukin-2 (IL-2) and interferon gamma (IFNgamma). |
| 2072 | 17709885 | Th1-type cytokines (IL-2 and IFNgamma) correlate with T1D, whereas Th2 (IL-4 and IL-10), Th3 (transforming growth factor beta [TGFbeta]), and T regulatory cell-type cytokines (IL-10 and TGFbeta) correlate with protection from T1D. |
| 2073 | 17709885 | Paradoxically, however, administrations of Th1-type cytokines (IL-2 and IFNgamma) and immunotherapies that induce Th1-type cytokine responses actually prevent T1D, at least in animal models. |
| 2074 | 17709885 | Type 1 diabetes (T1D) results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans by autoreactive T helper 1 (Th1) cells characterized by their cytokine secretory products, interleukin-2 (IL-2) and interferon gamma (IFNgamma). |
| 2075 | 17709885 | Th1-type cytokines (IL-2 and IFNgamma) correlate with T1D, whereas Th2 (IL-4 and IL-10), Th3 (transforming growth factor beta [TGFbeta]), and T regulatory cell-type cytokines (IL-10 and TGFbeta) correlate with protection from T1D. |
| 2076 | 17709885 | Paradoxically, however, administrations of Th1-type cytokines (IL-2 and IFNgamma) and immunotherapies that induce Th1-type cytokine responses actually prevent T1D, at least in animal models. |
| 2077 | 17940578 | The results are encouraging. (1) The long-term survival of allografts was received by blockade of both CD28/B7 and CD40/CD40L or CD28/B7 and OX40/OX40L costimulation signals. |
| 2078 | 17940578 | In the case of blockade of both CD28/B7 and OX40/OX40L, the islet allograft survival was over 150 days compared to the control 14 days. (2) The CTLA4Ig-FasL fusion molecule expressed by adenoviral vector containing CTLA4Ig-FasL gene can prevent the autoimmune diabetes of mice and significantly prolong the survival time of cardiac allografts in rats, indicating that Fas-FasL-mediated apoptosis is able to enhance CTLA4Ig-induced transplantation tolerance. (3) In the time-window of peripheral tolerance induced by various methods, the systemic infusion of donor bone marrow cells and spleen cells obtained stable allogeneic mixed chimerism and robust transplantation tolerance. |
| 2079 | 17940578 | In the case of CTLA4Ig-FasL treatment combined with donor bone marrow cells more than 20% donor-origin blood cells chimerism, and more than 200 days prolonged skin allograft survival were obtained or received. (4) The murine bone marrow stromal cell line QXMSC1 transfected with IL-6 gene or IL-2+IL-3 genes significantly improved the immune reconstitution of mice following allogeneic bone marrow transplantation. |
| 2080 | 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. |
| 2081 | 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. |
| 2082 | 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. |
| 2083 | 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. |
| 2084 | 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. |
| 2085 | 17999365 | Recently, association of celiac disease with common single-nucleotide polymorphism (SNP) variants in an extensive linkage-disequilibrium block of 480 kb containing the KIAA1109, Tenr, IL2, and IL21 genes has been demonstrated in three independent populations (rs6822844P combined=1.3 x 10(-14)). |
| 2086 | 17999365 | The KIAA1109/Tenr/IL2/IL21 block corresponds to the Idd3 locus in the nonobese diabetic mouse model of type 1 diabetes (T1D). |
| 2087 | 17999365 | We therefore aimed to investigate whether the KIAA1109/Tenr/IL2/IL21 region is involved in susceptibility to multiple autoimmune diseases. |
| 2088 | 17999365 | Our results replicate and extend the association found in the KIAA1109/Tenr/IL2/IL21 gene region with autoimmune diseases, implying that this locus is a general risk factor for multiple autoimmune diseases. |
| 2089 | 17999365 | Recently, association of celiac disease with common single-nucleotide polymorphism (SNP) variants in an extensive linkage-disequilibrium block of 480 kb containing the KIAA1109, Tenr, IL2, and IL21 genes has been demonstrated in three independent populations (rs6822844P combined=1.3 x 10(-14)). |
| 2090 | 17999365 | The KIAA1109/Tenr/IL2/IL21 block corresponds to the Idd3 locus in the nonobese diabetic mouse model of type 1 diabetes (T1D). |
| 2091 | 17999365 | We therefore aimed to investigate whether the KIAA1109/Tenr/IL2/IL21 region is involved in susceptibility to multiple autoimmune diseases. |
| 2092 | 17999365 | Our results replicate and extend the association found in the KIAA1109/Tenr/IL2/IL21 gene region with autoimmune diseases, implying that this locus is a general risk factor for multiple autoimmune diseases. |
| 2093 | 17999365 | Recently, association of celiac disease with common single-nucleotide polymorphism (SNP) variants in an extensive linkage-disequilibrium block of 480 kb containing the KIAA1109, Tenr, IL2, and IL21 genes has been demonstrated in three independent populations (rs6822844P combined=1.3 x 10(-14)). |
| 2094 | 17999365 | The KIAA1109/Tenr/IL2/IL21 block corresponds to the Idd3 locus in the nonobese diabetic mouse model of type 1 diabetes (T1D). |
| 2095 | 17999365 | We therefore aimed to investigate whether the KIAA1109/Tenr/IL2/IL21 region is involved in susceptibility to multiple autoimmune diseases. |
| 2096 | 17999365 | Our results replicate and extend the association found in the KIAA1109/Tenr/IL2/IL21 gene region with autoimmune diseases, implying that this locus is a general risk factor for multiple autoimmune diseases. |
| 2097 | 17999365 | Recently, association of celiac disease with common single-nucleotide polymorphism (SNP) variants in an extensive linkage-disequilibrium block of 480 kb containing the KIAA1109, Tenr, IL2, and IL21 genes has been demonstrated in three independent populations (rs6822844P combined=1.3 x 10(-14)). |
| 2098 | 17999365 | The KIAA1109/Tenr/IL2/IL21 block corresponds to the Idd3 locus in the nonobese diabetic mouse model of type 1 diabetes (T1D). |
| 2099 | 17999365 | We therefore aimed to investigate whether the KIAA1109/Tenr/IL2/IL21 region is involved in susceptibility to multiple autoimmune diseases. |
| 2100 | 17999365 | Our results replicate and extend the association found in the KIAA1109/Tenr/IL2/IL21 gene region with autoimmune diseases, implying that this locus is a general risk factor for multiple autoimmune diseases. |
| 2101 | 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. |
| 2102 | 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. |
| 2103 | 18062768 | This change in thinking occurred when a T regulatory cell defect was shown to be responsible for the lethal autoimmunity associated with IL-2/IL-2R deficiency. |
| 2104 | 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. |
| 2105 | 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. |
| 2106 | 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. |
| 2107 | 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. |
| 2108 | 18230955 | They are clustered into three groups: noxious (the 'bad', 8 members), comprising IL-1, IL-2, IL-6, IL-7, IL-8, IL-15, IL-17 and IL-18; protective (the 'good', 5 members), comprising IL-4, IL-10, IL-11, IL-12 and IL-13; and 'aloof' , comprising IL-5, IL-9, IL-14, IL-16 and IL-19 through IL-29 (15 members). |
| 2109 | 18230955 | IL-3 was reluctant to clustering and IL-30 through 33 were not included due to the scarce available data. |
| 2110 | 18242633 | We have therefore considered human IFN-gamma CD8(+) T cell responses against viral epitopes to analyze different variables which could be critical during the epitope-specific stimulation period. |
| 2111 | 18242633 | Incorporating both of these parameters into the ELISpot procedure proved capable of greatly amplifying (35.1-fold increase) the low grade CD8(+) T cell responses directed against beta-cell epitopes of type 1 diabetes patients, as compared to a previously optimized procedure using human serum-supplemented medium and low dose IL-2. |
| 2112 | 18299186 | Reduced CD4+T cell activation in children with type 1 diabetes carrying the PTPN22/Lyp 620Trp variant. |
| 2113 | 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. |
| 2114 | 18299186 | In conclusion, the LYP 620Trp variant is associated with reduced activation, proliferation and IL-2 production in CD4(+)T cells among T1D patients. |
| 2115 | 18299186 | Reduced CD4+T cell activation in children with type 1 diabetes carrying the PTPN22/Lyp 620Trp variant. |
| 2116 | 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. |
| 2117 | 18299186 | In conclusion, the LYP 620Trp variant is associated with reduced activation, proliferation and IL-2 production in CD4(+)T cells among T1D patients. |
| 2118 | 18338925 | The interleukins IL-2, IL-4, IL-10 and interferon gamma were quantified by ELISA. |
| 2119 | 18369459 | We replicated the previously reported association with interleukin 23 receptor and interleukin 12B (IL12B) polymorphisms in PS and PSA cohorts (IL23R: rs11209026, U.S. |
| 2120 | 18369459 | PSA, P = 1.3x10(-3)) and detected an independent association in the IL23R region with a SNP 4 kb upstream from IL12RB2 (P = 0.001). |
| 2121 | 18369459 | PS cohort included the region harboring lipoma HMGIC fusion partner (LHFP) and conserved oligomeric golgi complex component 6 (COG6) genes on chromosome 13q13 (combined P = 2x10(-6) for rs7993214; OR = 0.71), the late cornified envelope gene cluster (LCE) from the Epidermal Differentiation Complex (PSORS4) (combined P = 6.2x10(-5) for rs6701216; OR 1.45) and a region of LD at 15q21 (combined P = 2.9x10(-5) for rs3803369; OR = 1.43). |
| 2122 | 18369459 | This region is of interest because it harbors ubiquitin-specific protease-8 whose processed pseudogene lies upstream from HLA-C. |
| 2123 | 18369459 | This region of 15q21 also harbors the gene for SPPL2A (signal peptide peptidase like 2a) which activates tumor necrosis factor alpha by cleavage, triggering the expression of IL12 in human dendritic cells. |
| 2124 | 18369459 | This region harbors the interleukin 2 (IL2) and interleukin 21 (IL21) genes and was recently shown to be associated with four autoimmune diseases (Celiac disease, Type 1 diabetes, Grave's disease and Rheumatoid Arthritis). |
| 2125 | 18383559 | According to this concept, a T-helper lymphocyte of type 1 (Th1) subset of T-lymphocytes and their cytokine products, the type 1 cytokines [e.g. interleukin 2 (IL-2), interferon gamma (IFN-gamma) and tumour necrosis factor beta (TNF-beta)] prevail over immunoregulatory (anti-inflammatory) Th2 subset and its cytokine products, i.e. type 2 cytokines (e.g. |
| 2126 | 18383559 | IL-4, IL-6 and IL-10). |
| 2127 | 18383559 | Activation of sympathetic-corticotropin-releasing hormone (CRH) axis by psychological stress induces specifically Th1 cell overactivity that determines enhanced glutamine utilization and consequent poor L-arginine supply for nitric oxide (NO)-assisted insulin secretion. |
| 2128 | 18392872 | In this work, we assessed the in-vitro effects of eicosapentaenoic acid (EPA; C20:5n-3) and docosahexaenoic acid (DHA; C22:6n-3) (final concentration, 15 microM) on T cell blastogenesis, interleukin-2 and -4 (IL-2, IL-4) secretion, fatty acid composition and intracellular oxidative status in type I diabetic patients with or without complications. |
| 2129 | 18392872 | EPA and DHA diminished T-lymphocyte proliferation and IL-2 production but enhanced IL-4 secretion in both diabetic and control groups. |
| 2130 | 18392872 | In this work, we assessed the in-vitro effects of eicosapentaenoic acid (EPA; C20:5n-3) and docosahexaenoic acid (DHA; C22:6n-3) (final concentration, 15 microM) on T cell blastogenesis, interleukin-2 and -4 (IL-2, IL-4) secretion, fatty acid composition and intracellular oxidative status in type I diabetic patients with or without complications. |
| 2131 | 18392872 | EPA and DHA diminished T-lymphocyte proliferation and IL-2 production but enhanced IL-4 secretion in both diabetic and control groups. |
| 2132 | 18417224 | Interleukin-2 (IL-2) plays an established role in T-cell regulation through binding to the high-affinity IL-2 receptor (IL-2R). |
| 2133 | 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. |
| 2134 | 18417224 | Interleukin-2 (IL-2) plays an established role in T-cell regulation through binding to the high-affinity IL-2 receptor (IL-2R). |
| 2135 | 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. |
| 2136 | 18432585 | Plasma levels of Th1/Th2 type cytokine are associated with change of prolactin and GH/IGF-I in hemodialysis patients. |
| 2137 | 18432585 | The aims of the present study were to estimate the serum concentrations of Th1-Th2 cytokine, GH, insulin-like growth factor-I (IGF-I) and PRL, and to determine whether there are any correlations between the release of T-cell cytokines and disturbance of hormones in a group of patients on maintenance hemodialysis (MHD). |
| 2138 | 18432585 | Baseline serum concentrations of GH/IGF-I, PRL, IL-2, sIL-2R, IFN-gamma, IL-4 and IL-10 were measured in all patients and control subjects. |
| 2139 | 18432585 | Our results demonstrate that the fasting serum concentration of IGF-I, PRL, sIL-2R and Th1-type cytokine, including IL-2 and IFN-gamma, were significantly higher in HD patients compared to the healthy subjects. |
| 2140 | 18432585 | GH and Th2-type cytokine including IL-4 and IL-10 levels were slightly reduced, but no significant differences were observed between HD patients and the control group. |
| 2141 | 18432585 | In the group of HD patients, PRL correlated directly with IFN-gamma and correlated inversely with IL-10; IFN-gamma correlated inversely with IL-4; and GH also correlated inversely with IGF-I and IL-4. |
| 2142 | 18432585 | However, IGF-I correlated directly with IL-2 and IL-10. |
| 2143 | 18432585 | These data suggest that the Th1/Th2 imbalance in HD patients with an increase of Th1 type cytokines, associated with the altered GH/IGF-I axis and prolactin and immuno-endocrine dysfunction, probably plays a role in an impaired immune system in HD patients. |
| 2144 | 18432585 | Plasma levels of Th1/Th2 type cytokine are associated with change of prolactin and GH/IGF-I in hemodialysis patients. |
| 2145 | 18432585 | The aims of the present study were to estimate the serum concentrations of Th1-Th2 cytokine, GH, insulin-like growth factor-I (IGF-I) and PRL, and to determine whether there are any correlations between the release of T-cell cytokines and disturbance of hormones in a group of patients on maintenance hemodialysis (MHD). |
| 2146 | 18432585 | Baseline serum concentrations of GH/IGF-I, PRL, IL-2, sIL-2R, IFN-gamma, IL-4 and IL-10 were measured in all patients and control subjects. |
| 2147 | 18432585 | Our results demonstrate that the fasting serum concentration of IGF-I, PRL, sIL-2R and Th1-type cytokine, including IL-2 and IFN-gamma, were significantly higher in HD patients compared to the healthy subjects. |
| 2148 | 18432585 | GH and Th2-type cytokine including IL-4 and IL-10 levels were slightly reduced, but no significant differences were observed between HD patients and the control group. |
| 2149 | 18432585 | In the group of HD patients, PRL correlated directly with IFN-gamma and correlated inversely with IL-10; IFN-gamma correlated inversely with IL-4; and GH also correlated inversely with IGF-I and IL-4. |
| 2150 | 18432585 | However, IGF-I correlated directly with IL-2 and IL-10. |
| 2151 | 18432585 | These data suggest that the Th1/Th2 imbalance in HD patients with an increase of Th1 type cytokines, associated with the altered GH/IGF-I axis and prolactin and immuno-endocrine dysfunction, probably plays a role in an impaired immune system in HD patients. |
| 2152 | 18432585 | Plasma levels of Th1/Th2 type cytokine are associated with change of prolactin and GH/IGF-I in hemodialysis patients. |
| 2153 | 18432585 | The aims of the present study were to estimate the serum concentrations of Th1-Th2 cytokine, GH, insulin-like growth factor-I (IGF-I) and PRL, and to determine whether there are any correlations between the release of T-cell cytokines and disturbance of hormones in a group of patients on maintenance hemodialysis (MHD). |
| 2154 | 18432585 | Baseline serum concentrations of GH/IGF-I, PRL, IL-2, sIL-2R, IFN-gamma, IL-4 and IL-10 were measured in all patients and control subjects. |
| 2155 | 18432585 | Our results demonstrate that the fasting serum concentration of IGF-I, PRL, sIL-2R and Th1-type cytokine, including IL-2 and IFN-gamma, were significantly higher in HD patients compared to the healthy subjects. |
| 2156 | 18432585 | GH and Th2-type cytokine including IL-4 and IL-10 levels were slightly reduced, but no significant differences were observed between HD patients and the control group. |
| 2157 | 18432585 | In the group of HD patients, PRL correlated directly with IFN-gamma and correlated inversely with IL-10; IFN-gamma correlated inversely with IL-4; and GH also correlated inversely with IGF-I and IL-4. |
| 2158 | 18432585 | However, IGF-I correlated directly with IL-2 and IL-10. |
| 2159 | 18432585 | These data suggest that the Th1/Th2 imbalance in HD patients with an increase of Th1 type cytokines, associated with the altered GH/IGF-I axis and prolactin and immuno-endocrine dysfunction, probably plays a role in an impaired immune system in HD patients. |
| 2160 | 18481948 | Variants within the IL-2 (interleukin 2) and CD25 genes are associated with T1DM (Type 1 diabetes mellitus) in mice and humans respectively. |
| 2161 | 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. |
| 2162 | 18482207 | In the periphery, naturally occurring Foxp3+ CD4+ CD25+regulatory T (Treg) cells represent the master cells in dominant peripheral T-cell tolerance. |
| 2163 | 18482207 | The development and function of Treg cells are ultimately linked to IL-2 and Foxp3 expression. |
| 2164 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 2165 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 2166 | 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. |
| 2167 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 2168 | 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. |
| 2169 | 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. |
| 2170 | 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. |
| 2171 | 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. |
| 2172 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 2173 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 2174 | 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. |
| 2175 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 2176 | 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. |
| 2177 | 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. |
| 2178 | 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. |
| 2179 | 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. |
| 2180 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 2181 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 2182 | 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. |
| 2183 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 2184 | 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. |
| 2185 | 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. |
| 2186 | 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. |
| 2187 | 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. |
| 2188 | 18566388 | A function for IL-7R for CD4+CD25+Foxp3+ T regulatory cells. |
| 2189 | 18566388 | The IL-2/IL-2R interaction is important for development and peripheral homeostasis of T regulatory (Treg) cells. |
| 2190 | 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. |
| 2191 | 18566388 | Therefore, other gammac-cytokine(s) must be critically important during thymic development of CD4+CD25+Foxp3+ Treg cells apart from the IL-2. |
| 2192 | 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. |
| 2193 | 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. |
| 2194 | 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. |
| 2195 | 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. |
| 2196 | 18778952 | Four weeks later, splenocytes were harvested, mitogen stimulated, and analyzed for cytokine production (IL-2, IL-4, and IL-10) along with stimulation indices (SI). |
| 2197 | 18778952 | Stimulated IL-10 concentrations were elevated in STZ-treated CFTR-/- compared to LR-treated animals and controls (p<0.05). |
| 2198 | 18778952 | IL-2 levels were greater in CFTR-/- mice compared to controls (p<0.05), but unrelated to STZ. |
| 2199 | 18778952 | Reinforcing generalized cytokine up-regulation in CFTR-/-, IL-4 levels were greater in CFTR-/- mice compared to C57BL/6J, but FVB/NJ mice demonstrated greatest concentrations following STZ. |
| 2200 | 18778952 | Four weeks later, splenocytes were harvested, mitogen stimulated, and analyzed for cytokine production (IL-2, IL-4, and IL-10) along with stimulation indices (SI). |
| 2201 | 18778952 | Stimulated IL-10 concentrations were elevated in STZ-treated CFTR-/- compared to LR-treated animals and controls (p<0.05). |
| 2202 | 18778952 | IL-2 levels were greater in CFTR-/- mice compared to controls (p<0.05), but unrelated to STZ. |
| 2203 | 18778952 | Reinforcing generalized cytokine up-regulation in CFTR-/-, IL-4 levels were greater in CFTR-/- mice compared to C57BL/6J, but FVB/NJ mice demonstrated greatest concentrations following STZ. |
| 2204 | 18779574 | IL-21 is a pleiotropic type I cytokine that shares the common cytokine receptor gamma chain and plays important roles for normal Ig production, terminal B cell differentiation to plasma cells, and Th17 differentiation. |
| 2205 | 18779574 | IL-21 is elevated in several autoimmune diseases, and blocking its action has attenuated disease in MRL/lpr mice and in collagen-induced arthritis. |
| 2206 | 18779574 | The diabetes-associated Idd3 locus is at the Il2/Il21 locus, and elevated IL-21 was observed in the nonobese diabetic (NOD) mouse and suggested to contribute to diabetes by augmenting T cell homeostatic proliferation. |
| 2207 | 18780166 | The IL-2/CD25 pathway determines susceptibility to T1D in humans and NOD mice. |
| 2208 | 18780166 | Although the interleukin-2 (IL-2)/IL-2R signaling pathway has been the focus of numerous studies, certain aspects of its molecular regulation are not well characterized, especially in non-T cells, and a more complete understanding of the pathway is necessary to discern the functional basis of the genetic association between the IL-2-IL-21 and IL-2RA/CD25 gene regions and T1D in humans. |
| 2209 | 18780166 | Genetic variation in these regions may promote T1D susceptibility by influencing transcription and/or splicing and, hence, IL-2 and IL-2RA/CD25 expression at the protein level in different immune cell subsets; thus, there is a need to establish links between the genetic variation and immune cell phenotypes and functions in humans, which can be further investigated and validated in mouse models. |
| 2210 | 18780166 | The IL-2/CD25 pathway determines susceptibility to T1D in humans and NOD mice. |
| 2211 | 18780166 | Although the interleukin-2 (IL-2)/IL-2R signaling pathway has been the focus of numerous studies, certain aspects of its molecular regulation are not well characterized, especially in non-T cells, and a more complete understanding of the pathway is necessary to discern the functional basis of the genetic association between the IL-2-IL-21 and IL-2RA/CD25 gene regions and T1D in humans. |
| 2212 | 18780166 | Genetic variation in these regions may promote T1D susceptibility by influencing transcription and/or splicing and, hence, IL-2 and IL-2RA/CD25 expression at the protein level in different immune cell subsets; thus, there is a need to establish links between the genetic variation and immune cell phenotypes and functions in humans, which can be further investigated and validated in mouse models. |
| 2213 | 18780166 | The IL-2/CD25 pathway determines susceptibility to T1D in humans and NOD mice. |
| 2214 | 18780166 | Although the interleukin-2 (IL-2)/IL-2R signaling pathway has been the focus of numerous studies, certain aspects of its molecular regulation are not well characterized, especially in non-T cells, and a more complete understanding of the pathway is necessary to discern the functional basis of the genetic association between the IL-2-IL-21 and IL-2RA/CD25 gene regions and T1D in humans. |
| 2215 | 18780166 | Genetic variation in these regions may promote T1D susceptibility by influencing transcription and/or splicing and, hence, IL-2 and IL-2RA/CD25 expression at the protein level in different immune cell subsets; thus, there is a need to establish links between the genetic variation and immune cell phenotypes and functions in humans, which can be further investigated and validated in mouse models. |
| 2216 | 18785974 | Non-obese diabetic-recombination activating gene-1 (NOD-Rag1 null) interleukin (IL)-2 receptor common gamma chain (IL2r gamma null) null mice: a radioresistant model for human lymphohaematopoietic engraftment. |
| 2217 | 18785974 | We now describe a new immunodeficient radioresistant non-obese diabetic mice (NOD) stock based on targeted mutations in the recombination activating gene-1 (Rag1(null)) and interleukin (IL)-2 receptor common gamma chain (IL2rgamma(null)), and compare its ability to support lymphohaematopoietic cell engraftment with that achieved in radiosensitive NOD.CB17-Prkdc(scid) (NOD-Prkdc(scid)) IL2rgamma(null) mice. |
| 2218 | 18785974 | These data document that Rag1(null) and scid stocks of immunodeficient NOD mice harbouring the IL2rgamma(null) mutation support similar levels of human lymphohaematopoietic cell engraftment. |
| 2219 | 18785974 | Non-obese diabetic-recombination activating gene-1 (NOD-Rag1 null) interleukin (IL)-2 receptor common gamma chain (IL2r gamma null) null mice: a radioresistant model for human lymphohaematopoietic engraftment. |
| 2220 | 18785974 | We now describe a new immunodeficient radioresistant non-obese diabetic mice (NOD) stock based on targeted mutations in the recombination activating gene-1 (Rag1(null)) and interleukin (IL)-2 receptor common gamma chain (IL2rgamma(null)), and compare its ability to support lymphohaematopoietic cell engraftment with that achieved in radiosensitive NOD.CB17-Prkdc(scid) (NOD-Prkdc(scid)) IL2rgamma(null) mice. |
| 2221 | 18785974 | These data document that Rag1(null) and scid stocks of immunodeficient NOD mice harbouring the IL2rgamma(null) mutation support similar levels of human lymphohaematopoietic cell engraftment. |
| 2222 | 18805480 | In an effort to exploit these pathways to achieve control of aberrant immune activation we demonstrate that modulation of redox status suppresses cell proliferation and production of IL-2, IFN-gamma, TNF-alpha, and IL-17 in two robust CD8 T-cell-dependent in vitro mouse models: (1) response to alloantigen in an mixed leukocyte reaction and (2) CD8 T cell receptor transgenic OT-1 response to cognate peptide (SIINFEKL). |
| 2223 | 18805480 | To further examine the mechanisms of redox-mediated repression of CTL target cell lysis, we analyzed the expression of the effector molecules IFN-gamma, perforin, and granzyme B and the degranulation marker CD107a (LAMP-1). |
| 2224 | 18850043 | EEPHC significantly suppressed the expression of major histocompatibility complex (MHC) class II molecules and the costimulatory molecules CD40 and CD86 in NOD BM-DCs. |
| 2225 | 18850043 | Furthermore, splenocytes from the protected mice produced high amounts of IL-4 and IL-10 and low levels of IL-2 and interferon gamma, suggesting that these DCs deficient in NF- kappaB activity are responsible for the apparent shift in type 2 helper T cells. |
| 2226 | 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. |
| 2227 | 18855194 | CD4+ helper T (Th) cells play crucial role in priming, expansion and survival of CD8+ cytotoxic T lymphocytes (CTLs). |
| 2228 | 18855194 | However, how CD4+ Th cell's help is delivered to CD8+ T cells in vivo is still unclear. |
| 2229 | 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. |
| 2230 | 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. |
| 2231 | 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. |
| 2232 | 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. |
| 2233 | 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. |
| 2234 | 18940257 | In particular, the ability of certain cytokines, for example, IL-2, to provide vital survival signals to regulatory cells and to trigger death of effector T cells or impede IL-15 driven expansion of memory cells has spurred several trials. |
| 2235 | 18940257 | The ability of IFNgamma, IL-4, TNFalpha, and lymphotoxin to exert selective effects upon crucial lymphocyte subset populations in vivo may also enable translation into potent therapies. |
| 2236 | 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. |
| 2237 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 2238 | 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. |
| 2239 | 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. |
| 2240 | 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. |
| 2241 | 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. |
| 2242 | 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. |
| 2243 | 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. |
| 2244 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 2245 | 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. |
| 2246 | 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. |
| 2247 | 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. |
| 2248 | 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. |
| 2249 | 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. |
| 2250 | 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. |
| 2251 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 2252 | 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. |
| 2253 | 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. |
| 2254 | 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. |
| 2255 | 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. |
| 2256 | 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. |
| 2257 | 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. |
| 2258 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 2259 | 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. |
| 2260 | 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. |
| 2261 | 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. |
| 2262 | 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. |
| 2263 | 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. |
| 2264 | 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. |
| 2265 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 2266 | 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. |
| 2267 | 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. |
| 2268 | 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. |
| 2269 | 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. |
| 2270 | 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. |
| 2271 | 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. |
| 2272 | 18941219 | Type I diabetes (T1D) susceptibility is inherited through multiple insulin-dependent diabetes (Idd) genes. |
| 2273 | 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. |
| 2274 | 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. |
| 2275 | 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. |
| 2276 | 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. |
| 2277 | 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. |
| 2278 | 18988535 | To date the several loci involved to the T1DM development have been reliably identified by means of a number of approaches: MHC locus, VNTR within 5'-nontranscibed region of insulin (INS) gene, CTLA4 gene, encoding surface receptor of T cells, PTPN22 and PTPN2 genes, encoding tyrosine phosphatases of T lymphocytes, interleukin 2 (IL2) gene and alpha-chain of its receptor gene (IL2RA), as well as KIAA0350 gene (unknown function) and IFIH1 gene, encoding receptor of double-stranded DNA generated during viral infections. |
| 2279 | 18988535 | Thus the protein products of MHC, INS, PTPN22 and PTPN2 genes involve in the formation in thymus of T-lymphocyte repertoire, which provides the immune defense of organism. |
| 2280 | 18988535 | On the other hand the nonspecific activation of T cells, from that starts the autoimmune destruction of beta-cells of Langerhans islets of pancreas, in all probability, connects with the protein products of CTLA4, IL2, IL2RA genes, and, perhaps, PTPN22 and PTPN2 genes. |
| 2281 | 18988535 | To date the several loci involved to the T1DM development have been reliably identified by means of a number of approaches: MHC locus, VNTR within 5'-nontranscibed region of insulin (INS) gene, CTLA4 gene, encoding surface receptor of T cells, PTPN22 and PTPN2 genes, encoding tyrosine phosphatases of T lymphocytes, interleukin 2 (IL2) gene and alpha-chain of its receptor gene (IL2RA), as well as KIAA0350 gene (unknown function) and IFIH1 gene, encoding receptor of double-stranded DNA generated during viral infections. |
| 2282 | 18988535 | Thus the protein products of MHC, INS, PTPN22 and PTPN2 genes involve in the formation in thymus of T-lymphocyte repertoire, which provides the immune defense of organism. |
| 2283 | 18988535 | On the other hand the nonspecific activation of T cells, from that starts the autoimmune destruction of beta-cells of Langerhans islets of pancreas, in all probability, connects with the protein products of CTLA4, IL2, IL2RA genes, and, perhaps, PTPN22 and PTPN2 genes. |
| 2284 | 19013541 | Ursolic acid enhanced IL-2 and IFN-gamma production in response to Con A stimulation, whereas it inhibited TNF-alpha production in response to LPS stimulation. |
| 2285 | 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. |
| 2286 | 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. |
| 2287 | 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. |
| 2288 | 19106270 | Genetic association between the interleukin-2 receptor-alpha gene and mode of onset of type 1 diabetes in the Japanese population. |
| 2289 | 19111166 | Recent studies have identified likely causal genes in two congenic intervals associated with T1D, Idd3, and Idd5, and have documented the occurrence of gene-gene interactions, including "genetic masking", involving the genes encoding the critical immune molecules IL-2 and CTLA-4. |
| 2290 | 19119414 | IL2RA genetic heterogeneity in multiple sclerosis and type 1 diabetes susceptibility and soluble interleukin-2 receptor production. |
| 2291 | 19119414 | In addition, we tested the levels of soluble interleukin-2 receptor (sIL-2RA) in the serum from up to 69 healthy control subjects, 285 MS, and 1,317 T1D subjects. |
| 2292 | 19119414 | IL2RA genetic heterogeneity in multiple sclerosis and type 1 diabetes susceptibility and soluble interleukin-2 receptor production. |
| 2293 | 19119414 | In addition, we tested the levels of soluble interleukin-2 receptor (sIL-2RA) in the serum from up to 69 healthy control subjects, 285 MS, and 1,317 T1D subjects. |
| 2294 | 19201773 | Genetic variants in the region harbouring IL2/IL21 associated with ulcerative colitis. |
| 2295 | 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. |
| 2296 | 19209463 | IGRP is also a target of CD8 T cell responses in human T1D patients. |
| 2297 | 19209463 | In NOD mice, most IGRP-reactive CD8 T cells target the IGRP(206-214) epitope and are diabetogenic. |
| 2298 | 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. |
| 2299 | 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. |
| 2300 | 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. |
| 2301 | 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. |
| 2302 | 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. |
| 2303 | 19291704 | Our studies show that SEA can have a direct effect on CD4(+) T cells increasing expression of TGF-beta, integrin beta8 and galectins. |
| 2304 | 19295415 | The long-term outcome of pancreas transplant (PT) in African Americans (AA) using interleukin-2 receptor antibody induction has not been well documented. |
| 2305 | 19295415 | Excellent long-term patient and pancreas graft survivals can be achieved in AA recipients of PT by using interleukin-2 receptor antibody induction and combination of tacrolimus, mycophenolic acid, and steroid maintenance. |
| 2306 | 19295415 | The long-term outcome of pancreas transplant (PT) in African Americans (AA) using interleukin-2 receptor antibody induction has not been well documented. |
| 2307 | 19295415 | Excellent long-term patient and pancreas graft survivals can be achieved in AA recipients of PT by using interleukin-2 receptor antibody induction and combination of tacrolimus, mycophenolic acid, and steroid maintenance. |
| 2308 | 19455118 | Novel genetic risk markers for ulcerative colitis in the IL2/IL21 region are in epistasis with IL23R and suggest a common genetic background for ulcerative colitis and celiac disease. |
| 2309 | 19471255 | Novel association of the interleukin 2-interleukin 21 region with inflammatory bowel disease. |
| 2310 | 19557294 | These changes were associated with increased expression of TNF-alpha, IL-1beta, IL-2 and IL-6 in hippocampi of diabetic rats. |
| 2311 | 19592648 | Recent studies have ascribed a breakdown in tolerance to dysfunction in regulatory T cells that is secondary to reduced IL-2 production by T cells having the NOD diabetes susceptibility region insulin-dependent diabetes 3 (Idd3). |
| 2312 | 19654878 | Apoptosis of CD4+ CD25(high) T cells in type 1 diabetes may be partially mediated by IL-2 deprivation. |
| 2313 | 19701192 | Here we use polychromatic flow cytometry to show that differences in surface expression of the human interleukin-2 (IL-2) receptor alpha (IL2RA, or CD25) protein are restricted to particular immune cell types and correlate with several haplotypes in the IL2RA region that have previously been associated with two autoimmune diseases, type 1 diabetes (T1D) and multiple sclerosis. |
| 2314 | 19788505 | Disengaging the IL-2 receptor with daclizumab enhances IL-7-mediated proliferation of CD4(+) and CD8(+) T cells. |
| 2315 | 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. |
| 2316 | 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. |
| 2317 | 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. |
| 2318 | 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. |
| 2319 | 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. |
| 2320 | 19788505 | Disengaging the IL-2 receptor with daclizumab enhances IL-7-mediated proliferation of CD4(+) and CD8(+) T cells. |
| 2321 | 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. |
| 2322 | 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. |
| 2323 | 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. |
| 2324 | 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. |
| 2325 | 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. |
| 2326 | 19788505 | Disengaging the IL-2 receptor with daclizumab enhances IL-7-mediated proliferation of CD4(+) and CD8(+) T cells. |
| 2327 | 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. |
| 2328 | 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. |
| 2329 | 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. |
| 2330 | 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. |
| 2331 | 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. |
| 2332 | 19788505 | Disengaging the IL-2 receptor with daclizumab enhances IL-7-mediated proliferation of CD4(+) and CD8(+) T cells. |
| 2333 | 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. |
| 2334 | 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. |
| 2335 | 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. |
| 2336 | 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. |
| 2337 | 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. |
| 2338 | 19855244 | Treatment group showed increased serum interleukin (IL)-10 (twofold) and decreased inducible protein-10 and IL-4 (threefold) in luminex. |
| 2339 | 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. |
| 2340 | 19855244 | OA-treated grafts had significant reduced and delayed infiltration of CD4+ and CD8+ T cells. |
| 2341 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2342 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2343 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2344 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2345 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2346 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2347 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2348 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2349 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2350 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2351 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2352 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2353 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2354 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2355 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2356 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2357 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2358 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2359 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2360 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2361 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2362 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2363 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2364 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2365 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2366 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2367 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2368 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2369 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2370 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2371 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2372 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2373 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2374 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2375 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2376 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2377 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2378 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2379 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2380 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2381 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2382 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2383 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2384 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2385 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2386 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2387 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2388 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2389 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2390 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2391 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2392 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2393 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2394 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2395 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2396 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2397 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2398 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2399 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2400 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2401 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2402 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2403 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2404 | 19880748 | Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. |
| 2405 | 19880748 | IL-2 and IL-21 are two cytokines with great potential to affect autoimmune infiltration of nonlymphoid tissue, and are contained within the strongest non-MHC-linked locus for type 1 diabetes (T1D) susceptibility on the nonobese diabetic (NOD) mouse (Idd3). |
| 2406 | 19880748 | IL-21 is necessary for the development of diabetes in the NOD mouse, but a number of important studies argue that decreased expression of IL-2 explains Idd3. |
| 2407 | 19880748 | In this study, we demonstrate that the amount of IL-21, but not IL-2, correlated with T1D incidence. |
| 2408 | 19880748 | During our analyses of the IL-2/IL-21 interval, we found that mice segregate into one of two distinct expression profiles. |
| 2409 | 19880748 | In the first group, which includes the C57BL/6 strain, both Il2 and Il21 were expressed at low levels. |
| 2410 | 19880748 | In the other group, which includes the NOD strain, Il2 and Il21 were both highly expressed. |
| 2411 | 19880748 | The increased production of IL-21 in NOD mice was found to result from two single nucleotide polymorphisms within the distal promoter region that conferred increased binding affinity for the transcription factor Sp1. |
| 2412 | 19880748 | Our findings indicate that a loss of locus parity after decreased IL-2 mRNA stability ensures that the high-expressing IL-21 allele persists in nature and provides a basis for autoimmunity. |
| 2413 | 20033399 | Using logistic regression, we found that single-nucleotide polymorphisms (SNPs) at the INS, PTPN22, and IFIH1 loci were associated with late-onset disease (OR (95%CI) = 0.57(0.47-0.69), p = 2.77 x 10(-9); OR (95%CI) = 1.50 (1.27-1.78), p = 3.98 x 10(-6); and OR (95%CI) = 0.81(0.71-0.93), p = 0.0028, respectively). |
| 2414 | 20033399 | Thus, we believe the IL2/IL2R axis represents a potential therapeutic target for delaying the onset of disease. |
| 2415 | 20049409 | Patients' IL-2 serum levels were compared to IL-2 -330 T/G genotypes and tumor functional status and finally with known markers such as chromogranin A (CgA) and 5-hydroxyindolacetic acid (5-HIAA). |
| 2416 | 20049409 | Compared to CgA and 5-HIAA, IL-2 was more specific in detecting GEP-NET patients (p < 0.0001 and p < 0.0001, respectively). |
| 2417 | 20049409 | Patients' IL-2 serum levels were compared to IL-2 -330 T/G genotypes and tumor functional status and finally with known markers such as chromogranin A (CgA) and 5-hydroxyindolacetic acid (5-HIAA). |
| 2418 | 20049409 | Compared to CgA and 5-HIAA, IL-2 was more specific in detecting GEP-NET patients (p < 0.0001 and p < 0.0001, respectively). |
| 2419 | 20053369 | STZ administration elevated the levels of IL-2 as well as IFN-gamma and attenuated the level of TNF-alpha in the sera of diabetic animals. |
| 2420 | 20053369 | Investigating the oxidative stress responsive cell signaling pathways, increased expressions (immunoreactive concentrations) of phosphorylated p65 as well as its inhibitor protein phospho IkappaBalpha and phosphorylated mitogen activated protein kinases (MAPKs) have been observed in diabetic spleen tissue. |
| 2421 | 20053369 | Studies on isolated splenocytes revealed that hyperglycemia caused disruption of mitochondrial membrane potential, elevation in the concentration of cytosolic cytochrome c as well as activation of caspase 3 leading to apoptotic cell death. |
| 2422 | 20213480 | IL-2 and IFN-gamma in the retina of diabetic rats. |
| 2423 | 20354143 | PEA-15 is a death effector domain-containing phosphoprotein that binds ERK and restricts it to the cytoplasm. |
| 2424 | 20354143 | PEA-15 also binds to FADD and thereby blocks apoptosis induced by death receptors. |
| 2425 | 20354143 | However, PEA-15 deficient T cells had increased CD3/CD28-induced nuclear translocation of ERK and increased activation of IL-2 transcription and secretion in comparison to control wild-type littermates. |
| 2426 | 20354143 | In contrast, overexpression of PEA-15 in Jurkat T cells blocked nuclear translocation of ERK and IL-2 transcription. |
| 2427 | 20354143 | Finally, PEA-15-null T cells showed increased IL-2 dependent proliferation on stimulation. |
| 2428 | 20354143 | PEA-15 is a death effector domain-containing phosphoprotein that binds ERK and restricts it to the cytoplasm. |
| 2429 | 20354143 | PEA-15 also binds to FADD and thereby blocks apoptosis induced by death receptors. |
| 2430 | 20354143 | However, PEA-15 deficient T cells had increased CD3/CD28-induced nuclear translocation of ERK and increased activation of IL-2 transcription and secretion in comparison to control wild-type littermates. |
| 2431 | 20354143 | In contrast, overexpression of PEA-15 in Jurkat T cells blocked nuclear translocation of ERK and IL-2 transcription. |
| 2432 | 20354143 | Finally, PEA-15-null T cells showed increased IL-2 dependent proliferation on stimulation. |
| 2433 | 20354143 | PEA-15 is a death effector domain-containing phosphoprotein that binds ERK and restricts it to the cytoplasm. |
| 2434 | 20354143 | PEA-15 also binds to FADD and thereby blocks apoptosis induced by death receptors. |
| 2435 | 20354143 | However, PEA-15 deficient T cells had increased CD3/CD28-induced nuclear translocation of ERK and increased activation of IL-2 transcription and secretion in comparison to control wild-type littermates. |
| 2436 | 20354143 | In contrast, overexpression of PEA-15 in Jurkat T cells blocked nuclear translocation of ERK and IL-2 transcription. |
| 2437 | 20354143 | Finally, PEA-15-null T cells showed increased IL-2 dependent proliferation on stimulation. |
| 2438 | 20363978 | We have used the public sequencing and annotation of the mouse genome to delimit the previously resolved type 1 diabetes (T1D) insulin-dependent diabetes (Idd)18 interval to a region on chromosome 3 that includes the immunologically relevant candidate gene, Vav3. |
| 2439 | 20363978 | To test the candidacy of Vav3, we developed a novel congenic strain that enabled the resolution of Idd18 to a 604-kb interval, designated Idd18.1, which contains only two annotated genes: the complete sequence of Vav3 and the last exon of the gene encoding NETRIN G1, Ntng1. |
| 2440 | 20363978 | The T1D protection associated with B6 alleles of Idd18.1/Vav3 requires the presence of B6 protective alleles at Idd3, which are correlated with increased IL-2 production and regulatory T cell function. |
| 2441 | 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. |
| 2442 | 20476985 | Daclizumab: humanized monoclonal antibody to the interleukin-2 receptor. |
| 2443 | 20476985 | Daclizumab is a humanized antibody that binds to the alpha-chain of the interleukin-2 receptor and blocks the action of interleukin-2. |
| 2444 | 20476985 | Daclizumab: humanized monoclonal antibody to the interleukin-2 receptor. |
| 2445 | 20476985 | Daclizumab is a humanized antibody that binds to the alpha-chain of the interleukin-2 receptor and blocks the action of interleukin-2. |
| 2446 | 20483724 | The T cells from prediabetic NOD mice treated with an agonistic anti-CTLA-4 Ab-coated DC (anti-CTLA-4-Ab DC) showed significantly less proliferative response and enhanced IL-10 and TGF-beta1 production upon exposure to beta cell Ags. |
| 2447 | 20483724 | Furthermore, these mice showed increased frequency of Foxp3+ and IL-10+ T cells, less severe insulitis, and a significant delay in the onset of hyperglycemia compared with mice treated with control Ab-coated DCs. |
| 2448 | 20483724 | Further analyses showed that diabetogenic T cell function was modulated primarily through the induction of Foxp3 and IL-10 expression upon Ag presentation by anti-CTLA-4-Ab DCs. |
| 2449 | 20483724 | The induction of Foxp3 and IL-10 expression appeared to be a consequence of increased TGF-beta1 production by T cells activated using anti-CTLA-4-Ab DCs, and this effect could be enhanced by the addition of exogenous IL-2 or TGF-beta1. |
| 2450 | 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. |
| 2451 | 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. |
| 2452 | 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. |
| 2453 | 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. |
| 2454 | 20620534 | We evaluated the islet xenograft mean survival time as well as changes in interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) levels in transplanted mice. |
| 2455 | 20620534 | Within 1 week after transplantation the levels of IL-2 and TNF-alpha showed sharp increases in the untreated group, being significantly higher than those observed prior to transplantation. |
| 2456 | 20620534 | We evaluated the islet xenograft mean survival time as well as changes in interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) levels in transplanted mice. |
| 2457 | 20620534 | Within 1 week after transplantation the levels of IL-2 and TNF-alpha showed sharp increases in the untreated group, being significantly higher than those observed prior to transplantation. |
| 2458 | 20674317 | The pro-inflammatory cytokines, IL-1 and TNFα, as well as the Th1 cytokines, IL-2 and IFNγ were more elevated in female NOD mice whereas the Th2 cytokine, IL-4, was more depressed in these mice compared to their male counterparts. |
| 2459 | 20679400 | Low-dose IL-2 increases the number of T reg cells in the pancreas and induces expression of T reg cell-associated proteins including Foxp3, CD25, CTLA-4, ICOS (inducible T cell costimulator), and GITR (glucocorticoid-induced TNF receptor) in these cells. |
| 2460 | 20679403 | The strong perturbations induced by anti-CD3 overcame these niche limitations, in a process dependent on receptors for interleukin-2 (IL-2) and IL-7. |
| 2461 | 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. |
| 2462 | 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. |
| 2463 | 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. |
| 2464 | 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. |
| 2465 | 20847734 | Finally, while HFR decreased GWAT monocyte chemotactic protein-1 (MCP-1), interleukin-2 (IL-2), and PAI-1 levels, it did not affect several other cytokines including granulocyte-macrophage colony-stimulating factor, interferon-γ, IL-1β, IL-6, and IL-10. |
| 2466 | 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. |
| 2467 | 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. |
| 2468 | 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. |
| 2469 | 21038470 | Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF. |
| 2470 | 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. |
| 2471 | 21038470 | The induction of CD8(+) Treg by anti-CD3 mAb requires TNF and signaling through the NF-κB cascade. |
| 2472 | 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. |
| 2473 | 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. |
| 2474 | 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. |
| 2475 | 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. |
| 2476 | 21099113 | CD4+CD25+Foxp3+ Tregs play a major role in prevention of autoimmune diseases. |
| 2477 | 21099113 | In vivo experiments showed that this Treg boost was partially dependent on TNF but not on IL-2. |
| 2478 | 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. |
| 2479 | 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. |
| 2480 | 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. |
| 2481 | 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. |
| 2482 | 21168739 | Interleukin-2 receptor antagonists in liver transplantation: a meta-analysis of randomized trials. |
| 2483 | 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. |
| 2484 | 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. |
| 2485 | 21306187 | Five of these belonged to what is generally known as a Th1-mediated response (TNFα, IFNγ, IL-2, IL-1β and IL-12) and two were Th2 cytokines (IL-13 and IL-10). |
| 2486 | 21317396 | IL-2 and TGF-β1 play key roles in the immunobiology of Foxp3-expressing CD25(+)CD4(+) T cells (Foxp3(+)Treg). |
| 2487 | 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. |
| 2488 | 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. |
| 2489 | 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. |
| 2490 | 21442442 | Mile stones include the development of the calcineurin inhibitor Tacrolimus for immunosuppression as well as induction therapy using immune modulating substances like interleukin-2 receptor antagonists and antilymphocyte preparations. |
| 2491 | 21469091 | Reduced IL-2 expression in NOD mice leads to a temporal increase in CD62Llo FoxP3+ CD4+ T cells with limited suppressor activity. |
| 2492 | 21488898 | In this review, we discuss the influence of costimulation on intrinsic and extrinsic pathways of peripheral tolerance, with emphasis on members of the CD28 family, CD28, cytotoxic T-lymphocyte antigen-4 (CTLA-4), and programmed death-1 (PD-1), as well as the downstream cytokine interleukin-1 (IL-2). |
| 2493 | 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. |
| 2494 | 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). |
| 2495 | 21593413 | IL-21 is a pleiotropic type 1 cytokine that shares the common cytokine receptor γ-chain, γ(c), with IL-2, IL-4, IL-7, IL-9, and IL-15. |
| 2496 | 21593413 | IL-21 is most homologous to IL-2. |
| 2497 | 21593413 | Whereas IL-2 promotes development of regulatory T cells and confers protection from autoimmune disease, IL-21 promotes differentiation of Th17 cells and is implicated in several autoimmune diseases, including type 1 diabetes and systemic lupus erythematosus. |
| 2498 | 21593413 | However, the roles of IL-21 and IL-2 in CNS autoimmune diseases such as multiple sclerosis and uveitis have been controversial. |
| 2499 | 21593413 | Here, we generated Il21-mCherry/Il2-emGFP dual-reporter transgenic mice and showed that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina. |
| 2500 | 21593413 | IL-21 is a pleiotropic type 1 cytokine that shares the common cytokine receptor γ-chain, γ(c), with IL-2, IL-4, IL-7, IL-9, and IL-15. |
| 2501 | 21593413 | IL-21 is most homologous to IL-2. |
| 2502 | 21593413 | Whereas IL-2 promotes development of regulatory T cells and confers protection from autoimmune disease, IL-21 promotes differentiation of Th17 cells and is implicated in several autoimmune diseases, including type 1 diabetes and systemic lupus erythematosus. |
| 2503 | 21593413 | However, the roles of IL-21 and IL-2 in CNS autoimmune diseases such as multiple sclerosis and uveitis have been controversial. |
| 2504 | 21593413 | Here, we generated Il21-mCherry/Il2-emGFP dual-reporter transgenic mice and showed that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina. |
| 2505 | 21593413 | IL-21 is a pleiotropic type 1 cytokine that shares the common cytokine receptor γ-chain, γ(c), with IL-2, IL-4, IL-7, IL-9, and IL-15. |
| 2506 | 21593413 | IL-21 is most homologous to IL-2. |
| 2507 | 21593413 | Whereas IL-2 promotes development of regulatory T cells and confers protection from autoimmune disease, IL-21 promotes differentiation of Th17 cells and is implicated in several autoimmune diseases, including type 1 diabetes and systemic lupus erythematosus. |
| 2508 | 21593413 | However, the roles of IL-21 and IL-2 in CNS autoimmune diseases such as multiple sclerosis and uveitis have been controversial. |
| 2509 | 21593413 | Here, we generated Il21-mCherry/Il2-emGFP dual-reporter transgenic mice and showed that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina. |
| 2510 | 21593413 | IL-21 is a pleiotropic type 1 cytokine that shares the common cytokine receptor γ-chain, γ(c), with IL-2, IL-4, IL-7, IL-9, and IL-15. |
| 2511 | 21593413 | IL-21 is most homologous to IL-2. |
| 2512 | 21593413 | Whereas IL-2 promotes development of regulatory T cells and confers protection from autoimmune disease, IL-21 promotes differentiation of Th17 cells and is implicated in several autoimmune diseases, including type 1 diabetes and systemic lupus erythematosus. |
| 2513 | 21593413 | However, the roles of IL-21 and IL-2 in CNS autoimmune diseases such as multiple sclerosis and uveitis have been controversial. |
| 2514 | 21593413 | Here, we generated Il21-mCherry/Il2-emGFP dual-reporter transgenic mice and showed that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina. |
| 2515 | 21593413 | IL-21 is a pleiotropic type 1 cytokine that shares the common cytokine receptor γ-chain, γ(c), with IL-2, IL-4, IL-7, IL-9, and IL-15. |
| 2516 | 21593413 | IL-21 is most homologous to IL-2. |
| 2517 | 21593413 | Whereas IL-2 promotes development of regulatory T cells and confers protection from autoimmune disease, IL-21 promotes differentiation of Th17 cells and is implicated in several autoimmune diseases, including type 1 diabetes and systemic lupus erythematosus. |
| 2518 | 21593413 | However, the roles of IL-21 and IL-2 in CNS autoimmune diseases such as multiple sclerosis and uveitis have been controversial. |
| 2519 | 21593413 | Here, we generated Il21-mCherry/Il2-emGFP dual-reporter transgenic mice and showed that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina. |
| 2520 | 21606463 | Microarray and quantitative PCR analyses of livers from Ins2(Akita)Ldlr⁻/⁻ mice revealed altered expression of lipid homeostatic genes, including sterol-regulatory element binding protein (Srebp)1, liver X receptor (Lxr)α, Abca1, Cyp7b1, Cyp27a1, and Lpl, along with increased expression of pro-inflammatory cytokine genes, including interleukin (Il)1α, Il1β, Il2, tumor necrosis factor (Tnf)α, and Mcp1. |
| 2521 | 21688385 | Based on this review, we performed genetic analysis of the MYO9B gene and the IL-2/IL-21 locus by genotyping SNPs that have been previously associated with coeliac disease or schizophrenia in 223 families, 108 unrelated individuals with schizophrenia and 120 controls. |
| 2522 | 21691558 | Elevated pancreatic enzymes, IgM, soluble interleukin-2 receptor in anti-GADab(+) type 1 diabetes. |
| 2523 | 21724337 | Human pathogenesis of VL and reduced levels of leptin both are associated with increase in Th2 type immune response, characterized by secretion of cytokines such as IL-4 and IL-10. |
| 2524 | 21724337 | Whereas, the protective immune response during visceral leishmaniasis is associated with effective Th1 type immune response characterized by secretion of IFN-γ, IL-2 and IL-12, which correlates with leptin induction of T cells polarizing to Th1 population and secretion of proinflammatory cytokines, and also inhibition of Th2 type response. |
| 2525 | 21745722 | We found that these FoxP3(+) aTregs expressed high levels of the IL-7 receptor, IL-7Rα, without the high affinity receptor for IL-2, CD25, which is found on natural Treg cells (nTregs). |
| 2526 | 21875375 | Previous studies suggested the association of interleukin-2 (IL2) gene polymorphisms and its alpha- and beta-chain receptor (IL2RA and IL2RB) variants with different autoimmune diseases such as T1D, celiac disease, multiple sclerosis, and rheumatoid arthritis. |
| 2527 | 21875375 | We performed a genetic association study of chromosomal regions 4q27, 10p15, and 22q13 containing the IL2, IL2RA, and IL2RB genes in 445 T1D subjects and 828 healthy controls. |
| 2528 | 21875375 | The reported association with T1D patients of the IL2RA-rs41295061 located in the 10p15 region was replicated and our data suggest a trend of association of the polymorphisms IL2-rs17388568 and IL2-rs6822844 in 4q27. |
| 2529 | 21875375 | Previous studies suggested the association of interleukin-2 (IL2) gene polymorphisms and its alpha- and beta-chain receptor (IL2RA and IL2RB) variants with different autoimmune diseases such as T1D, celiac disease, multiple sclerosis, and rheumatoid arthritis. |
| 2530 | 21875375 | We performed a genetic association study of chromosomal regions 4q27, 10p15, and 22q13 containing the IL2, IL2RA, and IL2RB genes in 445 T1D subjects and 828 healthy controls. |
| 2531 | 21875375 | The reported association with T1D patients of the IL2RA-rs41295061 located in the 10p15 region was replicated and our data suggest a trend of association of the polymorphisms IL2-rs17388568 and IL2-rs6822844 in 4q27. |
| 2532 | 21875375 | Previous studies suggested the association of interleukin-2 (IL2) gene polymorphisms and its alpha- and beta-chain receptor (IL2RA and IL2RB) variants with different autoimmune diseases such as T1D, celiac disease, multiple sclerosis, and rheumatoid arthritis. |
| 2533 | 21875375 | We performed a genetic association study of chromosomal regions 4q27, 10p15, and 22q13 containing the IL2, IL2RA, and IL2RB genes in 445 T1D subjects and 828 healthy controls. |
| 2534 | 21875375 | The reported association with T1D patients of the IL2RA-rs41295061 located in the 10p15 region was replicated and our data suggest a trend of association of the polymorphisms IL2-rs17388568 and IL2-rs6822844 in 4q27. |
| 2535 | 22019586 | The mouse T1D susceptibility locus insulin-dependent diabetes susceptibility 3 (Idd3), which has a homologous genetic interval in humans, encodes cytokine genes Il2 and Il21 and regulates diabetes and other autoimmune diseases; however, the cellular and molecular mechanisms of this regulation are still being elucidated. |
| 2536 | 22019586 | Here we show that T cells from NOD mice produce more Il21 and less Il2 and exhibit enhanced Th17 cell generation compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele from a diabetes-resistant mouse strain. |
| 2537 | 22019586 | The mouse T1D susceptibility locus insulin-dependent diabetes susceptibility 3 (Idd3), which has a homologous genetic interval in humans, encodes cytokine genes Il2 and Il21 and regulates diabetes and other autoimmune diseases; however, the cellular and molecular mechanisms of this regulation are still being elucidated. |
| 2538 | 22019586 | Here we show that T cells from NOD mice produce more Il21 and less Il2 and exhibit enhanced Th17 cell generation compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele from a diabetes-resistant mouse strain. |
| 2539 | 22033476 | We studied in 38 newly diagnosed T1DM children with DKA, aged 7.68±3.07 years, plasma levels of cytokines IL-1β (interleukin-1β), IL-2, IL-6, IL-8, IL-10, TNF-α (tumour necrosis factor-α) and also WBC (white blood cell count), hs-CRP (high sensitivity C-reactive protein), GH (growth hormone) and cortisol, prior to, during and 120h after DKA management, with the aim to monitor their levels at different time-points and in different degrees of DKA severity. |
| 2540 | 22033476 | Prior to DKA management the levels of IL-6, IL-8, IL-10, WBC and cortisol were elevated, but were all reduced within 120 h after DKA management. |
| 2541 | 22033476 | In the group with moderate/severe DKA (ph≤7.2), IL-10 levels were the highest of all cytokines, but were significantly decreased after 6h (91.76 vs 18.04 pg/mL, p=0.008), with no further change, while IL-6 levels were decreased at 120 h (28.32 vs 11.9 pg/mL, p=0.003). |
| 2542 | 22033476 | In conclusion, in the children with DKA of our study, in the group with moderate/severe DKA the IL-10 levels were prematurely reduced at 6 hours, while the IL-6 levels remained high and were reduced at 120 hours after the DKA management. |
| 2543 | 22106155 | Type 1 diabetes genes within the interleukin (IL)-2, cytotoxic T-lymphocyte--associated protein 4 (CTLA-4), and natural resistance-associated macrophage protein (NRAMP1) pathways influence development of autoimmune diabetes in humans and NOD mice. |
| 2544 | 22106155 | In NOD mice, when present together, protective alleles encoding IL-2, Idd3 candidate gene, CTLA-4, NRAMP1, and acetyl-coenzyme A dehydrogenase, long-chain (ACADL) (candidate genes for the Idd5.1, Idd5.2, and Idd5.3 subregions) provide nearly complete diabetes protection. |
| 2545 | 22106155 | Type 1 diabetes genes within the interleukin (IL)-2, cytotoxic T-lymphocyte--associated protein 4 (CTLA-4), and natural resistance-associated macrophage protein (NRAMP1) pathways influence development of autoimmune diabetes in humans and NOD mice. |
| 2546 | 22106155 | In NOD mice, when present together, protective alleles encoding IL-2, Idd3 candidate gene, CTLA-4, NRAMP1, and acetyl-coenzyme A dehydrogenase, long-chain (ACADL) (candidate genes for the Idd5.1, Idd5.2, and Idd5.3 subregions) provide nearly complete diabetes protection. |
| 2547 | 22154614 | Serum levels of IgG were elevated in 67%, and soluble interleukin-2 receptor was elevated in 75%, when measured. |
| 2548 | 22186136 | These effects were accompanied by age-dependent changes in peripheral secretion of proinflammatory (interleukin [IL]-6 and tumor necrosis factor [TNF]-α) and T cell-related (IL-2 and interferon [IFN]-γ) cytokines and by increased release of the stress hormone corticosterone in periadolescence. |
| 2549 | 22211793 | Polymorphic variants of the IL2RA gene, which encodes high-affinity alpha subunit (CD25) of the interleukin-2 receptor, were recently found to affect the risk of several autoimmune disorders. |
| 2550 | 22227569 | We show that ICOS expression discriminates effector Foxp3(-) T cells from Foxp3(+) Tregs and specifically designates a dominant subset of intra-islet Tregs, endowed with an increased potential to expand, secrete IL-10, and mediate suppressive activity in vitro and in vivo. |
| 2551 | 22227569 | We further show that the ICOS(+) Tregs, in contrast to their ICOS(-) counterparts, are more sensitive to IL-2, a critical signal for their survival and functional stability. |
| 2552 | 22227569 | Lastly, the temporal loss in ICOS(+) Tregs is readily corrected by IL-2 therapy or protective Il2 gene variation. |
| 2553 | 22227569 | We show that ICOS expression discriminates effector Foxp3(-) T cells from Foxp3(+) Tregs and specifically designates a dominant subset of intra-islet Tregs, endowed with an increased potential to expand, secrete IL-10, and mediate suppressive activity in vitro and in vivo. |
| 2554 | 22227569 | We further show that the ICOS(+) Tregs, in contrast to their ICOS(-) counterparts, are more sensitive to IL-2, a critical signal for their survival and functional stability. |
| 2555 | 22227569 | Lastly, the temporal loss in ICOS(+) Tregs is readily corrected by IL-2 therapy or protective Il2 gene variation. |
| 2556 | 22270834 | Dendritic cells with TGF-β1 and IL-2 differentiate naive CD4+ T cells into alloantigen-specific and allograft protective Foxp3+ regulatory T cells. |
| 2557 | 22288305 | Biological drugs include TNF-alpha inhibitors (etanercept, infliximab and adalimumab) and ustekinumab which is an anti-IL 2/23 monoclonal antibody. |
| 2558 | 22447930 | Islets of aPC-treated mice exhibited markedly increased expression of insulin, aPC/protein C, endothelial protein C receptor, and matrix metalloproteinase (MMP)-2 when examined by immunostaining. |
| 2559 | 22447930 | The culture of NOD mouse spleen cells with aPC reduced the secretion of inflammatory cytokines interleukin (IL)-1β and interferon-γ but increased IL-2 and transforming growth factor-β1, two cytokines required for Treg differentiation. |
| 2560 | 22461703 | Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. |
| 2561 | 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. |
| 2562 | 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. |
| 2563 | 22461703 | Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. |
| 2564 | 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. |
| 2565 | 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. |
| 2566 | 22470201 | Serum concentration of IL-6, IL-2, TNF-α, and IFNγ in Vitiligo patients. |
| 2567 | 22519279 | In psoriasis there is an increased synthesis of proinflammatory proteins, such as: C-reactive protein (CRP), interleukin 1 (IL-1), IL-2, IL-6, IL-8, tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), alpha2-macroglobulin, alpha1-antitrypsin and ceruloplasmin. |
| 2568 | 22583338 | Interleukin-2 receptor antagonist does not decrease biopsy-proven acute rejection among adult Chinese kidney transplant recipients. |
| 2569 | 22583338 | Induction therapy with interleukin-2 receptor antagonist (IL2RA) is widely used for renal transplant recipients and this study aimed to examine the impact of IL2RA among Chinese renal transplant recipients. |
| 2570 | 22583338 | Interleukin-2 receptor antagonist does not decrease biopsy-proven acute rejection among adult Chinese kidney transplant recipients. |
| 2571 | 22583338 | Induction therapy with interleukin-2 receptor antagonist (IL2RA) is widely used for renal transplant recipients and this study aimed to examine the impact of IL2RA among Chinese renal transplant recipients. |
| 2572 | 22707198 | Microarray data demonstrated for the first time that overexpression of the genes encoding IL-1 receptor, lipid metabolic enzymes (e.g. |
| 2573 | 22707198 | Mte1, Ptdss1, and Sult2a1), myo-inositol oxygenase, glucagon, and somatostatin as well as down-regulation of olfactory receptor 984 and mitochondrial ribosomal protein, which are highly linked to T1DM etiology. |
| 2574 | 22707198 | The results of the microarray analysis revealed that up-regulation of IL-2, IL12a, and leptin receptor and down-regulation of PIK3 played important physiological roles in the onset of T2DM. |
| 2575 | 22771204 | In NOD mice, low dose IL-2 treatment at the initial time of diabetes can rescue insulin secretion by restoring proteins expression that are necessary for Tregs regulatory function in the pancreas. |
| 2576 | 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. |
| 2577 | 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. |
| 2578 | 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. |
| 2579 | 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. |
| 2580 | 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. |
| 2581 | 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. |
| 2582 | 22852057 | Zinc deficiency influences the generation of cytokines, including IL-1β, IL-2, IL-6, and TNF-α, and in response to zinc supplementation plasma cytokines exhibit a dose-dependent response. |
| 2583 | 22891215 | The alleles that confer susceptibility to type 1 diabetes at interleukin-2 (IL-2), IL2/4q27 (rs2069763) and renalase, FAD-dependent amine oxidase (RNLS)/10q23.31 (rs10509540), were associated with a lower age-at-diagnosis (P = 4.6 × 10⁻⁶ and 2.5 × 10⁻⁵, respectively). |
| 2584 | 22891215 | In addition to protein tyrosine phosphatase nonreceptor type 22 (PTPN22), evidence of statistical interaction between HLA class II genotypes and rs3087243 at cytotoxic T-lymphocyte antigen 4 (CTLA4)/2q33.2 was obtained (P = 7.90 × 10⁻⁵). |
| 2585 | 23023905 | Efficacy of omega-3 fatty acid supplementation on serum levels of tumour necrosis factor-alpha, C-reactive protein and interleukin-2 in type 2 diabetes mellitus patients. |
| 2586 | 23028375 | Here we apply PWAS ("proteome-wide analysis of SNPs"), a methodology based on quantitative mass spectrometry that enables rapid screening of SNPs for differential transcription factor binding, to 12 SNPs that are highly associated with type 1 diabetes at the IL2RA locus, encoding the interleukin-2 receptor CD25. |
| 2587 | 23028375 | We report differential, allele-specific binding of the transcription factors RUNX1, LEF1, CREB, and TFAP4 to IL2RA SNPs rs12722508*A, rs12722522*C, rs41295061*A, and rs2104286*A and demonstrate the functional influence of RUNX1 at rs12722508 by reporter gene assay. |
| 2588 | 23071669 | These included five that were common to both ages (TNF, HNF4A, IL15, Progesterone, and YWHAZ), and others that were unique to 2 weeks (e.g. |
| 2589 | 23071669 | MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g. |
| 2590 | 23071669 | IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C). |
| 2591 | 23071669 | Based on the literature, genes that may play a role in regulating metabolic pathways at 2 weeks include Myc and HNF4A, and at 4 weeks, beta-estradiol, p53, Akt, HNF4A and AR. |
| 2592 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 2593 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 2594 | 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). |
| 2595 | 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. |
| 2596 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 2597 | 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. |
| 2598 | 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. |
| 2599 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 2600 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 2601 | 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). |
| 2602 | 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. |
| 2603 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 2604 | 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. |
| 2605 | 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. |
| 2606 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 2607 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 2608 | 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). |
| 2609 | 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. |
| 2610 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 2611 | 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. |
| 2612 | 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. |
| 2613 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 2614 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 2615 | 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). |
| 2616 | 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. |
| 2617 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 2618 | 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. |
| 2619 | 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. |
| 2620 | 23180662 | IL-2 promotes the function of memory-like autoregulatory CD8+ T cells but suppresses their development via FoxP3+ Treg cells. |
| 2621 | 23180662 | IL-2 plays a critical role in both effector T-cell development and FoxP3(+) CD4(+) Treg-cell homeostasis. |
| 2622 | 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). |
| 2623 | 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. |
| 2624 | 23180662 | We show that decreased IL-2 production impairs the regulatory capacity of memory-like autoregulatory CD8(+) CD122(+) T cells. |
| 2625 | 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. |
| 2626 | 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. |
| 2627 | 23338919 | Comment on: efficacy of omega-3 fatty acid supplementation on serum levels of tumour necrosis factor-alpha, C-reactive protein and interleukin-2 in type 2 diabetes mellitus patients. |
| 2628 | 23415873 | Stimulation of human T cells with PHA or CD3/CD28 induced IL-2 mRNA expression and activated the endoplasmic reticulum (ER) stress response. |
| 2629 | 23415873 | The treatment of T cells with curcumin induced the unfolded protein response (UPR) signaling pathway, initiated by the phosphorylation of PERK and IRE1. |
| 2630 | 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. |
| 2631 | 23415873 | In PHA-activated T cells, curcumin further enhanced PHA-induced CHOP expression and reduced the expression of the anti-apoptotic protein Bcl-2. |
| 2632 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 2633 | 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. |
| 2634 | 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. |
| 2635 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 2636 | 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. |
| 2637 | 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. |
| 2638 | 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. |
| 2639 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 2640 | 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. |
| 2641 | 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. |
| 2642 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 2643 | 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. |
| 2644 | 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. |
| 2645 | 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. |
| 2646 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 2647 | 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. |
| 2648 | 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. |
| 2649 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 2650 | 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. |
| 2651 | 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. |
| 2652 | 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. |
| 2653 | 23418630 | Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. |
| 2654 | 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. |
| 2655 | 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. |
| 2656 | 23418630 | CD25 expression on CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation. |
| 2657 | 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. |
| 2658 | 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. |
| 2659 | 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. |
| 2660 | 23421092 | Trials of recombinant interleukin production in plants relate almost exclusively to tobacco, where through the transformation of the nuclear genome (agroinfection) monomeric (IL-2, IL-4, IL-13, IL-18), homodimeric (IL-10) and single-chain heterodimeric (IL-12) interleukins have been obtained. |
| 2661 | 23479229 | IL-21 promotes CD8+ CTL activity via the transcription factor T-bet. |
| 2662 | 23479229 | IL-21 is an IL-2 family cytokine and a growth factor for multiple lymphocyte effector lineages, including cytotoxic CD8(+) T cells. |
| 2663 | 23479229 | This is most likely the result of impaired CD8(+) CTL function in the absence of IL-21 signaling. |
| 2664 | 23479229 | Currently, the mechanisms by which IL-21 promotes CTL differentiation in CD8(+) T cells remain unclear, particularly the identity of the relevant transcription factor(s). |
| 2665 | 23479229 | We demonstrate that IL-21 induces the expression of the transcription factor T-bet in CD8(+) T cells, predominantly via STAT1, and that T-bet is required for the induction of cytolytic molecules, including perforin and granzyme B in response to IL-21. |
| 2666 | 23479229 | Finally, we show that IL-21-induced CTL function is T-bet dependent, as T-bet deficiency results in defective IL-21-dependent cytotoxicity in CD8(+) T cells in vitro and in vivo. |
| 2667 | 23479229 | Thus, IL-21 drives CD8(+) CTL differentiation via the actions of the transcription factor T-bet. |
| 2668 | 23499865 | CsA treatment down-regulates expression of gluconeogenic gene including Pepck, G6Pase and Pgc1α, leading to a decrease in blood glucose level and an improvement of glucose tolerance in the obese animals. |
| 2669 | 23499865 | RT-PCR analysis of genes involved in adipocyte differentiation and lipid metabolism in white adipose tissue reveal that CsA application reduces expression of Pparγ, Fas and Scd 1. |
| 2670 | 23499865 | The productions of pro-inflammatory cytokines (IL-1β, IL-2, IL-12 and TNFα) and JNK activity were remarkably reduced in the CsA-treated obese animals. |
| 2671 | 23600826 | Concentrations of proinflammatory cytokines interleukin (IL)-1β, IL-2, IL-12(p70), IL-18, IFN-γ, of regulatory cytokines IL-4, IL-10, IL-17 and chemokine CCL2 (MCP-1) were measured by multiplex-bead technology from supernatants. |
| 2672 | 23600826 | Co-incubation of fatty acids with uric acid resulted in a significant reduction of IL-10, IL-12(p70), IFN-γ and CCL2 (MCP-1) concentrations in supernatants compared to incubation with uric acid alone (P < 0·0001). |
| 2673 | 23600826 | Similarly, co-incubation of fatty acids with glucose diminished secretion of IL-10, IFN-γ and CCL2 (monocyte chemotactic protein-1), while IL-8 was up-regulated (P < 0·001). |
| 2674 | 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. |
| 2675 | 23670972 | Our objective was to study the effect of higher IL-2 doses (250,000-500,000 IU daily) as well as low-dose IL-2 (25,000 IU daily) and RAPA (1 mg/kg daily) (RAPA/IL-2) combination. |
| 2676 | 23707775 | The transcriptional profiles of T-bet, GATA3, and RORγt in the pancreatic lymphatic node samples derived from the NOD mice were detected by RT-PCR. |
| 2677 | 23707775 | This protective status was correlated with a substantially decreased production of interferon (IFN)-γ and interleukin (IL)-2, increased IL-10 and transforming growth factor (TGF)-β, and a reduced IL-17. |
| 2678 | 23707775 | Andrographolide also increased GATA3 mRNA expression but decreased T-bet and RORγt mRNA expressions. |
| 2679 | 23735822 | As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. |
| 2680 | 23735822 | Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. |
| 2681 | 23735822 | As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. |
| 2682 | 23735822 | Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. |
| 2683 | 23735822 | The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. |
| 2684 | 23735822 | Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. |
| 2685 | 23769592 | Plasma concentrations of interleukin (IL)-5, IL-6, IL-7, tumor necrosis factor-α (TNF-α), and granulocyte-monocyte colony-stimulating factor (GM-CSF) were significantly higher in the prediabetic group, as compared to the control group (all p<0.05). |
| 2686 | 23769592 | Plasma concentrations of all the other cytokines, interferon-γ (IFN-γ), IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 and IL-13, seemed to be elevated in the prediabetic group, but failed to reach statistical significances. |
| 2687 | 23769592 | Upon merging both groups, HbA1c was found to be positively correlated with IFN-γ, IL-1β, IL-2, IL-5, IL-7, IL-8, TNF-α and GM-CSF. |
| 2688 | 23769592 | Plasma concentrations of interleukin (IL)-5, IL-6, IL-7, tumor necrosis factor-α (TNF-α), and granulocyte-monocyte colony-stimulating factor (GM-CSF) were significantly higher in the prediabetic group, as compared to the control group (all p<0.05). |
| 2689 | 23769592 | Plasma concentrations of all the other cytokines, interferon-γ (IFN-γ), IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 and IL-13, seemed to be elevated in the prediabetic group, but failed to reach statistical significances. |
| 2690 | 23769592 | Upon merging both groups, HbA1c was found to be positively correlated with IFN-γ, IL-1β, IL-2, IL-5, IL-7, IL-8, TNF-α and GM-CSF. |
| 2691 | 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. |
| 2692 | 23776180 | Regulatory T cells, CD4(+)CD25(hi)Foxp3(+), develop normally, but pathogenic effector cells are severely reduced in number. |
| 2693 | 23776180 | Mechanistically, Foxp3(+) cells produce IL-17 but do not produce IFN-γ, whereas Foxp3(-) Th40 cells produce IFN-γ and IL-2. |
| 2694 | 23780417 | At the TNF-α, IL-2, IL-6 and IL-10 levels no difference was found (p > 0.05). |
| 2695 | 23878307 | CD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response. |
| 2696 | 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. |
| 2697 | 23878307 | Antigen-specific, DEC1-deficient CD4(+) T cells have cell-intrinsic defects in survival and proliferation. |
| 2698 | 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. |
| 2699 | 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. |
| 2700 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2701 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2702 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2703 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2704 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2705 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2706 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2707 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2708 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2709 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2710 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2711 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2712 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2713 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2714 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2715 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2716 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2717 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2718 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2719 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2720 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2721 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2722 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2723 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2724 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2725 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2726 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2727 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2728 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2729 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2730 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2731 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2732 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2733 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2734 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2735 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2736 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2737 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2738 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2739 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2740 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2741 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2742 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2743 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2744 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2745 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2746 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2747 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2748 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 2749 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 2750 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 2751 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 2752 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 2753 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 2754 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 2755 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 2756 | 23895744 | Destabilization of peptide:MHC interaction induces IL-2 resistant anergy in diabetogenic T cells. |
| 2757 | 23895744 | By treating a monoclonal diabetogenic T cell population with an MHC variant peptide, the cells are rendered unresponsive to the wild type ligand, as measured by both proliferation and IL-2 production. |
| 2758 | 23895744 | Stimulation of T cells with MHC variant peptides results in minimal Erk1/2 phosphorylation or cell division. |
| 2759 | 23895744 | Destabilization of peptide:MHC interaction induces IL-2 resistant anergy in diabetogenic T cells. |
| 2760 | 23895744 | By treating a monoclonal diabetogenic T cell population with an MHC variant peptide, the cells are rendered unresponsive to the wild type ligand, as measured by both proliferation and IL-2 production. |
| 2761 | 23895744 | Stimulation of T cells with MHC variant peptides results in minimal Erk1/2 phosphorylation or cell division. |
| 2762 | 23934388 | Interleukin (IL)-7 is one of the IL-2 family cytokines comprised of IL-2, IL-4, IL-7, IL-9, IL-15, as well as IL-21. |
| 2763 | 23982206 | Activation of the transcriptional function of the NF-κB protein c-Rel by O-GlcNAc glycosylation. |
| 2764 | 23982206 | Blocking the O-GlcNAcylation of this residue abrogated c-Rel-mediated expression of the cytokine-encoding genes IL2, IFNG, and CSF2 in response to T cell receptor (TCR) activation, whereas increasing the extent of O-GlcNAcylation of cellular proteins enhanced the expression of these genes. |
| 2765 | 23982206 | TCR- or tumor necrosis factor (TNF)-induced expression of other NF-κB target genes, such as NFKBIA (which encodes IκBα) and TNFAIP3 (which encodes A20), occurred independently of the O-GlcNAcylation of c-Rel. |
| 2766 | 24006086 | Soluble interleukin-2 receptor alpha in preclinical type 1 diabetes. |