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Gene Information
Gene symbol: CD8A
Gene name: CD8a molecule
HGNC ID: 1706
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 21925515 | (lyp/lyp) rat double negative, double positive and CD8 single positive (SP) thymocytes while expression of Gimap8, Gimap6, and Gimap7 was reduced only in CD8 SP thymocytes. |
| 2 | 2530249 | This occurred in parallel to the appearance of her insulin-specific CD8+ T cells, which inhibited the response of her A-loop-specific CD4+ T cells to insulin. |
| 3 | 2530249 | Our data demonstrate that CD8+ T cells play an important role in controlling peripheral tolerance to insulin and may abrogate IIR in a diabetic patient treated with SBI. |
| 4 | 2187189 | We conclude that IGF-I has important effects on the thymocyte number and the presence of CD4+/CD8+ immature cells in the thymus of diabetic rats despite persisting hyperglycemia. |
| 5 | 1899142 | These findings seem to indicate that the CD4+ cells are the helper cells for the activation of cytotoxic CD8+ cells that directly destroy islet beta cells in type I diabetes. |
| 6 | 2132756 | Results indicate that: 1) the first islet-infiltrating leukocytes are class II+, Ig- monocytes and CD8+ T lymphocytes, 2) after a slight decrease in the CD8+ cell population, an influx of CD4+ T lymphocytes occurs, accompanied by increasing numbers of CD8+ T cells, as well as IgM+ and IgG+ B lymphocytes, 3) whereas all the IgM+ B cells appear to be CD5+, between 70-95% of IgG+ B cells express CD5, and 4) throughout the response, the class II+, IgG-cell population remains relatively constant. |
| 7 | 1677834 | The percentage of CD8+CD11b+ cells containing suppressor/effector lymphocytes was decreased in the IDDM patients as compared with the controls (P less than 0.01) but no significant difference was seen in total CD8+ cells. |
| 8 | 1628775 | CD4+ T-cells may secrete cytokines, which in turn activate effector cell populations, whereas CD8+ T-cells may act as a final effector directly involved in beta-cell destruction. |
| 9 | 1286542 | Both the number of CD-4 and CD-8 positive cells increased significantly (p < 0.05), although no change in the CD-4:CD-8 ratio was observed. |
| 10 | 8420039 | Granzyme A is a serine protease expressed by populations of human and mouse natural killer cells and activated CD4+ and CD8+ cytotoxic lymphocytes; its expression marks a subset of inflammatory cells in allografts, autoimmune diabetes, and a number of other inflammatory lesions. |
| 11 | 8096128 | Hence, T cells expressing the CD8 phenotype specifically respond to idiotypic or ergotypic determinants on the inducing activated CD4+V beta 8+ T cells and effectively suppress a diabetogenic disease process by a mechanism that may involve T-T cell interactions. |
| 12 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 13 | 8318452 | First, CD4+ T cells from diabetic animals are required to transfer diabetes to non-diabetic recipients in conjunction with CD8+ effector T cells. |
| 14 | 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. |
| 15 | 8245789 | The number of resting CD4+ and CD8+ T cells positive for anti-p60 antibody binding (34.2 and 58.5%, respectively) increased to 92 and 90% of cells after 48-h stimulation with PHA. |
| 16 | 8306503 | Sera from both groups of IDDM patients and from healthy siblings exhibited soluble CD8 mean levels significantly higher than controls (P = 0.0001, P < 0.003, P < 0.03 respectively). |
| 17 | 7909401 | The helper functions of adult CD4 T cells to induce Ig-secreting cells from adult and the patient were strikingly suppressed by adult CD8 T cells. |
| 18 | 7909401 | Moreover, the patient's CD8 T cells stimulated rather than suppressed the induction of Ig-secreting cells from the patient when stimulated with the patient's CD4 T cells. |
| 19 | 8178053 | It consists of HLA class I genes and molecules (A, B and C) which control CD8+ cell-mediated antiviral responses, and class II genes and molecules (DR, DQ and DP) which control CD4+ cell responses (anti-bacterial and anti-toxin). |
| 20 | 8011155 | Suppression can be adoptively transferred by CD8+ T lymphocytes which act by releasing TGF-beta and IL-4 following antigen-specific triggering. |
| 21 | 8025212 | From 3 patients with newly-diagnosed Type 1 diabetes 184 clones were generated, the majority of which (39%) were CD4+TCR alpha beta+, whilst 31% were CD8+TCR alpha beta+. |
| 22 | 8025213 | Generally, there was an increase in the CD4:CD8 ratio in the peripheral lymphoid organs during the onset of insulitis which was largely due to an increase in the CD4 T cell population while the ratio decreased after the onset of diabetes. |
| 23 | 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. |
| 24 | 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. |
| 25 | 7525431 | These findings suggest that in peripheral blood of PBC patients reduced numbers of T cells may occur due to a selective intrahepatic sequestration of CD8+ T cells, and that the decreased expression of Leu-8 antigen by B cells may be associated with their participation in autoimmune processes. |
| 26 | 7833679 | In further similar studies, CD8+ cells from patients with Graves' disease (GD) are induced normally in response to glutamic acid decarboxylase-65 (GAD-65), the putative beta cell antigen important in insulin-dependent diabetes mellitus (IDDM), but significantly less to synthetic TSH receptor (TSHR). |
| 27 | 7833679 | Conversely, CD8+ cells from patients with IDDM are activated normally in response to TSHR, but significantly less to GAD-65. |
| 28 | 7841749 | Half a year after transplantation TII group remained stable for the requirement of insulin, whereas the control group gradually increased the dose of insulin. (1) Islet transplantation could adjust the immunological disorder in IDDM patients, increase the numbers of T lymphocyte subset such as CD2, CD4, CD8 while the chronic immuno-rejective response occurred. (2) T II inhibited both the numbers and function of T lymphocyte subpopulation and normalized the ratio of CD4/CD8. (3) TII prolonged the survival time of grafts in IDDM patients and suppressed immunological rejection. |
| 29 | 7889411 | By contrast, induction of an anti-self (anti-viral) CD8+ CTL response to the same virus later in life caused IDDM (incidence < 90%) in both transgenic lines, although the kinetics and requirements for CD4 help, the affinity and avidity of CD8+ CTL differed in each line. |
| 30 | 7714099 | Quite differently, the activation of CD8+ T lymphocytes from both hyper GD and eu GD group in response to TSHR peptides was impaired compared to HT, IDDM, and the N group; in contrast to the findings with CD4+ T lymphocytes, this was independent of thyroid hormone levels. |
| 31 | 7612149 | In addition, within both CD4 and CD8 subpopulations isolated from islet infiltrates, CD11b+ and CD49e+ cells were increased with respect to the same subset of cells isolated from the periphery. |
| 32 | 7789642 | Susceptibility of MIN6N8a cells to lysis by a NOD islet-derived CD8+ cytotoxic T-cell clone was greatly enhanced by IFN-gamma pretreatment, and this enhancement was abolished by anti-ICAM-1 and anti-LFA-1 mAbs. |
| 33 | 8666914 | Consistent with the induction of an active tolerance mechanism, splenic CD4+ (but not CD8+) T cells from GAD65 peptide-treated mice, inhibited the adoptive transfer of IDDM to NOD-scid/scid mice. |
| 34 | 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. |
| 35 | 10631549 | In the nonobese diabetic mouse model, there is new evidence that insulin plays an important role: not only is it an antigen for pathogenic CD4+ T cells but also it is recognised by highly diabetogenic CD8+ T cells. |
| 36 | 10787223 | Exclusive to POF patients was a statistically significant increase in CD8 density on T cells. |
| 37 | 10969850 | It has recently been demonstrated that one member of this family, CD30, plays a central role in maintaining peripheral tolerance by controlling the expansion of autoreactive CD8+ T-cells. |
| 38 | 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. |
| 39 | 11165713 | Here we show that a short (2 to 3 h) activation of T cells through the TCR simultaneously induces an increase in CD95L mRNA and a dramatic decrease in caspase-8 mRNA levels and proteolytic activity in human CD8(+) T cells. |
| 40 | 12905770 | In the infiltrating cells, the expression of CD8 was correlated with FasL (positively, P < 0.01); it was also found that there was a negative correlation between Fas+ islet cells and CD8+ mononucleated cells (P < 0.05). |
| 41 | 12917258 | CD8+ T cells triggered NO production by macrophages, while macrophages triggered IFN-gamma production by CD8+ T cells. |
| 42 | 12930356 | In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. |
| 43 | 12947308 | Ribonuclease protection assay was used to determine gene expression for cell markers F4/80 (macrophages), CD8 (type I T cells), CD4 (type II T cells), and CD 19 (natural killer cells), and for chemokines IP-10, MIP-1alpha, MIP-1beta, MCP-1, and RANTES. |
| 44 | 15778366 | Taken together, these results demonstrate that the BB rat Ian5 mutation alters the survival and function of regulatory CD8(-)4(+)25(+) T cells at the post-thymic level, resulting in clonal expansion of diabetogenic T cells among peripheral CD8(-)4(+)25(+) cells. |
| 45 | 15908957 | Here, we examine the antidiabetogenic properties of altered peptide ligands of CD8+ T cells recognizing an epitope of islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP206-214), a prevalent population of autoreactive T cells in autoimmune diabetes. |
| 46 | 15935691 | Subsequently, an attempt was made to correlate the presence of this mutation with the ability of CD4+ or CD8+ lymphocytes from these individuals to release IFN-gamma following mitogenic stimulation. |
| 47 | 15937548 | We have carried out comprehensive studies of the diabetogenic CD8 T cell population that targets residues 206-214 of the beta cell antigen islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP(206-214)) and undergoes avidity maturation as disease progresses. |
| 48 | 15977097 | At T1DM onset we observed significantly lower percentage of peripheral CD4 + and CD8 + cells producing IFN-gamma in patients compared to controls and subjects at risk. |
| 49 | 15977097 | The 15-month follow-up patients showed significantly lower percentage of CD4 + and CD8 + cells producing IFN-gamma compared to the other groups. |
| 50 | 15942943 | BMP2 belongs to the TGFbeta superfamily, and the BMP2-BMP4 genes are involved in thymocyte differentiation by blocking progression from CD4-CD8- to CD4+CD8+ while maintaining a sufficient pool of immature precursors. |
| 51 | 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). |
| 52 | 16082337 | Graft rejection requires CD4 T-cells, is facilitated by B-cells, and does not require CD8 T-cells. |
| 53 | 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. |
| 54 | 16424185 | These alloreactive CD8+ T cells 1) expressed the proliferation marker Ki-67, 2) up-regulated CD44, and 3) failed to undergo apoptosis. |
| 55 | 16493087 | In this study, we show that transgenic expression in NOD mice of HLA-A*0201, in the absence of murine class I MHC molecules, is sufficient to mediate autoreactive CD8+ T cell responses contributing to T1D development. |
| 56 | 16879996 | Neither the introduction of activated, self-antigen-specific CD4(+) helper T cells nor a global inflammatory stimulus were sufficient to activate the low-avidity CD8(+) T cells and did not break tolerance. |
| 57 | 17127455 | Type 1 Diabetes (T1D) is an autoimmune disease requiring contributions from effectors in both CD4+ and CD8+ T cell compartments in order to destroy insulin producing pancreatic beta cells. |
| 58 | 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. |
| 59 | 17163450 | This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells. |
| 60 | 17163450 | In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide. |
| 61 | 17163450 | The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population. |
| 62 | 17376833 | We hypothesized that critical genetic susceptibility loci that control progression to T1D, designated as insulin-dependent diabetes (Idd) loci, would be responsible for preventing CD8 T cell tolerance. |
| 63 | 17376840 | The aim of this study was to assess whether an epitope derived from the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP), IGRP(265-273,) which has recently been identified as a target in non-obese diabetic (NOD) mice and is fully homologous to the human epitope, is a target of human diabetogenic CD8(+) T cells. |
| 64 | 17617855 | Therefore, we determined whether perforin and/or FasL (CD95L) were required by donor MHC-restricted ('direct') CD8(+) T cells to reject islet allografts in vivo. |
| 65 | 17785799 | Activated DCs from GM-CSF-protected mice expressed lower levels of MHC class II and CD80/CD86 molecules, produced more IL-10 and were less effective in stimulating diabetogenic CD8+ T cells than DCs of PBS-treated NOD mice. |
| 66 | 18430797 | To do so, we delivered a mimotope peptide, recognized by the diabetogenic CD8(+) T cell clone AI4, to DCs in NOD mice via the endocytic receptor DEC-205. |
| 67 | 18431511 | In this issue of the JCI, Monti et al. report that immune conditioning via use of the Edmonton protocol - a treatment approach in which T1DM patients infused with pancreatic islets from multiple cadaveric donors simultaneously receive immunosuppressive drugs - results in lymphopenia that is associated with elevated serum levels of the homeostatic cytokines IL-7 and IL-15, which causes in vivo expansion of the autoreactive CD8(+) T cell population (see the related article beginning on page 1806). |
| 68 | 18483268 | Treatment with 1D11 increased infiltration of natural killer cells and T cells at the metastatic site, and enhanced expression of coactivators (NKG2D) and cytotoxic effectors (perforin and granzyme B) on CD8+ T cells. |
| 69 | 18483277 | We showed that CD8+ splenocytes from tumor-bearing mice expressed elevated interleukin (IL)-17 when compared with naive mice, and that CD8+ T cells could be induced to make IL-17 on addition of TGF-beta and IL-6 in vitro. |
| 70 | 19118506 | CD4(+) helper T (Th) cells play pivotal roles in induction of CD8(+) CTL immunity. |
| 71 | 19120302 | Incubation of human peripheral blood mononuclear cells (PBMC) with mAb in vitro has been shown to induce CD8(+) regulatory T cells (Tregs) capable of inhibiting proliferation of CD4(+) T cells. |
| 72 | 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. |
| 73 | 19209463 | IGRP is also a target of CD8 T cell responses in human T1D patients. |
| 74 | 19208910 | There was good selection of CD8 T-cells with a predominance of CD8 single-positive thymocytes, in spite of thymic insulin expression. |
| 75 | 19659777 | We therefore tested the hypothesis that the level of endothelial MHC class I molecule expression in diabetes-prone mice directly influences autoreactive CD8 T cell migration. |
| 76 | 19659777 | In addition, we examined whether the level of expression of MHC class I molecules influences autoantigen-driven CD8 T cell transmigration. |
| 77 | 19659777 | Using endothelial cell lines that expressed 'high' (NOD mouse), medium (NOD x C3H/HeJ F(1) generation mice) and no (C3H/HeJ) H-2K(d), we demonstrated in vitro that MHC levels have a profound effect on the activation, adhesion and transmigration of pathogenic, islet autoreactive CD8 T cells. |
| 78 | 19752223 | In this study, we describe the function of the adhesion molecule class I-restricted T cell-associated molecule (CRTAM) in regulating CD8+ T cell retention within the lymph node and eventually effector function. |
| 79 | 19922665 | Furthermore, the percentage of activated (CD69+) influenza-specific and IL-2 producer CD8+ T-cells was higher in adult mice compared to aged ones. |
| 80 | 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. |
| 81 | 20061825 | NKG2D is a surface receptor expressed on NK cells but also on CD8(+) T cells, gammadelta T cells, and auto-reactive CD4(+)/CD28(-) T cells of patients with rheumatoid arthritis. |
| 82 | 20045101 | The first was located in the major histocompatibility complex (MHC), with multiple SNPs strongly associated with CD4:CD8 ratio (rs2524054, p = 2.1 x 10(-28)). |
| 83 | 20045101 | The MHC association with CD4:CD8 replicated convincingly (p = 1.4 x 10(-9)) in an independent panel of 988 individuals. |
| 84 | 20045101 | Conditional analyses indicate that there are two major independent quantitative trait loci (QTL) in the MHC region that regulate CD4:CD8 ratio: one is located in the class I cluster and influences CD8 levels, whereas the second is located in the class II cluster and regulates CD4 levels. |
| 85 | 20519645 | In this study, we examined whether CD8 T cells that accumulate in suppressor of cytokine signaling 1 (SOCS1)-deficient mice because of increased IL-15 signaling in vivo would respond to an autoantigen expressed at a very low level using a mouse model of autoimmune diabetes. |
| 86 | 20519645 | Notwithstanding the Ag-specific proliferation defect, SOCS1-null P14 cells produced IFN-gamma and displayed potent cytolytic activity upon Ag stimulation, suggesting that SOCS1-null CD8 T cells underwent cytokine-driven functional differentiation that selectively compromised their proliferative response to Ag but not to cytokines. |
| 87 | 20519645 | These findings suggest that by attenuating cytokine-driven proliferation and functional differentiation, SOCS1 not only controls the pathogenicity of autoreactive cells but also preserves the ability of CD8 T cells to proliferate in response to Ags. |
| 88 | 20565292 | Here we demonstrate that CD103, an alpha E integrin necessary for T-cell homing and retention in the gut and other epithelia expressed by the majority of naïve CD8(+), and CD4(+)CD25(+) T cells and some DC subsets, is unnecessary for controlling T-cell responses during chronic lymphocytic choriomeningitis virus clone 13 (LCMV cl13) infection. |
| 89 | 20565292 | Interestingly, CD103 levels on the effector CD8(+) T cells became reduced soon after virus infection, with a small proportion of cells co-expressing PD-1 and CD103. |
| 90 | 20637454 | In addition, LPS-stimulated GM.BMDCs possessed a reduced capacity to activate diabetogenic CD8(+) T cells in a PD-1/PD-L1-dependent manner. |
| 91 | 18796632 | We show that selective gene ablation of the mouse gimap5 gene impairs the final intrathymic maturation of CD8 and CD4 T cells and compromises the survival of postthymic CD4 and CD8 cells, replicating findings in the BB rat model. |
| 92 | 20536791 | In the adoptively transferred model, the use of anti-CD134L mAb effectively prevented activation of CD4(+) memory T cells and significantly prolonged islet survival, similar to the action of anti-CD122 mAb to CD8(+) memory T cells. |
| 93 | 19966211 | We sought to incorporate this characteristic into an HLA-transgenic model of the disease and to determine the influence of reduced thymic insulin expression on CD8+ T cell responses to preproinsulin. |
| 94 | 19966211 | Our results suggest that insulin alleles that predispose to type 1 diabetes in humans do so, at least in part, by facilitating CD8+ T cell responses to the protein. |
| 95 | 21235534 | The CD4:CD8 ratio was reduced drastically upon LCMV infection due to an expansion of CD8 effectors but ameliorated in ATG-treated mice. |
| 96 | 20877570 | Here it was found that specific inhibition of cathepsin L affords strong protection from cyclophosphamide (CY)-induced insulitis and diabetes of NOD mice at the advanced stage of CD8(+) T cell infiltration via inhibiting granzyme activity. |
| 97 | 20877570 | It was discovered that cathepsin L inhibition prevents cytotoxic activity of CD8(+) T cells in the pancreatic islets through controlling dipeptidyl peptidase I activity. |
| 98 | 21330637 | DPP-4 inhibition significantly prevented adipose tissue infiltration by CD8(+) T-cells and M1 macrophages and decreased the expression of PAI-1. |
| 99 | 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. |
| 100 | 20855871 | In addition, transfer of CD8(+) T cells from diabetic animals into DORmO.RAG2(-/-) mice promoted insulitis by OVA-specific CD4(+) T cells. |
| 101 | 21430227 | In this paper, we report that prior stimulation with IL-15 and IL-21 also enables CD8(+) T cells to respond to weakly agonistic TCR ligands, resulting in proliferation, cytokine secretion, and cytolytic activity. |
| 102 | 21430227 | Using a transgenic mouse model of autoimmune diabetes, we show that cytokine-primed autoreactive CD8(+) T cells induce disease following stimulation by weak TCR ligands, but their diabetogenic potential is dependent on continuous availability of IL-15 in vivo. |
| 103 | 21511186 | However, in contrast to Tfh cells, CCR9+ Th cells displayed limited expression of CXCR5 and the targets of CCR9+ Th cells were CD8+ T cells whose responsiveness to IL-21 was necessary for the development of diabetes. |
| 104 | 21272093 | Interestingly, when the two conditions, HH condition and the infection, were associated, the mice showed a decrease in the percentage of CD4(+) CD8(-) blood lymphocytes that are involved in the modulation of immune response and have direct cytotoxic effects on the fungus. |
| 105 | 21340621 | Our goal was to determine the effect of TLR7 stimulation on the priming and activation of diabetogenic CD8(+) T cells. |
| 106 | 19342624 | Our results thus demonstrate an important role for BTLA in the induction of peripheral tolerance of both CD4(+) and CD8(+) T cells in vivo. |
| 107 | 20484136 | RIP-B7.1 mice expressing the costimulator molecule B7.1 (CD80) on pancreatic beta-cells are a well established model to characterize preproinsulin-specific CD8 T-cell responses and experimental autoimmune diabetes (EAD). |
| 108 | 20484136 | An imbalance between costimulator (B7.1) and coinhibitor (B7-H1) signals on pancreatic beta-cells can trigger pancreatic beta-cell-destruction by preproinsulin-specific CD8 T-cells. |
| 109 | 21697456 | Taken together, these data demonstrate that the PD-L1:B7-1 pathway inhibits potentially pathogenic self-reactive effector CD4(+) and CD8(+) T cell responses in vivo, and suggest that the immunoinhibitory functions of this pathway may be particularly important during the later phases of diabetogenesis. |
| 110 | 21538351 | The level of NKG2A expression on resting CD8+ T cells inversely correlated with acquisition of regulatory function when activated. |
| 111 | 21832162 | In contrast, CD4(+) or CD8(+) T cells do not produce IL-17A in response to acute or protracted viral infection with lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lymphocytic choriomeningitis virus-induced model of type 1 diabetes. |
| 112 | 21737880 | CCL22 expression increased the frequency of Tregs, produced higher levels of TGF-? in the CD4+ T cell population near islets, and decreased the frequency of circulating autoreactive CD8+ T cells and CD8+ IFN-??producing T cells. |
| 113 | 21873518 | Adoptive transfer experiments revealed that LAG-3 was primarily responsible for limiting the pathogenic potential of CD4(+) T cells and, to a lesser extent, CD8(+) T cells. |
| 114 | 21873518 | We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting autoimmunity in disease-prone environments. |
| 115 | 21785903 | Fasting serum DPP-4 enzymatic activity, plasma glucose (FPG), CD26 expression on CD3+, CD4+ and CD8+ lymphocytes, HbA1c and body mass index (BMI) were assessed. |
| 116 | 21785903 | Determination of the CD26 expression on CD3+, CD4+ and CD8+ lymphocytes was performed by flow-cytometric analysis. |
| 117 | 21998398 | PPI(6-14)-specific CD8(+) T cells detected in one healthy control displayed Il-10 mRNA expression, which was not observed in diabetic patients. |
| 118 | 21998398 | Our data support the hypothesis that insulin therapy may contribute to the expansion of autoreactive CD8(+) T cells in the long term. |