Gene expression profiles of effector T cells
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ABSTRACT:
PROVIDER: PRJNA141349 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29606: Gene expression profiles of effector T cells induced by mTOR inhibition GSE29607: Comparison of gene expression profiles of effector T cells from leptin-receptor-deficient mice and wild type mice Refer to individual Series
2012-09-05 | E-GEOD-29608 | biostudies-arrayexpress
Project description:Effector CD8+ T cells are believed to be terminally differentiated cells having cytotoxic activity and the ability to produce effector cytokines such as INF-M-NM-3 and TNF-M-NM-1. We investigated the difference between CXCR1+ and CXCR1- subsets of human effector CD27-CD28-CD8+ T cells. Both subsets similarly expressed cytolytic molecules and exerted substantial cytolytic activity, whereas only the CXCR1- subset had IL-2 productivity and self-proliferative activity and was more resistant to cell death than the CXCR1+ subset. These differences were explained by the specific up-regulation of CAMK4, SPRY2, and IL-7R in the CXCR1- subset and that of pro-apoptotic DAPK1 in the CXCR1+ subset. The IL-2 producers were more frequently found in the IL-7R+ subset of the CXCR1- effector CD8+ T cells than in the IL-7R- subset. IL-7/IL-7R signaling promoted cell survival only in the CXCR1- subset. The present study has highlighted a novel subset of effector CD8+ T cells producing IL-2 and suggests the importance of this subset in the homeostasis of effector CD8+ T cells. To find the genes that potentially cause the difference in IL-2 productivity and cell survival between the CXCR1+ and CXCR1- human effector CD8+ T cell subsets, we performed microarray gene expression analysis. We highly purified each CD3+CD8+ subset for this analysis (> 95.3%) from 5 healthy individuals, and then compared the gene expression profiles of each subset.
2011-01-27 | E-GEOD-26890 | biostudies-arrayexpress
Project description:To further develop our gene expression approach to treatment of autoimmunity, we have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed upon immunosuppressor treatment responsible for inhibition of T cell effector functions. Human CD4+CD25- cells from healthy donors were pretreated or not with rapamycin and stimulated with anti-CD3 and anti-CD28 for 12h. mTOR (Mammalian Target of Rapamycin) inhibition-induced gene expression was evaluated in human effector T cells after 1 hour rapamycin pretreatment and compared to vehicle-pretreated cells. Three independent experiments were performed for each of the two different experimental conditions using different donors for each experiment.
2012-09-05 | E-GEOD-29606 | biostudies-arrayexpress
Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype. DNA microarray analysis was performed of DbGP33-41 and DbNP396-404 tetramer-positive effector CD8+ T cells FACS-sorted at day 8 post-LCMV infection from four independent samples of either Blimp-1 conditional knockout mice (CKO; Blimp-1flox/flox x GranzymeB-cre+) or wildtype (WT) littermate controls.
2010-08-19 | E-GEOD-17211 | biostudies-arrayexpress
Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype.
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Project description:Microarray analyses was employed to determine the gene expression profiles of LCMV-specific p14 CD8+ effector T cells eight days after an acute LCMV Armstrong infection providing a framework to compare and contrast effector function potential of distinct immune cell subsets to CD8+ effector T cells.
2015-06-01 | GSE44410 | GEO
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed during leptin receptor deficiency, which is partly responsible for the inhibition of T cell effector functions. Mouse CD4+CD25- T cells were purified from leptin-receptor-deficient mice and wild type mice, and stimulated with anti-CD3 and anti-CD28 for 12h. Six mice of each genotype were used. Leptin receptor deficiency-induced gene expression profiles were evaluated in mouse effector T cells from db/db mice and compared to the ones observed in their WT counterpart (db/+ mice). Two independent experiments were performed, and in each of them, 3 mice/group were pooled.
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Project description:To further develop our gene expression approach to treatment of autoimmunity, we have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed upon immunosuppressor treatment responsible for inhibition of T cell effector functions. Human CD4+CD25- cells from healthy donors were pretreated or not with rapamycin and stimulated with anti-CD3 and anti-CD28 for 12h.
2012-09-05 | GSE29606 | GEO
Project description:Effector CD8+ T cells are believed to be terminally differentiated cells having cytotoxic activity and the ability to produce effector cytokines such as INF-γ and TNF-α. We investigated the difference between CXCR1+ and CXCR1- subsets of human effector CD27-CD28-CD8+ T cells. Both subsets similarly expressed cytolytic molecules and exerted substantial cytolytic activity, whereas only the CXCR1- subset had IL-2 productivity and self-proliferative activity and was more resistant to cell death than the CXCR1+ subset. These differences were explained by the specific up-regulation of CAMK4, SPRY2, and IL-7R in the CXCR1- subset and that of pro-apoptotic DAPK1 in the CXCR1+ subset. The IL-2 producers were more frequently found in the IL-7R+ subset of the CXCR1- effector CD8+ T cells than in the IL-7R- subset. IL-7/IL-7R signaling promoted cell survival only in the CXCR1- subset. The present study has highlighted a novel subset of effector CD8+ T cells producing IL-2 and suggests the importance of this subset in the homeostasis of effector CD8+ T cells.
2011-01-27 | GSE26890 | GEO