Comparision of expression profile between CD4+ helper T cells and CD8+ cytotoxic T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Yoshinori Naoe
PROVIDER: E-GEOD-67204 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We compared gene expression profiling between CD4+ helper T cells and CD8+ cytotoxic T cells
2015-06-30 | GSE67204 | GEO
Project description:We investigated transcriptional changes in CD4CD8aa and CD4 intraepthelial lymphocytes. TCRαβ thymocytes differentiate to either CD8αβ cytotoxic T lymphocytes or CD4 T helper cells. This functional dichotomy is controlled by key transcription factors, including the T helper master regulator, ThPOK, which suppresses the cytolytic-program in MHC class II restricted CD4 thymocytes. ThPOK continues to repress CD8-lineage genes in mature CD4 T cells, even as they differentiate to T helper effector subsets. Surprisingly, we show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8-lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes. Intraepithelial_CD4_CD8a neg vs CD8a pos. Two sample set of CD4CD8aa and CD4 intraepthelial lymphocytes (IEL) from small intestine of RAG knockout mice ( 8 weeks after transfer of naive CD4 cells, adoptive tranfer model of colitis), were prepared via cell sorting, and RNA was prepared by TRIZol (Invitrogen, USA) . Data were analyzed in GeneSpring GX10. For microarray analysis, RNA was labeled and hybridized to GeneChip Mouse Genome 430 2.0 arrays according to the Affymetrix protocols. Data were analyzed in GeneSpring GX10.
2013-01-08 | E-GEOD-41257 | biostudies-arrayexpress
Project description:We show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8- lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper- program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes Small intestine CD4 intraepithelial T lymphocytes from ThPOK-GFP reposter mice were isolated and sorted (FACS Aria) based on ThPOK and CD8aa expression. Cell were isolated either from non-experimental ThPOK-GFP reporter mice (WT) or after transfering CD4 naive T cells from ThPOK-GFP reporter mice to RAG-/-recipient animals (TR) as an experimental colitis model. Experimet was done in duplicate.
2012-12-10 | E-GEOD-42277 | biostudies-arrayexpress
Project description:We investigated transcriptional changes in CD4CD8aa and CD4 intraepthelial lymphocytes. TCRαβ thymocytes differentiate to either CD8αβ cytotoxic T lymphocytes or CD4 T helper cells. This functional dichotomy is controlled by key transcription factors, including the T helper master regulator, ThPOK, which suppresses the cytolytic-program in MHC class II restricted CD4 thymocytes. ThPOK continues to repress CD8-lineage genes in mature CD4 T cells, even as they differentiate to T helper effector subsets. Surprisingly, we show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8-lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes.
2013-01-08 | GSE41257 | GEO
Project description:CD4+ T cells (T helper cells) are cytokine-producing adaptive immune cells that activate or regulate the responses of different immune cells. They are known to play crucial roles in antibody class switching in B cells, neutrophil recruitment and activation of macrophages and CD8+ cytotoxic T cells. The activation and functional status of CD4+ T cells is important for adequate responses to pathogen infections but has also been associated with auto-immune disorders and survival in several cancers. In the current study, we carried out proteomic profiling of SUP-T1 cells.
2021-09-09 | PXD021272 | Pride
Project description:Disturbed expression of microRNAs (miRNAs) in regulatory T-cells (Tregs) leads to development of autoimmunity in experimental mouse models. However, the miRNA expression signature characterizing Tregs of autoimmune diseases, such as rheumatoid arthritis (RA) has not been determined yet. Moreover, the technical limitations prevented the analysis of such minute T-cell population as naive and memory Tregs. In this study we have used a microarray approach to comprehensively analyze miRNA expression signatures of naive Tregs (CD4+CD45RO-CD25++), memory Tregs (CD4+CD45RO+CD25+++), as well as conventional naive (CD4+CD45RO-CD25-) and memory (CD4+CD45RO+CD25-) T-cells (Tconvs) derived from peripheral blood of RA patients, and matched healthy controls. Differential expression of selected miRNAs was validated by TaqMan-based qRT-PCR. We found a positive correlation between increased expression of miR-451 in T-cells of RA patients and disease activity score (DAS28), ESR levels, and serum levels of IL-6. Moreover, we found characteristic, disease and treatment independent, global miRNA expression signatures defining naive Tregs, memory Tregs, naive Tconvs and memory Tconvs. The analysis allowed us to define miRNAs characteristic for a general naive phenotype (e.g. miR-92a), a general memory phenotype (e.g. miR-21, miR-155), and most importantly miRNAs specifically expressed in both naive and memory Tregs, defining as such the Treg phenotype (i.e. miR-146a, miR-3162, miR-1202, miR-1246a, and miR-4281). MicroRNA profiling was performed in four CD4+ T-cell subsets: naive Tconventional (CD3+CD8-CD45RO-CD25-), naive Tregulatory (CD3+CD8-CD45RO-CD25+), memory Tconventional (CD3+CD8-CD45RO+CD25-), and memory Tregulatory (CD3+CD8-CD45RO+CD25+) derived from 2 healthy controls, and 6 rheumatoid arthritis patients (total n=8).
2014-01-22 | E-GEOD-50646 | biostudies-arrayexpress
Project description:We performed genome-wide RNA sequencing to analyze gene expression in CD4 and CD8 LN T cells from B6 and FlipFlop mice. We first identified 335 genes in B6 mice that were differentially expressed in CD4 helper and CD8 cytotoxic T cells. Assessment of these genes in FlipFlop mice further revealed that FlipFlop CD4 T cells resembled B6 CD8 T cells, while FlipFlop CD8 T cells resembled B6 CD4 T cells.
2021-02-07 | GSE166296 | GEO
Project description:We show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8- lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper- program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes
2012-12-10 | GSE42277 | GEO
Project description:CD4+ T cells (T helper cells) are cytokine-producing adaptive immune cells that activate or regulate the responses of different immune cells. They are known to play crucial roles in antibody class switching in B cells, neutrophil recruitment and activation of macrophages and CD8+ cytotoxic T cells. The activation and functional status of CD4+ T cells is important for adequate responses to pathogen infections but has also been associated with auto-immune disorders and survival in several cancers. In the current study, we carried out proteomic profiling of resting and activated primary human CD4+ T cells from healthy donors. In addition to identifying known markers of CD4+ T cell activation, we also identified protein kinases, protein phosphatases, and cytokines to be differentially expressed.
2023-01-18 | PXD021250 | Pride
Project description:During a binary cell fate decision, a progeny silences the gene expression program associated with the alternative fate. Helper versus cytotoxic lineage decision in the thymus has been studied as a model for gene silencing of alternative lineage genes, including Cd4. While RUNX3 is required for the initiation of Cd4 silencing, it remains unknown how silenced states of Cd4 and other helper lineage genes are maintained. We show that the histone methyltransferase G9a is necessary for heritable silencing of Cd4 and other helper lineage genes in CD8 T cells. Despite normal Cd4 downregulation during the development, G9a-deficient CD8 T cells fail to maintain silencing of helper lineage genes when they repeatedly divide under non-inflammatory conditions. However, Cd4 depression is prevented during division driven by elevated TCR signaling and an inflammatory cytokine signaling. These results reveal the requirement for G9a in silencing of helper lineage genes in CD8 T cells and also suggest that CD8 T cells employ an alternative mechanism to maintain their cellular identity during immune responses.
2018-03-21 | GSE101730 | GEO