Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA279262 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
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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 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.
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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.
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