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Fli1 as transcriptional safeguard that restrains effector CD8 T cell differentiation

ABSTRACT: Fli1 as transcriptional safeguard that restrains effector CD8 T cell differentiation

PROVIDER: PRJNA630251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11685204_1.fastq.gz	Fastqsanger.gz
	SRR11685204_2.fastq.gz	Fastqsanger.gz
	SRR11685205_1.fastq.gz	Fastqsanger.gz
	SRR11685205_2.fastq.gz	Fastqsanger.gz
	SRR11685206_1.fastq.gz	Fastqsanger.gz

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In vivo CRISPR screening identifies Fli1 as transcriptional safeguard that restrains effector CD8 T cell differentiation [RNA-seq]

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In vivo CRISPR screening identifies Fli1 as transcriptional safeguard that restrains effector CD8 T cell differentiation [RNA-seq]

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Fli1 as transcriptional safeguard that restrains effector CD8 T cell differentiation

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ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.

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Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. P14 TCR transgenic CD8+ T cells from wild-type or BATF-/- mice were examined either as naÃ¯ve cells or after 3 days of in vitro stimulation with antibodies to CD3 and CD28 in the presence of IL-2

2014-03-02 | E-GEOD-54215 | biostudies-arrayexpress

Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs

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Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs

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Project description:Transcriptome analyses of naive, effector and memory CD8 TCRP1A lymphocytes expressing or not an active form of the transcription factor Stat5. TCRP1A CD8 T lymphocytes were activated by their cognate Ag for 72h to induce their differentiation in effector T cells (TCRP1A eTL 72h: 4 replicates S1, S2, S3, S4). In some samples, an active form of Stat5 was introduced (TCRP1A Stat5ca eTL 72h: 2 replicates S9, S10). These 72h activated T cells were either purified and analyzed directly (samples mentioned above) or injected in congeneic hosts and recovered more than 20 days later from the host spleen and lymph nodes: TCRP1A eTL >d20: 2 replicates– S30, S32; TCRP1A Stat5ca eTL >d20: 4 replicates S11, S12, S13, S14). Naive TCRP1A CD8 T lymphocytes (TCRP1A-naive: 4 replicates S33, S34, S35, S36) are included as controls. TCRP1A CD8 T lymphocytes were activated by anti-CD3/CD28. After 24h, an active form of Stat5 was introduced in activated cells. Culture was continued for another 48h to induce their differentiation in effector T cells. These 72h activated T cells were either directly injected in congeneic hosts and recovered more than 14 days later from the host spleen and lymph nodes: T-BetKO Stat5ca >d14: 3 replicates S39, S40, S41.

2013-09-13 | E-GEOD-26945 | biostudies-arrayexpress

Gene expression profiles of human effector CD8+ T cell subsets

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.

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