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T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation [ATAC-seq]

ABSTRACT: T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation [ATAC-seq]

PROVIDER: PRJNA765391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16016168.fastq.gz	Fastqsanger.gz
	SRR16016169.fastq.gz	Fastqsanger.gz
	SRR16016170.fastq.gz	Fastqsanger.gz
	SRR16016171.fastq.gz	Fastqsanger.gz
	SRR16016172.fastq.gz	Fastqsanger.gz

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T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation.

Project description:T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation.

| PRJNA765387 | ENA

T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation [ATAC-seq]

Project description:TGF-beta signaling is required for the differentiation of gut-resident memory CD8 T cells. Here, we showed that the deficiency of transcription factor T-bet partially rescued the differentiation of TGF-beta receptor deficient gut-resident memory CD8 T cells.

2021-10-06 | GSE184628 | GEO

T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation [RNA-seq]

2021-10-06 | GSE184627 | GEO

T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation [RNA-seq]

Project description:T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation [RNA-seq]

| PRJNA765390 | ENA

T-bet deficiency and Hic1 induction override TGF-b-dependency in the formation of CD103+ intestine-resident memory CD8+ T cells

2024-03-10 | GSE260630 | GEO

T-bet Suppresses TGF-b-independent Gut-resident Memory CD8+ T Cell Differentiation.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-10-06 | GSE184629 | GEO

BET bromodomain inhibition suppresses TH17-mediated pathology

Project description:IL-17-producing T helper (TH17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine TH17 differentiation from naM-CM-/ve CD4+ T cells, as well as in the activation of previously differentiated TH17 cells. We provide evidence that BET controls TH17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector TH17-associated cytokines, including IL17, IL21 and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in TH17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in TH17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and TH17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions. 4 samples were analyzed: two conditions in duplicate. Naive T cells were placed in conditions leading to TH17 differentiation, with and without BET inhibitor. RNA was collected at 48 hours.

2013-09-20 | E-GEOD-37270 | biostudies-arrayexpress

T-bet-depended but IFN-gamma-independent genes in GVHD

Project description:Given T-bet is a master regulator for Th1 differentiation that produce IFN-gamma, underlining mechanisms accounted for the distinct GVHD outcomes caused by T-bet- versus IFN-gamma-deficient donor T cells are unclear. We hypothesize that GVHD is regulated by T-bet-dependent but IFN-gamma-independent molecules. To identify these molecules, we isolated donor T cells from spleen cells of the recipients that were transplanted with WT, T-bet-/- or IFN-gamma-/- CD4 T cells for 7 days. The gene profile of isolated T cells was measured by microarray analysis using GeneChip Mouse Genome 430 2.0 arrays (Affymetrix) according to the manufacturerM-^Rs instructions. Array images were analyzed and processed by robust multi-array average (RMA) procedure.

2014-10-30 | E-MTAB-2198 | biostudies-arrayexpress

BET Bromodomain Inhibition Blocks the Function of a Critical AR-Independent Master Regulator Network in Lethal Prostate Cancer

Project description:BET bromodomain inhibitors are known to block prostate cancer cell survival through suppression of c-Myc and androgen receptor (AR) function. However, little is known about other transcriptional modulators whose function is blocked by these drugs and the anti-tumor activity of BET bromodomain inhibition in AR-independent castration-resistant prostate cancers (CRPC), whose frequency may be increasing. In this study we determined that BET bromodomain inhibition suppresses survival of a diverse set of CRPC cell models, including those that do not express the AR or in which c-Myc is not suppressed. To identify additional transcriptional regulators whose suppression contributes to the anti-tumor effects of BET bromodomain inhibition, we treated multiple CRPC cell lines with the BET bromodomain inhibitor JQ1, measured genome-wide gene expression changes, and then used the Master Regulator Inference Algorithm (MARINa). This approach identified transcriptional regulators whose function is blocked by JQ1 and whose suppression recapitulates the effects of BET bromodomain inhibition. High Expression of these Master Regulators in aggressive human CRPC demonstrates their clinical relevance.

2019-03-20 | GSE98069 | GEO

FOXA1 suppresses cancer immunity independent of DNA binding

Project description:FOXA1 suppresses cancer immunity independent of DNA binding

| PRJNA596242 | ENA