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

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

PROVIDER: PRJNA765390 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16016176_1.fastq.gz	Fastqsanger.gz
	SRR16016176_2.fastq.gz	Fastqsanger.gz
	SRR16016177_1.fastq.gz	Fastqsanger.gz
	SRR16016177_2.fastq.gz	Fastqsanger.gz
	SRR16016178.fastq.gz	Fastqsanger.gz

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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.

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

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

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

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

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

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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

Migratory DCs activate TGF-β to precondition naïve CD8+ T cells for tissue-resident memory fate

Project description:Epithelial resident memory T (eTRM) cells serve as sentinels in barrier tissues to guard against previously encountered pathogens. How eTRM cells are generated has important implications for efforts to elicit their formation through vaccination or prevent it in autoimmune disease. Here, we show that during immune homeostasis, the cytokine transforming growth factor β (TGF-β) epigenetically conditions resting naïve CD8+ T cells and prepares them for the formation of eTRM cells in a mouse model of skin vaccination. Naïve T cell conditioning occurs in lymph nodes (LNs), but not in the spleen, through major histocompatibility complex class I–dependent interactions with peripheral tissue–derived migratory dendritic cells (DCs) and depends on DC expression of TGF-β–activating αV integrins. Thus, the preimmune T cell repertoire is actively conditioned for a specialized memory differentiation fate through signals restricted to LNs.

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Comparative analysis reveals a role for TGF-β in shaping the residency-related transcriptional signature in tissue-resident memory CD8+ T cells

Project description:Tissue-resident CD8+ memory T (TRM) cells are immune cells that permanently reside at tissue sites where they play an important role in providing rapid protection against reinfection. They are not only phenotypically and functionally distinct from their circulating memory counterparts, but also exhibit a unique transcriptional profile. To date, the local tissue signals required for their development and long-term residency are not well understood. So far, the best-characterised tissue-derived signal is transforming growth factor-β (TGF-β), which has been shown to promote the development of these cells within tissues. In this study, we aimed to determine to what extent the transcriptional signatures of TRM cells from multiple tissues reflects TGF-β imprinting. We activated murine CD8+ T cells, stimulated them in vitro by TGF-β, and profiled their transcriptomes using RNA-seq. Upon comparison, we identified a TGF-β-induced signature of differentially expressed genes between TGF-β-stimulated and -unstimulated cells. Next, we linked this in vitro TGF-β-induced signature to a previously identified in vivo TRM-specific gene set and found considerable (>50%) overlap between the two gene sets, thus showing that a substantial part of the TRM signature can be attributed to TGF-β signalling. Finally, gene set enrichment analysis further revealed that the altered gene signature following TGF-β exposure reflected transcriptional signatures found in TRM cells from both epithelial and non-epithelial tissues. In summary, these findings show that TGF-β has a broad footprint in establishing the residency-specific transcriptional profile of TRM cells, which is detectable in TRM cells from diverse tissues. They further suggest that constitutive TGF-β signaling might be involved for their long-term persistence at tissue sites.

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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

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