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STAT4 and T-bet control follicular helper T cells development in viral infections

ABSTRACT: STAT4 and T-bet control follicular helper T cells development in viral infections

PROVIDER: PRJNA415458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6203720_1.fastq.gz	Fastqsanger.gz
	SRR6203720_2.fastq.gz	Fastqsanger.gz
	SRR6203721_1.fastq.gz	Fastqsanger.gz
	SRR6203721_2.fastq.gz	Fastqsanger.gz
	SRR6203712_1.fastq.gz	Fastqsanger.gz

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Early T-helper 1 Differentiation Is Marked by A Follicular Helper-like Transition: Differential Roles of STAT4 and T-bet

Project description:Follicular helper T (Tfh) cells comprise an important subset of helper T cells; however, their relationship with other helper lineages is incompletely understood. Herein, we show IL-12 acting via signal transducer and activator of transcription 4 (STAT4) induced both Il21 and Bcl6 genes, generating cells with features of both Tfh and Th1 cells. However, STAT4 also induced T-bet. Using ChIP-seq, we defined the genome-wide targets of T-bet and found that it repressed Bcl6 and other markers of Tfh cells, thereby attenuating the nascent Tfh-like phenotype in the late phase of Th1 specification. Finally, Tfh-like T cells were rapidly generated following Toxoplasma gondii infection in mice, but T-bet constrained Tfh cells expansion and consequent germinal center formation and antibody production. Our data argue that Tfh and Th1 share a transitional stage through the signal mediated by STAT4, which promotes both phenotypes. However, T-bet represses Tfh functionalities, promoting full Th1 differentiation. The roles of STAT4 and T-bet to determine T helper cell fate were investigated by comparing DNA binding profiles of STAT4 and T-bet in Th1 conditions. The functional outcome was further evaluated by profiling DNase hypersensitivity sites and histone epigenetic marks between WT and STAT4-deficient or T-bet-deficient T cells in Th1 conditions.

2011-12-27 | E-GEOD-33802 | biostudies-arrayexpress

STAT4 and T-bet control follicular helper T cells development in viral infections [ATAC-seq]

Project description:Follicular helper T (Tfh) cells promote germinal center (GC) B cell survival and proliferation, and guide their differentiation and Ig isotype switching by delivering contact-dependent and soluble factors, including IL-21, IL-4, IL-9, and IFN-g. IL-21 and IFN-g are co-expressed by Tfh cells during acute and chronic infections, but transcriptional regulation of these cytokines in the GC is incompletely understood. We show that the Th1 transcriptional regulators T-bet and STAT4 are co-expressed with Bcl6 in Tfh cells following acute murine lymphocytic choriomeningitis virus infection, albeit with temporal decline in T-bet expression as the GC response evolved. T-bet was important for Tfh cell production of IFN-g, but not IL-21, and for the generation of a robust germinal center reaction. STAT4, phosphorylated in Tfh cells upon infection, was required for their expression of T-bet and Bcl6, and that of IFN-g and IL-21. These data indicate that T-bet is concomitantly expressed with Bcl6 in Tfh cells and is required alongside STAT4 phosphorylation to coordinate Tfh cell IL-21 and IFN-g production, and for promotion of the GC response following acute viral challenge.

2017-11-22 | GSE105807 | GEO

STAT4 and T-bet control follicular helper T cells development in viral infections [RNA-seq]

2017-11-22 | GSE105806 | GEO

Early T-helper 1 Differentiation Is Marked by A Follicular Helper-like Transition: Differential Roles of STAT4 and T-bet

2011-12-27 | GSE33802 | GEO

STAT4 and T-bet control follicular helper T cells development in viral infections [ATAC-seq]

Project description:STAT4 and T-bet control follicular helper T cells development in viral infections [ATAC-seq]

| PRJNA415459 | ENA

STAT4 and T-bet control follicular helper T cells development in viral infections [RNA-seq]

Project description:STAT4 and T-bet control follicular helper T cells development in viral infections [RNA-seq]

| PRJNA415460 | ENA

STAT4 and T-bet control follicular helper T cell development in viral infections.

Project description:Follicular helper T (Tfh) cells promote germinal center (GC) B cell survival and proliferation and guide their differentiation and immunoglobulin isotype switching by delivering contact-dependent and soluble factors, including IL-21, IL-4, IL-9, and IFN-?. IL-21 and IFN-? are coexpressed by Tfh cells during viral infections, but transcriptional regulation of these cytokines is not completely understood. In this study, we show that the T helper type 1 cell (Th1 cell) transcriptional regulators T-bet and STAT4 are coexpressed with Bcl6 in Tfh cells after acute viral infection, with a temporal decline in T-bet in the waning response. T-bet is important for Tfh cell production of IFN-?, but not IL-21, and for a robust GC reaction. STAT4, phosphorylated in Tfh cells upon infection, is required for expression of T-bet and Bcl6 and for IFN-? and IL-21. These data indicate that T-bet is expressed with Bcl6 in Tfh cells and is required alongside STAT4 to coordinate Tfh cell IL-21 and IFN-? production and for promotion of the GC response after acute viral challenge.

| S-EPMC5748849 | biostudies-literature

Discrete Roles of STAT4 and STAT6 Transcription Factors in Tuning Epigenetic Modifications and Transcription during Helper T Cell Differentiation

Project description:This SuperSeries is composed of the following subset Series: GSE22081: Discrete Roles of STAT4 and STAT6 Transcription Factors in Tuning Epigenetic Modifications and Transcription during Helper T Cell Differentiation (gene expression) GSE22104: Discrete Roles of STAT4 and STAT6 Transcription Factors in Tuning Epigenetic Modifications and Transcription during Helper T Cell Differentiation (ChIP-Seq) Refer to individual Series

2010-06-17 | E-GEOD-22105 | biostudies-arrayexpress

Transcription profiling of mouse vivo follicular helper CD4 T cells (TFH) versus non follicular helper CD4 T cells (non-TFH)

Project description:Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) follicular helper CD4 T cells (CXCR5high),versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection. A paper including data analysis of these experiments has been accepted for publication (Robert J. Johnston et al. Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of follicular helper CD4 T cell differentiation). Experiment Overall Design: Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) follicular helper CD4 T cells (CXCR5high), versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection.

2009-08-07 | E-GEOD-16697 | biostudies-arrayexpress

Discrete Roles of STAT4 and STAT6 Transcription Factors in Tuning Epigenetic Modifications and Transcription during Helper T Cell Differentiation (ChIP-Seq)

Project description:Signal transducer and activator of transcription 4 (STAT4) and STAT6 are key factors in the specification of helper T cells; however, their direct roles in driving differentiation are not well understood. Using chromatin immunoprecipitation and massive parallel sequencing, we quantitated the full complement of STAT-bound genes, concurrently assessing global STAT-dependent epigenetic modifications and gene transcription using cells from cognate STAT-deficient mice. STAT4 and STAT6 each bound over 4000 genes with distinct binding motifs. Both played critical roles in maintaining chromatin configuration and transcription of a core subset of genes through the combination of different epigenetic patterns. Globally, STAT4 had a more dominant role in promoting active epigenetic marks, whereas STAT6 had a more prominent role in antagonizing repressive marks. Clusters of genes negatively regulated by STATs were also identified, highlighting previously unappreciated repressive roles. Therefore, STAT4 and STAT6 play wide regulatory roles in T helper specification. The roles of STAT proteins to shape T helper cell phenotype was investigated by comparing DNA binding profiles of STAT4 and STAT6 in Th1 and Th2 conditions. The functional outcome of STAT bindings was further evaluated by profiling histone epigenetic marks and gene expression changes between WT and STAT-deficient T cells in Th1 and Th2 conditions.

2010-06-18 | E-GEOD-22104 | biostudies-arrayexpress

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