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Ets1 suppresses the expression of key TFH genes to block TFH differentiation

ABSTRACT: Ets1 suppresses the expression of key TFH genes to block TFH differentiation

PROVIDER: PRJNA434187 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6726040_1.fastq.gz	Fastqsanger.gz
	SRR6726040_2.fastq.gz	Fastqsanger.gz
	SRR6726050_1.fastq.gz	Fastqsanger.gz
	SRR6726050_2.fastq.gz	Fastqsanger.gz
	SRR6726051_1.fastq.gz	Fastqsanger.gz

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Ets1 modulates epigentic landscape of key TFH genes in T naïve cells

Project description:Ets1 can directly bind key TFH genes, regulating their expression . Loss of Ets1 results in the pre-mature expression of TFH-genes in Non-TFH cells. We wished to analyze if loss of Ets1 correlated with changes in chromatin accessibility especially in TFH gene loci.

2019-03-03 | GSE110594 | GEO

Upregulation of TFH profile in absence of Ets1 expression

Project description:To characterize the effect of loss of Ets1 in Non-TFH and TFH cells, we performed gene expression RNAseq analysis for T follicular helper (TFH) and Non-T follicular helper (Non-TFH) cells in WT (Ets1 fl/fl) and Ets1 KO (CD4-cre Ets1 fl/fl) mice.

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Ets1 modulates epigentic landscape of key TFH genes in T naïve cells

Project description:Ets1 modulates epigentic landscape of key TFH genes in T naïve cells

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Ets1 suppresses the expression of key TFH genes to block TFH differentiation

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

2019-03-03 | GSE110647 | GEO

Upregulation of TFH profile in absence of Ets1 expression

Project description:Upregulation of TFH profile in absence of Ets1 expression

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Ets1 suppresses adipose beiging process via bidirectional regulation of mitochondrial biogenesis and clearance

Project description:Beige adipocytes accumulates mitochondria and alleviates metabolic disorder via activating energy expenditure. Whether the opposing process of mitochondrial biogenesis and clearance are integrated regulated in beige adipocytes is beyond known. Here we show that DNA binding protein Ets1 suppresses beige adipocyte formation via bidirectional regulation of mitochondrial biogenesis and clearance. The expression level of Ets1 was down-regulated in browning adipocytes, and up-regulated in the subcutaneous fat of obese mice. Adipocyte Ets1 heterozygous knock-in mice showed suppressed beige adipocytes formation under cold stress, while the homozygous knock-in mice are cold intolerance. On the other hand, knocking out Ets1 in adipocytes enhanced energy expenditure and protect the mice from high fat diet induced metabolic disorders. Mechanical assay suggests Ets1 binds to the promoter region of mitochondria complex coding genes and autophagy related genes, transcriptionally suppresses mitochondrial biogenesis and activates its clearance. Our results indicate that Ets1 integrally regulates the balance of mitochondria generation and degradation, hence acts as a pivotal governor of mitochondria content and negatively regulates beige adipocyte formation.

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Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses

Project description:Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses

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M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

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Gene expression analysis of Ets1-/- CD4+ CD8+ thymocytes

Project description:We performed ChIP-Seq for hallmark TFs (Ets1, Runx1), histone modification marks (H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3), total RNA Pol II, short RNA-Seq as well as nucleosome mapping mainly in murine Rag2 -/- thymocytes. We also performed ChIP-Seq for E47 as well as nucleosome mapping, gene expression microarray analysis in CD4+ CD8+ WT and Ets1-/- DP thymocytes. Overall, we find a key role for the transcription factor Ets1, contributing towards alpha beta T cell lineage commitment via differential transactivation of stage-specific genes orchestrated by dynamic, co-association -mediated chromatin remodeling, as well as transcription dependent generation of a specialized chromatin structure at the TCR beta locus. Genome-wide analysis via ChIP-Seq for Ets1, Runx1, total RNA Pol II binding, H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3, short RNA-Seq, Mnase-Seq in murine Rag2 -/- thymocytes, ChIP-Seq for E47, Mnase-Seq and gene expression microarray analysis in DP thymocytes Gene expression analysis of Ets1-/- CD4+ CD8+ thymocytes

2015-12-19 | E-GEOD-73849 | biostudies-arrayexpress

Expression Data from in vivo Tfh vs GC Tfh vs non-Tfh

Project description:CD4 T cell help is critical for both the generation and maintenance of germinal centers, and T follicular helper (TFH) cells are the CD4 T cell subset required for this process. SAP (SH2D1A) expression in CD4 T cells is essential for germinal center development. However, SAP-deficient mice have only a moderate defect in TFH differentiation as defined by common TFH surface markers. CXCR5+ TFH cells are found within the germinal center as well as along the boundary regions of T/B cell zones. Here we show that germinal center associated T cells (GC TFH) can be identified by their co-expression of CXCR5 and the GL7 epitope, allowing for phenotypic and functional analysis of TFH and GC TFH populations. Here we show GC TFH are a functionally discrete subset of further polarized TFH cells, with enhanced B cell help capacity and a specialized ability to produce IL-4 in a TH2-independent manner. Strikingly, SAP-deficient mice have an absence of the GC TFH subset and SAP- TFH are defective in IL-4 and IL-21 production. We further demonstrate that SLAM (Slamf1, CD150), a surface receptor that utilizes SAP signaling, is specifically required for IL-4 production by GC TFH. GC TFH cells require IL-4 and IL-21 production for optimal help to B cells. These data illustrate complexities of SAP-dependent SLAM family receptor signaling, revealing a prominent role for SLAM receptor ligation in IL-4 production by germinal center CD4 T cells but not in TFH and GC TFH differentiation. Analysis of in vivo polyclonal GC Tfh vs Tfh vs Non-Tfh eight days after LCMV viral infection. Analysis of in vivo follicular helper CD4 T cells (CXCR5high GL7low), versus germinal center follicular helper CD4 T cells (CXCR5hi GL7hi), versus non-follicular helper CD4 T cells (CXCR5low) eight days after viral infection.

2010-04-28 | E-GEOD-21380 | biostudies-arrayexpress

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