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HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS

ABSTRACT: HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS

PROVIDER: PRJNA601171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10885500.fastq.gz	Fastqsanger.gz
	SRR10885501.fastq.gz	Fastqsanger.gz
	SRR10885502.fastq.gz	Fastqsanger.gz
	SRR10885503.fastq.gz	Fastqsanger.gz
	SRR10885504.fastq.gz	Fastqsanger.gz

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HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS [RNA-seq]

Project description:Cytotoxic T cells play a key role in adaptive immunity by killing infected or cancerous cells. While the transcriptional control of CD8 T cell differentiation and effector function following T cell activation has been extensively studied, little is known about epigenetic regulation of these processes. Here we show that the histone deacetylase HDAC3 inhibits CD8 T cell cytotoxicity early during activation and is required for persistence of activated CD8 T cells following resolution of an acute infection. Mechanistically, HDAC3 inhibits gene programs associated with cytotoxicity and effector differentiation of CD8 T cells including genes encoding essential cytotoxicity proteins and key transcription factors. These data identify HDAC3 as an epigenetic regulator of the CD8 T cell cytotoxicity program.

2020-04-22 | GSE143643 | GEO

HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS [ChIP-seq]

2020-04-22 | GSE143642 | GEO

HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS [ChIP-seq]

Project description:HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS [ChIP-seq]

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HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS [RNA-seq]

Project description:HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS [RNA-seq]

| PRJNA601173 | ENA

Hdac3 is an epigenetic inhibitor of the cytotoxicity program in CD8 T cells.

| S-EPMC7336313 | biostudies-literature

HDAC3 requirement for the inflammatory gene expression program in macrophages

Project description:This SuperSeries is composed of the following subset Series: GSE33162: HDAC3 requirement for the inflammatory gene expression program in macrophages [gene expression] GSE33163: HDAC3 requirement for the inflammatory gene expression program in macrophages [ChIP_Seq] Refer to individual Series

2012-07-08 | E-GEOD-33164 | biostudies-arrayexpress

HDAC3 requirement for the inflammatory gene expression program in macrophages [ChIP_Seq]

Project description:Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents. Chromatin immuno-precipitations of H4 histone pan-acetylation followed by multiparallel sequencing performed in murine bone marrow-derive macrophages. Experiments carried out in untreated cells as well as in cells treated for 4hrs with lipopolysaccharide (LPS), for both HDAC3 +/- (wt) and HDAC3 -/- (KO) mice.

2012-07-08 | E-GEOD-33163 | biostudies-arrayexpress

HDAC3 requirement for the inflammatory gene expression program in macrophages [gene expression]

Project description:Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents. Gene expression profiles for bone marrow-derived macrophages from either HDAC3 +/- (wt) or HDAC3 -/- (KO). Cells were left untreated or challenged with lipopolysaccharide (LPS) for 4hrs. Each genotype-treatment combination was performed in triplicate.

2012-07-08 | E-GEOD-33162 | biostudies-arrayexpress

HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS

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

2020-04-22 | GSE143644 | GEO

HDAC3 requirement for the inflammatory gene expression program in macrophages

Project description:HDAC3 requirement for the inflammatory gene expression program in macrophages

| PRJNA149173 | ENA