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CUT&RUN for “HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection”

ABSTRACT: CUT&RUN for “HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection”

PROVIDER: PRJNA1262402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33554839_1.fastq.gz	Fastqsanger.gz
	SRR33554839_2.fastq.gz	Fastqsanger.gz
	SRR33554840_1.fastq.gz	Fastqsanger.gz
	SRR33554840_2.fastq.gz	Fastqsanger.gz
	SRR33554841_1.fastq.gz	Fastqsanger.gz

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CUT&RUN for “HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection”

Project description:CD8+ T cell exhaustion is a complex process involving the differentiation of persistently activated CD8+ T cells into functionally distinct cell subsets. Here, we investigated the role of the key epigenetic regulator histone deacetylase 1 (HDAC1) in the differentiation of exhausted T (Tex) cells during chronic viral infection. We uncovered that HDAC1 controls the generation and maintenance of effector-like CX3CR1+ Tex cells in a CD8+ T cell-intrinsic manner. Deletion of HDAC1 led to expansion of an alternative Tex subset characterized by high expression of T cell exhaustion markers, and this was accompanied by elevated viremia. HDAC1 bound to and facilitated an open chromatin state of effector-like signature gene loci in progenitor Tex cells, thereby priming cell fate specification toward the CX3CR1+ Tex subset. Our study un-covers a selective role for HDAC1 in CX3CR1+ Tex subset differentiation, which is essential for controlling viral load during chronic infection.

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HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection

Project description:CD8+ T cell exhaustion is a complex process involving the differentiation of persistently acti-vated CD8+ T cells into functionally distinct cell subsets. Here, we investigated the role of the key epigenetic regulator histone deacetylase 1 (HDAC1) in the differentiation of exhausted T (Tex) cells during chronic viral infection. We uncovered that HDAC1 controls the generation and maintenance of effector-like CX3CR1+ Tex cells in a CD8+ T cell-intrinsic manner. Dele-tion of HDAC1 led to expansion of an alternative Tex subset characterized by high expression of T cell exhaustion markers, and this was accompanied by elevated viremia. HDAC1 bound to and facilitated an open chromatin state of effector-like signature gene loci in progenitor Tex cells, thereby priming cell fate specification toward the CX3CR1+ Tex subset. Our study un-covers a selective role for HDAC1 in CX3CR1+ Tex subset differentiation, which is essential for controlling viral load during chronic infection.

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HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection

Project description:HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection

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HDAC1 regulates effector CD8+ T cell differentiation during chronic viral infection

Project description:Hdac1 is a known epigenetic regulator of gene expression. The aim of this study is to investigate whether Hdac1 influences CD8+ T cell fate during chronic infection. We demonstrate that the genetic ablation of Hdac1 reduces the generation of Tex-Int cells

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ATAC-seq for “HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection”

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scRNA-seq for “HDAC1 controls the generation and maintenance of effector-like CD8+ T cells during chronic viral infection”

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HDAC1 regulates effector CD8+ T cell differentiation during chronic viral infection

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Collateral lethality between HDAC1 and HDAC2 exploits cancer-specific NuRD complex vulnerabilities [Cut & Run]

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