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

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

PROVIDER: PRJNA1132170 | ENA |

REPOSITORIES: ENA

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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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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 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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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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Transcription profiling of mouse naive, effector, memory and exhausted virus-specific CD8 T cells after chronic viral infection

Project description:CD8 T cells normally differentiate from resting naÃ¯ve T cells into function effector and then memory CD8 T cells following acute infections. During chronic viral infections, however, virus-specific CD8 T cells often become exhausted. We used microarrays to examine the gene expression differences between naive, effector, memory and exhausted virus-specific CD8 T cells following lymphocytic choriomeningitis virus infection. Experiment Overall Design: Three or four independent samples were sorted by flow cytometry for each cell type (naive, effector, memory and exhausted) virus-specific CD8 T cells. RNA was extracted and hybridized to Affymetrix microarrays.

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A role of Hdac1 in fate decision to exhausted CD8+ T cells in response to chronic viral infection

Project description:The goal of this study is to determine how an epigenetic regulator, Hdac1, mediates control of exhausted CD8 T cell fate decision and differentiation at the early stage of responses to chronic viral infection.

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Chronic viral infection of naive, effector, memory and exhausted virus-specific CD8 T cells

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