Abstract
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 Tay et al.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylation / drug effects
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Acrylamides / pharmacology
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Animals
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Antigens / metabolism
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Base Sequence
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CD8-Positive T-Lymphocytes / drug effects
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CD8-Positive T-Lymphocytes / immunology*
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Core Binding Factor Alpha 3 Subunit / metabolism
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Epigenesis, Genetic* / drug effects
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Histone Deacetylase Inhibitors / pharmacology
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Histone Deacetylases / deficiency
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Histone Deacetylases / metabolism*
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Histones / metabolism
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Lymph Nodes / drug effects
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Lymph Nodes / metabolism
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Lymphocyte Activation / drug effects
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Lymphocyte Activation / immunology
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Lymphocytic choriomeningitis virus / physiology
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Lysine / metabolism
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Mice, Inbred C57BL
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Mice, Knockout
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Phenotype
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Phenylenediamines / pharmacology
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Positive Regulatory Domain I-Binding Factor 1 / metabolism
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T-Lymphocytes, Cytotoxic* / drug effects
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Transcription, Genetic / drug effects
Substances
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Acrylamides
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Antigens
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Core Binding Factor Alpha 3 Subunit
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Histone Deacetylase Inhibitors
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Histones
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Phenylenediamines
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Prdm1 protein, mouse
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RGFP966
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Positive Regulatory Domain I-Binding Factor 1
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Histone Deacetylases
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histone deacetylase 3
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Lysine