{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tay RE"],"funding":["Massachusetts Institute of Technology","Dr. Miriam and Sheldon G. Adelson Medical Research Foundation","Dana-Farber/Harvard Cancer Center","NCI NIH HHS","A*STAR","National Institutes of Health","NIAMS NIH HHS"],"pagination":["e20191453"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7336313"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["217(7)"],"pubmed_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 "],"journal":["The Journal of experimental medicine"],"pubmed_title":["Hdac3 is an epigenetic inhibitor of the cytotoxicity program in CD8 T cells."],"pmcid":["PMC7336313"],"funding_grant_id":["P01 CA163222","NCI R01 CA238039","R01 AR043369","R01 AR043369-19","R01 CA222871","R01 CA238039","R01 AR072304"],"pubmed_authors":["Tay RE","Wucherpfennig KW","Long HW","Cejas P","Xie Y","Weng QY","Brown M","Olawoyin O","Fisher DE","Ito Y","Kim HJ","Meyer CA"],"additional_accession":[]},"is_claimable":false,"name":"Hdac3 is an epigenetic inhibitor of the cytotoxicity program in CD8 T cells.","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 ","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jul","modification":"2026-04-18T03:07:44.76Z","creation":"2026-04-18T03:06:29.515Z"},"accession":"S-EPMC7336313","cross_references":{"pubmed":["32374402"],"doi":["10.1084/jem.20191453"]}}