{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cui K"],"funding":["Intramural NIH HHS","NIGMS NIH HHS"],"pagination":["944-958.e6"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10175192"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["56(5)"],"pubmed_abstract":["Interferon-γ (IFN-γ) is a key cytokine in response to viral or intracellular bacterial infection in mammals. While a number of enhancers are described to promote IFN-γ responses, to the best of our knowledge, no silencers for the Ifng gene have been identified. By examining H3K4me1 histone modification in naive CD4<sup>+</sup> T cells within Ifng locus, we identified a silencer (CNS-28) that restrains Ifng expression. Mechanistically, CNS-28 maintains Ifng silence by diminishing enhancer-promoter interactions within Ifng locus in a GATA3-dependent but T-bet-independent manner. Functionally, CNS-28 restrains Ifng transcription in NK cells, CD4<sup>+</sup> cells, and CD8<sup>+</sup> T cells during both innate and adaptive immune responses. Moreover, CNS-28 deficiency resulted in repressed ty"],"journal":["Immunity"],"pubmed_title":["Restraint of IFN-γ expression through a distal silencer CNS-28 for tissue homeostasis."],"pmcid":["PMC10175192"],"funding_grant_id":["P20 GM121322","ZIA BC011801"],"pubmed_authors":["Ren G","Cui K","Zhu J","Chen Z","Fang D","Hu G","Wei D","Cao Y","Wu C","Liu S","Liu C","Zhao K"],"additional_accession":[]},"is_claimable":false,"name":"Restraint of IFN-γ expression through a distal silencer CNS-28 for tissue homeostasis.","description":"Interferon-γ (IFN-γ) is a key cytokine in response to viral or intracellular bacterial infection in mammals. While a number of enhancers are described to promote IFN-γ responses, to the best of our knowledge, no silencers for the Ifng gene have been identified. By examining H3K4me1 histone modification in naive CD4<sup>+</sup> T cells within Ifng locus, we identified a silencer (CNS-28) that restrains Ifng expression. Mechanistically, CNS-28 maintains Ifng silence by diminishing enhancer-promoter interactions within Ifng locus in a GATA3-dependent but T-bet-independent manner. Functionally, CNS-28 restrains Ifng transcription in NK cells, CD4<sup>+</sup> cells, and CD8<sup>+</sup> T cells during both innate and adaptive immune responses. Moreover, CNS-28 deficiency resulted in repressed ty","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2026-06-01T20:23:35.567Z","creation":"2026-05-20T03:07:48.901Z"},"accession":"S-EPMC10175192","cross_references":{"pubmed":["37040761"],"doi":["10.1016/j.immuni.2023.03.006"]}}