{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shan Q"],"funding":["BLRD VA","U.S. Department of Health &amp; Human Services | NIH | National Institute of Allergy and Infectious Diseases","NIAID NIH HHS","U.S. Department of Veterans Affairs"],"pagination":["1222-1235"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9579964"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(8)"],"pubmed_abstract":["CD8<sup>+</sup> T cell homeostasis is maintained by the cytokines IL-7 and IL-15. Here we show that transcription factors Tcf1 and Lef1 were intrinsically required for homeostatic proliferation of CD8<sup>+</sup> T cells. Multiomics analyses showed that Tcf1 recruited the genome organizer CTCF and that homeostatic cytokines induced Tcf1-dependent CTCF redistribution in the CD8<sup>+</sup> T cell genome. Hi-C coupled with network analyses indicated that Tcf1 and CTCF acted cooperatively to promote chromatin interactions and form highly connected, dynamic interaction hubs in CD8<sup>+</sup> T cells before and after cytokine stimulation. Ablating CTCF phenocopied the proliferative defects caused by Tcf1 and Lef1 deficiency. Tcf1 and CTCF controlled a similar set of genes that regulated cell c"],"journal":["Nature immunology"],"pubmed_title":["Tcf1-CTCF cooperativity shapes genomic architecture to promote CD8<sup>+</sup> T cell homeostasis."],"pmcid":["PMC9579964"],"funding_grant_id":["R01 AI121080","BX005771","R01 AI112579","I01 BX005771","AI112579","AI121080","AI139874","R01 AI139874"],"pubmed_authors":["Yuan S","Li X","Xue HH","Liu J","Peng W","Shan Q","Chen X","Zhu S"],"additional_accession":[]},"is_claimable":false,"name":"Tcf1-CTCF cooperativity shapes genomic architecture to promote CD8<sup>+</sup> T cell homeostasis.","description":"CD8<sup>+</sup> T cell homeostasis is maintained by the cytokines IL-7 and IL-15. Here we show that transcription factors Tcf1 and Lef1 were intrinsically required for homeostatic proliferation of CD8<sup>+</sup> T cells. Multiomics analyses showed that Tcf1 recruited the genome organizer CTCF and that homeostatic cytokines induced Tcf1-dependent CTCF redistribution in the CD8<sup>+</sup> T cell genome. Hi-C coupled with network analyses indicated that Tcf1 and CTCF acted cooperatively to promote chromatin interactions and form highly connected, dynamic interaction hubs in CD8<sup>+</sup> T cells before and after cytokine stimulation. Ablating CTCF phenocopied the proliferative defects caused by Tcf1 and Lef1 deficiency. Tcf1 and CTCF controlled a similar set of genes that regulated cell c","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-10T06:51:50.137Z","creation":"2025-02-19T03:25:54.521Z"},"accession":"S-EPMC9579964","cross_references":{"pubmed":["35882936"],"doi":["10.1038/s41590-022-01263-6"]}}