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Deletion of\n            <jats:italic toggle=\"yes\">Clns1a<\/jats:italic>\n            in T cells resulted in DNA damage, cell cycle arrest, impaired T cell proliferation, and effector function, thereby protecting mice from both EAE and IBD. We found that CLNS1A interacts with protein arginine methyl transferase 5 (PRMT5). Moreover, CLNS1A regulates symmetric histone dimethylation and the expression of genes involved in DNA repair, replication, and cell cycle progression. Thus, CLNS1A plays an important role in CD4 T cells by promoting genome stability and cell cycle progression.\n          <\/jats:p>","DOI":"10.1126\/sciimmunol.adq8860","type":"journal-article","created":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T17:58:17Z","timestamp":1750442297000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":6,"title":["CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-1666-4058","authenticated-orcid":true,"given":"Liwei","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pathology, New York University Grossman School of Medicine, New York, NY, 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