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Similarly, the posttranscriptional regulation of the highly heterogenic CD8<jats:sup>+<\/jats:sup> T cell populations and their effector function in IBD also remains poorly understood. Here, we find that <jats:italic>miR\u201029a<\/jats:italic> and <jats:italic>\u201029b (miR\u201029a\/b<\/jats:italic>) regulate T cell fate, and their expression is higher near damaged colon tissue in patients with IBD compared to controls. In mice, we find that <jats:italic>miR\u201029a\/b<\/jats:italic> suppresses the differentiation of CD8<jats:sup>+<\/jats:sup> T cells and the secretion of pro\u2010inflammatory and chemotactic factors during severe colitis by inhibiting transcriptional pathways, including those involving the T cell receptor and JAK\u2010STAT signaling. Furthermore, we identify <jats:italic>Ifng<\/jats:italic>, an inflammatory factor that drives immune response and the reshaping of CD8<jats:sup>+<\/jats:sup> T cell fate, as a potential target of the miRNAs. Finally, we show that delivery of miR\u201029 mimics to the colon of mice is sufficient to alleviate DSS\u2010induced inflammation. Together, these data show that <jats:italic>miR\u201029<\/jats:italic> plays an important role in suppressing T cell overactivation during inflammatory diseases.<\/jats:p>","DOI":"10.1002\/exp.20240363","type":"journal-article","created":{"date-parts":[[2025,6,12]],"date-time":"2025-06-12T11:05:26Z","timestamp":1749726326000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["<i>MiR\u201029a\/b<\/i> Suppresses CD8<sup>+<\/sup> T Cell Effector Function and Intestinal Inflammation"],"prefix":"10.1002","volume":"5","author":[{"given":"Yingying","family":"Lin","sequence":"first","affiliation":[{"name":"College of Food Science and Nutritional Engineering China Agricultural University  Beijing China"},{"name":"Key Laboratory of Functional Dairy, Department of Nutrition and Health China Agricultural University  Beijing 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