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MiR‐29a/b Suppresses CD8+ T Cell Effector Function and Intestinal Inflammation
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MiR‐29a/b Suppresses CD8+ T Cell Effector Function and Intestinal Inflammation
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Journal Article
MiR‐29a/b Suppresses CD8+ T Cell Effector Function and Intestinal Inflammation
2025
Overview
The role of CD8+ T cells in the pathogenesis of ulcerative colitis (UC) remains unclear. Similarly, the posttranscriptional regulation of the highly heterogenic CD8+ T cell populations and their effector function in IBD also remains poorly understood. Here, we find that miR‐29a and ‐29b (miR‐29a/b) 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 miR‐29a/b suppresses the differentiation of CD8+ T cells and the secretion of pro‐inflammatory and chemotactic factors during severe colitis by inhibiting transcriptional pathways, including those involving the T cell receptor and JAK‐STAT signaling. Furthermore, we identify Ifng, an inflammatory factor that drives immune response and the reshaping of CD8+ T cell fate, as a potential target of the miRNAs. Finally, we show that delivery of miR‐29 mimics to the colon of mice is sufficient to alleviate DSS‐induced inflammation. Together, these data show that miR‐29 plays an important role in suppressing T cell overactivation during inflammatory diseases. Our findings suggest that miR‐29a/b is a critical regulator of CD8+ T cells, possibly via the Ifng‐JAK‐STAT signal in IBD patients and the upregulation of miR‐29a/b relieves the development of significant inflammation in the colon of DSS‐induced colitis‐affected mice.
