2. Academic Validation
  3. MiR-29a/b Suppresses CD8+ T Cell Effector Function and Intestinal Inflammation

MiR-29a/b Suppresses CD8+ T Cell Effector Function and Intestinal Inflammation

  • Exploration (Beijing). 2025 Jun 10;5(4):20240363. doi: 10.1002/EXP.20240363.
Yingying Lin 1 2,  Yuqi Wang 1,  Yuning Zhang 1,  Yao Lu 1,  Juan Chen 2,  Yongting Luo 2,  Jian He 3,  Qingfeng Luo 4,  Heng Quan 2,  Weiru Yu 2,  Yujia Luo 2,  Peng Xue 1,  Yi Xue 2,  Xiaoya Lin 2,  Rui Ding 2,  Lining Chen 1,  Yiran Wang 2,  Zenghui Xia 1,  Liang Zhao 1,  Hao Zhang 1,  Ran Wang 2,  Qingyu Wang 2,  Xifan Wang 5,  Jiaqi Su 6,  Fazheng Ren 2,  Cong Lv 2,  Yixuan Li 2,  Huiyuan Guo 1 2 3
Affiliations

Affiliations

  • 1 College of Food Science and Nutritional Engineering China Agricultural University Beijing China.
  • 2 Key Laboratory of Functional Dairy, Department of Nutrition and Health China Agricultural University Beijing China.
  • 3 Nutrition and Health Research Center National Center of Technology Innovation for Dairy Hohhot China.
  • 4 Department of Gastroenterology, Beijing Hospital, National Center of Gerontology Institute of Geriatric Medicine, Chinese Academy of Medical Science Beijing China.
  • 5 Department of Obstetrics and Gynecology Columbia University New York New York USA.
  • 6 Department of Health Sciences and Technology ETH Zurich Zurich Switzerland.
PMID: 40873647 DOI: 10.1002/EXP.20240363
Abstract

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.

Keywords

CD8+ T cell; Ifng‐JAK‐STAT; differentiation; miR‐29a/b; ulcerative colitis.

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