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miRNAs Alter T Helper 17 Cell Fate in the Pathogenesis of Autoimmune Diseases

期刊

FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.593473

关键词

miRNAs; T helper 17 cell; systemic lupus erythematosus; rheumatoid arthritis; multiple sclerosis; inflammatory bowel disease; autoimmune disease

资金

  1. Medical Guide Project from Science and Technology Commission of Shanghai Municipality (CN) [20ZR1411500, 19411962500]
  2. National Natural Science Foundation of China [82073436]
  3. Outstanding Youth Medical Talents of Shanghai (Rising Stars of Medical Talent) Youth Development Program
  4. Zhuoxue Plan of Fudan University

向作者/读者索取更多资源

Th17 cells play a crucial role in the immune response against bacterial and fungal infections, but excessive IL-17 production can lead to immunopathology and inflammatory autoimmune diseases. Understanding the regulation of Th17 cells by miRNAs has enhanced our knowledge of their function in immune response and disease, including recent advances in miRNA-mediated dysregulation of Th17 cell fate in autoimmune diseases.
T helper 17 (Th17) cells are characterized by the secretion of the IL-17 cytokine and are essential for the immune response against bacterial and fungal infections. Despite the beneficial roles of Th17 cells, unrestrained IL-17 production can contribute to immunopathology and inflammatory autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. Although these diverse outcomes are directed by the activation of Th17 cells, the regulation of Th17 cells is incompletely understood. The discovery that microRNAs (miRNAs) are involved in the regulation of Th17 cell differentiation and function has greatly improved our understanding of Th17 cells in immune response and disease. Here, we provide an overview of the biogenesis and function of miRNA and summarize the role of miRNAs in Th17 cell differentiation and function. Finally, we focus on recent advances in miRNA-mediated dysregulation of Th17 cell fate in autoimmune diseases.

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