The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways

Multiple sclerosis is a chronic autoimmune disease driven by pathogenic Th17 cells. In this study, we dissected the role of - in pathogenic Th17 cells by autoantigen-specific disease models. We first showed that was upregulated in peripheral lymphoid organs and spinal cords of mice developed autoimm...

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Bibliographic Details
Published in:ImmunoHorizons 2020-06, Vol.4 (6), p.308-318
Main Authors: Wang, Li, Qiu, Rong, Zhang, Zhaoyang, Han, Zhijun, Yao, Chao, Hou, Guojun, Dai, Dai, Jin, Wenfei, Tang, Yuanjia, Yu, Xiang, Shen, Nan
Format: Article
Language:English
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Summary:Multiple sclerosis is a chronic autoimmune disease driven by pathogenic Th17 cells. In this study, we dissected the role of - in pathogenic Th17 cells by autoantigen-specific disease models. We first showed that was upregulated in peripheral lymphoid organs and spinal cords of mice developed autoimmune encephalomyelitis. Although - was upregulated in multiple Th cell subsets, it was dispensable for Th cell differentiation in vitro. Whereas mice exhibited milder symptoms of disease in an active experimental autoimmune encephalomyelitis model, adoptive transfer of 2D2 Th17 cells into naive recipient mice promoted higher disease incidence and severity compared with mice transferred with control 2D2 Th17 cells. Global transcriptional analysis of deficient pathogenic Th17 cells revealed upregulated genes in phosphatase and tensin homologue (PTEN)-mediated pathways, and was further identified as one of its potential targets. Therefore, we identified that Th17 cell-intrinsic could protect mice from autoimmunity by targeting PTEN-regulated pathways.
ISSN:2573-7732
2573-7732
DOI:10.4049/immunohorizons.2000008