实验性自身免疫性脑脊髓炎
张力素
PTEN公司
下调和上调
自身免疫
生物
免疫学
过继性细胞移植
癌症研究
小RNA
自身免疫性疾病
多发性硬化
T细胞
作者
Li Wang,Rong Qiu,Zhaoyang Zhang,Zhijun Han,Chao Yao,Guojun Hou,Dai Dai,Wenfei Jin,Yuanjia Tang,Xiang Yu,Nan Shen
出处
期刊:ImmunoHorizons
[The American Association of Immunologists]
日期:2020-06-01
被引量:2
标识
DOI:10.4049/immunohorizons.2000008
摘要
Multiple sclerosis is a chronic autoimmune disease driven by pathogenic Th17 cells. In this study, we dissected the role of miR-22 in pathogenic Th17 cells by autoantigen-specific disease models. We first showed that miR-22 was upregulated in peripheral lymphoid organs and spinal cords of mice developed autoimmune encephalomyelitis. Although miR-22 was upregulated in multiple Th cell subsets, it was dispensable for Th cell differentiation in vitro. Whereas miR-22-/- mice exhibited milder symptoms of disease in an active experimental autoimmune encephalomyelitis model, adoptive transfer of miR-22-/- 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 miR-22-deficient pathogenic Th17 cells revealed upregulated genes in phosphatase and tensin homologue (PTEN)-mediated pathways, and Pten was further identified as one of its potential targets. Therefore, we identified that Th17 cell-intrinsic miR-22 could protect mice from autoimmunity by targeting PTEN-regulated pathways.
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