Xuebin Qu, Jun Zhou, Ting Wang, Jingjing Han, Li Ma, Hongli Yu, Deqin Geng, Hongbin Fan, Qingshan Zhang, Fang Hua, Ruiqin Yao
Brain, behavior, and immunity 2016 OctT helper cells 17 (Th17) are recognized as key participants in the pathogenesis of chronic autoimmune diseases such as multiple sclerosis (MS). Regulation of Th17 differentiation is a valuable strategy for diagnosis and treatment of these complicated immune disorders. Here, by genome-wide expression profiling of microRNAs (miRs), we screened miR-30a, whose level was greatly decreased during Th17 differentiation and the process of demyelination disease, both in MS patients and experimental autoimmune encephalomyelitis (EAE) mice. Enforced constitutive expression of miR-30a in naïve T cells inhibited their differentiation into Th17, and in vivo overexpression of miR-30a resulted in fewer Th17 and alleviative EAE. Moreover, target prediction analysis and dual luciferase report assay revealed that interleukin-21 receptor (IL-21R) was a direct target of miR-30a, a finding consistent with the results that miR-30a downregulated the expression of IL-21R, while overexpression of IL-21R alleviated the inhibitory effect of miR-30a on Th17 differentiation. Taken together, our findings imply that miR-30a inhibits Th17 differentiation and the pathogenesis of MS by targeting IL-21R. Copyright © 2016 Elsevier Inc. All rights reserved.
Xuebin Qu, Jun Zhou, Ting Wang, Jingjing Han, Li Ma, Hongli Yu, Deqin Geng, Hongbin Fan, Qingshan Zhang, Fang Hua, Ruiqin Yao. MiR-30a inhibits Th17 differentiation and demyelination of EAE mice by targeting the IL-21R. Brain, behavior, and immunity. 2016 Oct;57:193-199
PMID: 27006279
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