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Brain Behav Immun. 2016 Oct;57:193-199. doi: 10.1016/j.bbi.2016.03.016. Epub 2016 Mar 19.

MiR-30a inhibits Th17 differentiation and demyelination of EAE mice by targeting the IL-21R.

Author information

1
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221004, Jiangsu, China.
2
Department of Neurology, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, Jiangsu, China.
3
Department of Neurology, Xuzhou Central Hospital, Xuzhou 221004, Jiangsu, China.
4
Department of Neurology, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, Jiangsu, China; Institute of Neurological Diseases of Xuzhou Medical College, Xuzhou 221002, Jiangsu, China.
5
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221004, Jiangsu, China. Electronic address: wenxi_yao@163.com.

Abstract

T 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.

KEYWORDS:

Demyelination; IL-21R; MiR-30a; Th17

PMID:
27006279
DOI:
10.1016/j.bbi.2016.03.016
[Indexed for MEDLINE]

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