Premium
Linc‐MAF‐4 regulates T h 1/T h 2 differentiation and is associated with the pathogenesis of multiple sclerosis by targeting MAF
Author(s) -
Zhang Fang,
Liu Guiyou,
Wei Changjuan,
Gao Chao,
Hao Junwei
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201600838r
Subject(s) - pathogenesis , gene knockdown , peripheral blood mononuclear cell , multiple sclerosis , immunology , t cell , biology , microbiology and biotechnology , in vitro , cell culture , immune system , genetics
In this study, we strove to substantiate the ability of linc-MAF-4 to act as a regulator of pathogenesis during multiple sclerosis (MS). We recruited 34 patients who were diagnosed with MS according to the revised McDonald criteria. Six patients with MS and 5 healthy volunteers contributed peripheral blood mononuclear cells for microarray analysis. Subsequent knockdown and overexpression of linc-MAF-4 in naive CD4 + T cells from the additional 28 patients with MS was performed to track changes in CD4 + T-cell subsets and their function, as well as to confirm results from the prior microarray analysis. Expression of linc-MAF-4 increased significantly in peripheral blood mononuclear cells of patients with MS compared with those of control participants. In addition, linc-MAF-4 regulated encephalitogenic T helper (T h )1-cell differentiation in patients with MS. Transfection of synthetic linc-MAF-4 into naive CD4 + T cells facilitated T h 1-cell differentiation and inhibited T h 2-cell differentiation by directly inhibiting MAF, which is a T h 2-cell transcription factor. Linc-MAF-4 also promoted activation of CD4 + T cells from patients with MS. Expression level of linc-MAF-4 correlated with the annual relapse rate in patients with MS. Our results suggest that linc-MAF-4 is involved in the pathogenesis of MS, specifically via regulation of encephalitogenic T cells.-Zhang, F., Liu, G., Wei, C., Gao, C., Hao, J. Linc-MAF-4 regulates T h 1/T h 2 differentiation and is associated with the pathogenesis of multiple sclerosis by targeting MAF.