Linc‐MAF‐4 regulates Th1/Th2 differentiation and is associated with the pathogenesis of multiple sclerosis by targeting MAF. Issue 2 (18th October 2016)

• Record Type: Journal Article
• Authors: Zhang, Fang; Liu, Guiyou; Wei, Changjuan; Gao, Chao; Hao, Junwei
• Is Part Of: FASEB journal. Volume 31:Issue 2(2017)
• Page Start: 519
• Page End: 525
• Publication Date: 2016-10-18
• Subjects: CD4+ T cell -- long noncoding RNAs -- autoimmune diseases; Biology -- Periodicals; Biology, Experimental -- Periodicals; 570
• DOI: 10.1096/fj.201600838R
• Languages: English
• ISSNs: 0892-6638

Abstract

ABSTRACT: 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 (Th )1‐cell differentiation in patients with MS. Transfection of synthetic linc‐MAF‐4 into naive CD4 + T cells facilitated Th 1‐cell differentiation and inhibited Th 2‐cell differentiation by directly inhibiting MAF, which is a Th 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 Th1/Th2 differentiation and is associated with the pathogenesis of multiple sclerosis by targeting MAF. FASEB J. 31, 519–525 (2017). http://www.fasebj.org