MicroRNA-155 modulates Th1 and Th17 cell differentiation and is associated with multiple sclerosis and experimental autoimmune encephalomyelitis

Jing Zhang  ¹ , Ye Cheng  ¹ , Wei Cui  ¹ , Meixi Li  ¹ , Bin Li  ¹ , Li Guo  ²

Affiliations

• ¹ The Department of Neurology of the Second Hospital of Hebei Medical University, China.
• ² The Department of Neurology of the Second Hospital of Hebei Medical University, China. Electronic address: docshuangq@126.com.

Abstract

Mammalian noncoding microRNAs (miRNAs) are suggested to be involved in immune system function. We found that miR-155 expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). Knockdown of miR-155 resulted in low Th1 and Th17 cells and mild EAE, and its overexpression led to more Th1 and Th17 cells and severe EAE. MiR-155 promoted the development of inflammatory Th17/Th1 cell subsets. These findings demonstrate that miR-155 confers susceptibility to EAE by affecting inflammatory T cell responses and can be a new target for therapy of multiple sclerosis.

Keywords: Experimental autoimmune encephalomyelitis; MicroRNAs; Multiple sclerosis; Th1 cells; Th17 cells.