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
- 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: email@example.com.
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.