miR-485 regulates Th17 generation and pathogenesis in experimental autoimmune encephalomyelitis through targeting STAT3

• DOI: 10.1016/j.jneuroim.2023.578100
• Publication Date: 2023-05-04T15:37:20Z
• Authors: Yumei Xue; Lu Zhang; Ruoyi Guo; Xi Shao; Mengya Shi; Congcong Yuan; Xiaobing Li; Bin Li
• Keywords: Pathogenesis; Proinflammatory cytokine

Experimental autoimmune encephalomyelitis (EAE) is an induced disease widely used as animal model for multiple sclerosis, which mainly characterized by demyelination, axonal loss, well neurodegeneration of central nervous system (CNS). T-helper (Th) 17 cell that generate interleukin-17 (IL-17) plays a key role in its pathogenesis. Their activity and differentiation are tightly regulated some cytokines transcription factors. Certain microRNAs (miRNAs) involved the pathogenesis various disorders, including EAE. Our research detected novel miRNA can regulate According to results, during EAE, expression miR-485 notably lowered, STAT3 was significantly increased. It discovered knockdown vivo upregulated Th17-associated aggravated while overexpressed down-regulated mitigated The up-regulation miRNA-485 vitro inhibited within EAE CD4+ T cells. Furthermore, revealed target prediction dual-luciferase reporter assays, directly targets STAT3, gene encodes protein responsible Th17 generation. Overall, exert vital functions generation