The RNA-binding protein HuR contributes to neuroinflammation by promoting C-C chemokine receptor 6 (CCR6) expression on Th17 cells
作者： Jing Chen , Jennifer L Martindale , Carole Cramer , Myriam Gorospe , Ulus Atasoy
关键词:
摘要: In both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), the C-C chemokine receptor 6 (CCR6) is critical for pathogenic T helper 17 (Th17) cell migration to central nervous system (CNS). Whereas many cytokines their receptors are potently regulated via post-transcriptional mechanisms in response various stimuli, how CCR6 expression post-transcriptionally Th17 cells unknown. Here, using RNA-binding protein HuR conditional knock-out (KO) wild-type (WT) mice, we present evidence that regulates by binding stabilizing Ccr6 mRNA promoting translation. We also found down-regulates several microRNA expressions, which could target 3'-UTR of decay. Accordingly, reduced on impaired CNS compared with WT thereby ameliorated EAE. Together, these findings highlight contributes cell-mediated neuroinflammation support notion targeting might be a potential therapeutic intervention managing disorders CNS.
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