Glatiramer acetate biases dendritic cells towards an anti-inflammatory phenotype by modulating OPN, IL-17, and RORγt responses and by increasing IL-10 production in experimental allergic encephalomyelitis

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作者：

S Begum-Haque，M Christy，Y Wang，E Kasper，J Ochoa-Reparaz，JY Smith，A Haque，LH Kasper

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摘要：

Paralleling our previous mechanistic studies of glatiramer acetate (GA; Copaxone) activity, we show that GA curbs the expression of Toll-like receptor (TLR) 9 and the universal adapter protein Myd88 in mice with EAE, the animal model for multiple sclerosis. Concurrent with enhanced dendritic cell (DC) production of IL-10, GA interferes with OPN, IL-17, and ROR gamma expression in DCs of mice with EAE, and suppresses brain expression of the EAE-induced chemokines, MIP1α and β, IP-10 and RANTES. Thus GA not only biases dendritic cells towards an anti-inflammatory phenotype, but also suppresses the expression of factors that affect the blood–brain barrier penetration during neuroinflammation.

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关键词：

EAE, experimental allergic encephalomyelitis GA, glatiramer acetate DC, dendritic cells OPN, osteopontin TLR, toll related receptor MyD88, myeloid differentiation primary response gene 88 IL, interleukin Th, T helper LN, lymph node