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
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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DOI：
10.1016/j.jneuroim.2012.10.003
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发表时间：
2013-01-15
影响因子：
3.3
通讯作者：
Kasper, Lloyd H.
中科院分区：
文献类型：
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作者：
Begum-Haque, Sakhina;Christy, Marc;Kasper, Lloyd H.
与我们之前对醋酸格拉替默（GA; Copaxone）活性的机制研究相似，我们发现GA抑制了多发性硬化症动物模型EAE小鼠中toll样受体（TLR） 9和通用适配蛋白Myd88的表达。在增强树突状细胞（DC）产生IL-10的同时，GA干扰EAE小鼠DC中OPN、IL-17和ROR γ的表达，并抑制EAE诱导的趋化因子MIP1 α和β、IP-10和RANTES的脑表达。因此，GA不仅使树突状细胞偏向抗炎表型，而且还抑制神经炎症期间影响血脑屏障穿透的因子的表达。(C) 2012 Elsevier B.V.版权所有
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, MIP1 alpha and beta, 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. (C) 2012 Elsevier B.V. All rights reserved.