کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6020754 1580420 2013 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
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
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
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
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 254, Issues 1–2, 15 January 2013, Pages 117-124
نویسندگان
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