کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5630215 | 1580371 | 2017 | 10 صفحه PDF | دانلود رایگان |
- Innate immune receptors contribute to the pathogenesis of autoimmunity in a more substantial way than previously appreciated
- In particular, they can mediate certain effects of infections on the susceptibility and clinical course of multiple sclerosis
- This review focuses on the role of Toll-like receptor 2 (TLR2) in controlling infections and modulating autoimmune responses
Innate immunity relies on a set of germline-encoded receptors including Toll-like receptors (TLRs) that enable the host to discriminate between self and non-self. Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the central nervous system (CNS). Infections are thought to play an important role in disease susceptibility. The role of innate immunity in MS has been recently appreciated. TLR2, a member of the TLR family, forms heterodimers with either TLR1 or TLR6 and detects a wide range of microbial as well as self-derived molecular structures. It may thus be important both in fighting infection and in activating autoimmunity. In this review, we discuss innate regulation of autoimmunity in MS with a focus on the role of TLR2 signaling.
Journal: Journal of Neuroimmunology - Volume 304, 15 March 2017, Pages 11-20