Toll-Like Receptors in Multiple Sclerosis

被引：45

作者：

Racke, Michael K. ^{[2
,3
]}

Drew, Paul D. ^{[1
]}

机构：

[1] Univ Arkansas Med Sci, Dept Neurobiol & Dev Sci, Little Rock, AR 72205 USA

[2] Ohio State Univ, Med Ctr, Dept Neurol, Columbus, OH 43210 USA

[3] Ohio State Univ, Med Ctr, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA

来源：

TOLL-LIKE RECEPTORS: ROLES IN INFECTION AND NEUROPATHOLOGY | 2009年 / 336卷

关键词：

EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYD88-DEPENDENT SIGNALING PATHWAY; CHLAMYDIA-PNEUMONIAE INFECTION; ENCEPHALITOGENIC T-CELLS; PLACEBO-CONTROLLED TRIAL; INNATE IMMUNITY; INTERLEUKIN-1; RECEPTOR; DEMYELINATING DISEASES;

D O I：

10.1007/978-3-642-00549-7_9

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) characterized by inflammation, demyelination, and axonal pathology. The exact causes of MS are unknown, but environmental factors including pathogens are believed to contribute to the development of disease. Toll-like receptors (TLRs) are a family of receptors important in pathogen recognition and host defense. TLRs are expressed by a variety of peripheral immune cells as well as resident cells of the CNS. Studies indicate that TLRs play a significant role in modulating MS, as well as experimental autoimmune encephalomyelitis (EAE), an animal model of MS. This review will discuss the current understanding of the role of TLRs in modulating EAE and MS.

引用

页码：155 / 168

页数：14

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