Glial toll-like receptor signaling in central nervous system infection and autoimmunity

被引：149

作者：

Carpentier, Pamela A. ^{[3
,4
]}

Duncan, D'Anne S. ^{[1
,2
]}

Miller, Stephen D. ^{[1
,2
]}

机构：

[1] Northwestern Univ, Feinburg Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA

[2] Northwestern Univ, Feinburg Sch Med, Interdept Immunobiol Ctr, Chicago, IL 60611 USA

[3] Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA USA

[4] Stanford Univ, Sch Med, Inst Stem Cell Biol & Regenerat med, Stanford, CA USA

来源：

BRAIN BEHAVIOR AND IMMUNITY | 2008年 / 22卷 / 02期

关键词：

innate immunity; toll-like receptors; CNS; glial cells; astrocytes; microglia; autoimmunity; neurotoxicity; cytokines;

D O I：

10.1016/j.bbi.2007.08.011

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Innate immunity in the CNS depends primarily on the functions of glial cells, astrocytes and microglia, which are important for the early control of pathogen replication and direct the recruitment and activation of cells of the adaptive immune system required for pathogen clearance. Efficient immune responses are required for clearance of an invading pathogen, but dysregulation of a pro-inflammatory response in the CNS could lead to the development of autoimmunity. This review summarizes the activation of toll-like receptors (TLRs) expressed on glial cells and the functional outcome of these interactions for CNS health and disease which depends on a delicate balance of the protective and toxic effects of molecules induced in the CNS following TLR ligation. (C) 2007 Elsevier Inc. All rights reserved.

引用

页码：140 / 147

页数：8

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