The role of antigen presenting cells in multiple sclerosis

被引:197
|
作者
Chastain, Emily M. L. [1 ,2 ]
Duncan, D'Anne S. [1 ,2 ]
Rodgers, Jane M. [1 ,2 ]
Miller, Stephen D. [1 ,2 ]
机构
[1] Northwestern Univ, Feinberg Sch Med, Dept Microbiol Immunol, Chicago, IL USA
[2] Northwestern Univ, Feinberg Sch Med, Interdept Immunobiol Ctr, Chicago, IL USA
关键词
Multiple sclerosis; EAE; TMEV-IDD; Microglia; Astrocyte; Dendritic cell; CENTRAL-NERVOUS-SYSTEM; MHC CLASS-II; MURINE ENCEPHALOMYELITIS VIRUS; COSTIMULATORY MOLECULES B7-1; NECROSIS-FACTOR-ALPHA; TOLL-LIKE RECEPTOR-3; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; ADAPTIVE IMMUNE-RESPONSES; BRAIN DENDRITIC CELLS;
D O I
10.1016/j.bbadis.2010.07.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Multiple sclerosis (MS) is a debilitating T cell mediated autoimmune disease of the central nervous system (CNS). Animal models of MS, such as experimental autoimmune encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) have given light to cellular mechanisms involved in the initiation and progression of this organ-specific autoimmune disease. Within the CNS, antigen presenting cells (APC) such as microglia and astrocytes participate as first line defenders against infections or inflammation. However, during chronic inflammation they can participate in perpetuating the self-destructive environment by secretion of inflammatory factors and/or presentation of myelin epitopes to autoreactive T cells. Dendritic cells (DC) are also participants in the presentation of antigen to T cells, even within the CNS. While the APCs alone are not solely responsible for mediating the destruction to the myelin sheath, they are critical players in perpetuating the inflammatory milieu. This review will highlight relevant studies which have provided insight to the roles played by microglia, DCs and astrocytes in the context of CNS autoimmunity. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:265 / 274
页数:10
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