Molecular pathogenesis of multiple sclerosis

被引：93

作者：

Bar-Or, A

Oliveira, EML

Anderson, DE

Hafler, DA

机构：

[1] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Boston, MA 02115 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 1999年 / 100卷 / 1-2期

关键词：

multiple sclerosis; central nervous system; relapsing-remitting; primary-progressive; secondary-progressive; EAE; pathogenesis; autoreactive T cells; Th1; Th2; myelin epitopes; blood-brain barrier; cerebrospinal fluid; MBP; PLP; chemokines; adhesion molecules; interferon-beta; extracellular matrix; matrix metalloproteinases; costimulation; B7-1 (CD80); B7-2 (CD86); proinflammatory cytokines; molecular mimicry;

D O I：

10.1016/S0165-5728(99)00193-9

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 best understood as an inflammatory disease of the central nervous system (CNS) white matter characterized by demyelination, focal T cell and macrophage infiltrates, axonal injury and loss of neurological function. Our current understanding invokes proinflammatory cells and mediators that may be triggered by environmental factors to mediate disease in a genetically susceptible host. Five major themes which have been associated with the pathogenesis of MS lesions will be discussed: (1) The differential activation states of myelin-reactive T cells from MS patients vs. normal individuals, (2) the selective expression of chemokines, adhesion molecules and matrix metalloproteinases, (3) the proposed roles of the B7 costimulatory pathway, (4) the proinflammatory cytokines and (5) the role of molecular mimicry. (C) 1999 Elsevier Science B,V. All rights reserved.

引用

页码：252 / 259

页数：8

共 97 条

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