Targeting the B7/CD28:CTLA-4 costimulatory system in CNS autoimmune disease

被引：44

作者：

Karandikar, NJ

Vanderlugt, CL

Bluestone, JA

Miller, SD

机构：

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

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

[3] Univ Chicago, Ben May Inst Canc Res, Chicago, IL 60637 USA

[4] Univ Chicago, Comm Immunol, Chicago, IL 60637 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 1998年 / 89卷 / 1-2期

关键词：

central nervous system (CNS); B7/CD28 : CTLA-4 costimulatory system; experimental autoimmune encephalomyelitis (EAE);

D O I：

10.1016/S0165-5728(98)00058-7

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The B7/CD28:CTLA-4 costimulatory pathway plays a critical role in determining the fate of immmune responses (activation vs. down-regulation) and is a highly promising therapeutic target for treating autoimmune diseases. In this review, we highlight the mechanisms by which this costimulatory pathway operates emphasizing the role of the different components in the pathogenesis of relapsing experimental autoimmmune encephalomyelitis, a CD4 T cell-mediated autoimmune model of multiple sclerosis. The separate and distinct roles of B7-1, B7-2 and CTLA-4 in positive and negative regulation of autoimmune pathogenesis are considered and a working model is proposed. (C) 1998 Elsevier Science B.V. All rights reserved.

引用

页码：10 / 18

页数：9