Novel molecular targets in the treatment of systemic lupus erythematosus

被引：36

作者：

Crispin, Jose C. ^{[1
]}

Tsokos, George C. ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Beth Israel Med Ctr, Div Rheumatol, Boston, MA 02115 USA

来源：

AUTOIMMUNITY REVIEWS | 2008年 / 7卷 / 03期

关键词：

autoimmunity; CD3; zeta; pathogenesis; PP2A; systemic lupus erythematosus; therapy;

D O I：

10.1016/j.autrev.2007.11.020

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

T cells from patients with systemic lupus erythematosus (SLE) display a number of biochemical abnormalities which include altered expression of key signaling molecules, heightened calcium responses, and skewed expression of transcription factors. These defects are involved in the altered behavior of SLE T cells and are probably central in the disease pathogenesis. The aim of this communication is to review the defects that have been consistently documented in SLE T cells, highlighting molecules and pathways that represent therapeutic targets. (C) 2007 Elsevier B.V. All rights reserved.

引用

页码：256 / 261

页数：6

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