Regulation of CD40 ligand expression in systemic lupus erythematosus

被引:52
作者
Crow, MK
Kirou, KA
机构
[1] Cornell Univ, Hosp Special Surg, Dept Med, New York, NY 10021 USA
[2] Cornell Univ, Weill Med Coll, New York, NY USA
关键词
D O I
10.1097/00002281-200109000-00004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Production of pathogenic autoantibodies in systemic lupus erythematosus (SLE) requires T cell help, along with ligation of the B cell surface immunoglobulin receptor by antigen. It is likely that macrophages, dendritic cells, and endothelial cells are also activated by interactions with T cells and contribute to lupus pathology. CD40 ligand (CD40L, CD154), a member-of the tumor necrosis factor family of cell surface molecules, mediates these contact dependent signals delivered by CD4(+) T helper cells to CD40(+) target cells. Recent data from SLE patients and murine lupus models have demonstrated prolonged expression of CD40L on lupus T cells and its capacity to mediate excessive B cell activation. This review summarizes the current information regarding transcriptional and post-transcriptional regulation of CD40L expression in normal and SLE T cells. More complete characterization of the mechanisms that regulate the magnitude and duration of CD40L expression should suggest new approaches to modulate this promising therapeutic target.(C) 2001 Lippincott Williams & Wilkins, Inc.
引用
收藏
页码:361 / 369
页数:9
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