B cells, BAFF/zTNF4, TACl, and systemic lupus erythematosus

被引:18
作者
Dörner, T
Putterman, C
机构
[1] Charite, Dept Med, D-10098 Berlin, Germany
[2] Charite, Dept Rheumatol, D-10098 Berlin, Germany
[3] Charite, Dept Clin Immunol, D-10098 Berlin, Germany
[4] Montefiore Med Ctr, Albert Einstein Coll Med, Dept Med, Div Rheumatol, Bronx, NY 10467 USA
关键词
BAFF; SLE; TACl; TNF; TNF receptor superfamily;
D O I
10.1186/ar299
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
B cells and B-cell/T-cell collaborations are instrumental in the pathophysiology of systemic lupus erythematosus (SLE). This commentary highlights in particular the newly discovered role of B-cell-activating factor (BAFF; also known as TALL-1, THANK, BlyS, and zTNF4) as a positive regulator of B-cell functions, such as B-cell activation and differentiation. Two members of the tumor necrosis factor(TNF)-receptor superfamily were recently identified as receptors for BAFF on B cells. The interaction between BAFF and its receptors may be important in the pathogenesis of lupus. Advances in our understanding of abnormalities in immune regulation in lupus might provide the opportunity to improve our current therapeutic approaches to this disorder.
引用
收藏
页码:197 / 199
页数:3
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