Signaling lymphocyte activation molecule family in systemic lupus erythematosus

被引:10
|
作者
Comte, Denis [1 ,2 ]
Karampetsou, Maria P. [3 ]
Humbel, Morgane [1 ,2 ]
Tsokos, George C. [4 ]
机构
[1] Lausanne Univ Hosp, Div Immunol, Lausanne, Switzerland
[2] Lausanne Univ Hosp, Div Allergy, Lausanne, Switzerland
[3] Evaggelismos Gen Hosp, Div Rheumatol, Athens, Greece
[4] Harvard Med Sch, Boston, MA 02115 USA
基金
瑞士国家科学基金会;
关键词
LOW-DOSE INTERLEUKIN-2; T-CELL DEFECTS; DIFFERENTIAL EXPRESSION; SUSCEPTIBILITY LOCI; THERAPEUTIC TARGET; ALTERED EXPRESSION; ADHESION MOLECULE; DENDRITIC CELLS; CD229; LY9; SLAM;
D O I
10.1016/j.clim.2018.11.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease characterized by a breakdown in immune tolerance leading to the development of auto reactive lymphocytes and autoantibodies. Recent findings have provided new insight on the role of the signaling lymphocytic activation molecule family (SLAMF) receptors, a group of nine co-regulatory molecules involved in the activation of hematopoietic cells, and their downstream protein SLAM-associated protein (SAP), into the pathogenesis of SLE. This review summarizes the current knowledge on SLAMF in human SLE immunopathogenesis, and the importance of SLAMF molecules as new therapeutic targets.
引用
收藏
页码:57 / 63
页数:7
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