FcγRIIB, FcγRIIIB, and systemic lupus erythematosus

被引：72
作者：
Niederer, Heather A.
Clatworthy, Menna R.
Willcocks, Lisa C.
Smith, Kenneth G. C. [1 ]
机构：
[1] Univ Cambridge, Addenbrookes Hosp, Sch Clin Med, Cambridge Inst Med Res, Cambridge CB2 0XY, England
来源：
YEAR IN IMMUNOLOGY 2 | 2010年 / 1183卷
关键词：
systemic lupus erythematosus; low-affinity Fc receptors; Fc gamma RIIB; Fc gamma RIIIB; FCGR2B; FCGR3B; copy number variability; COPY NUMBER VARIATION; GENOME-WIDE ASSOCIATION; ALTERS RECEPTOR EXPRESSION; B-CELL TOLERANCE; HUMAN-NEUTROPHILS; IMMUNE-COMPLEX; PROMOTER HAPLOTYPE; T-CELLS; GENETIC SUSCEPTIBILITY; FOLLICULAR EXCLUSION;
D O I：
10.1111/j.1749-6632.2009.05132.x
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 autoimmune disease systemic lupus erythematosus (SLE) is characterized by the deposition of immune complexes in organs such as the kidney. This Occurs as a result of multiple immunological abnormalities, including the production of high levels of autoantibody and dysregulated handling of immune complexes. Receptors for the Fc portion of IgG are critically involved in immune complex handling and clearance and in the regulation of B-cell activation. Polymorphisms in the low-affinity Fc gamma receptors have been associated with susceptibility to a number of autoimmune diseases, including SLE. We review the role of two such receptors in the pathogenesis of lupus-the inhibitory receptor Fc gamma RIIB and the glycosylphosphatidylinositol-linked activatory receptor Fc gamma RIIIB. Recent work has enhanced our understanding of the mechanism of action of the Fc gamma RIIB 1232T polymorphism and the overall role of this receptor in SLE. The human neutrophil antigen-1 allotypes of Fc gamma RIIIB and the role of the receptor in SLE are discussed with regard to the recent determination of copy number variation in FCGR3B and the association of low copy number with SLE.
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页码：69 / 88
页数：20
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