The role of Fc receptors and complement in autoimmunity

被引：54

作者：

Mihai, Sidonia ^{[1
]}

Nimmerjahn, Falk ^{[1
]}

机构：

[1] Univ Erlangen Nurnberg, Inst Genet, Dept Biol, D-91058 Erlangen, Germany

来源：

AUTOIMMUNITY REVIEWS | 2013年 / 12卷 / 06期

关键词：

Autoantibodies; FcRs; Complement; Autoimmune diseases; ANTIBODY-INDUCED ARTHRITIS; PASSIVE TRANSFER MODEL; II COLLAGEN ANTIBODY; GAMMA RECEPTORS; ALTERNATIVE PATHWAY; EFFECTOR PHASE; ACTIVATION; NEPHRITIS; PROTECTION; INDUCTION;

D O I：

10.1016/j.autrev.2012.10.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Autoantibodies interact with the innate immune system, including the complement network and Fc receptors (FcRs) bearing effector cells, resulting in the induction of tissue injury. It was suggested that these two pro-inflammatory pathways might mediate distinct effector responses, and that only one or the other effector arm may usually dominate an inflammatory response. Recent studies, however, support the notion that autoantibody-induced tissue injury may depend on both, FcRs and selected pathways of the complement network. This review summarizes our current knowledge on the interactions between autoantibodies, FcRs and complement components as essential triggers of tissue injury in autoimmune diseases like rheumatoid arthritis, anti-glomerular basement membrane glomerulonephritis and subepidermal blistering diseases. Manipulation of these connective pathways might be of therapeutic use to control antibody-mediated autoimmune diseases. (C) 2012 Elsevier B.V. All rights reserved.

引用

页码：657 / 660

页数：4

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