The role of the complement and the FcγR system in the pathogenesis of arthritis

doi:10.1186/ar1761

Arthritis Research & Therapy

Volume 7
Issue 4

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The role of the complement and the FcγR system in the pathogenesis of arthritis

Samuel Solomon¹, Daniela Kassahn¹ and Harald Illges¹^,2^,3

¹Immunology, Department of Biology, Faculty of Sciences, University of Konstanz, Konstanz, Germany

²Biotechnology Institute Thurgau, Tägerwilen, Switzerland

³University of Applied Sciences, Department of Natural Sciences, Immunology and Cell Biology, Rheinbach, Germany

author email corresponding author email

Arthritis Research & Therapy 2005, 7:129-135doi:10.1186/ar1761


Published:	16 May 2005

Abstract

Autoantibodies in sera from patients with autoimmune diseases have long been known and have become diagnostic tools. Analysis of their functional role again became popular with the availability of mice mutant for several genes of the complement and Fcγ receptor (FcγR) systems. Evidence from different inflammatory models suggests that both systems are interconnected in a hierarchical way. The complement system mediators such as complement component 5a (C5a) might be crucial in the communication between the complement system and FcγR-expressing cells. The split complement protein C5a is known to inactivate cells by its G-protein-coupled receptor and to be involved in the transcriptional regulation of FcγRs, thereby contributing to the complex regulation of autoimmune disease.