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

Samuel Solomon1, Daniela Kassahn1 and Harald Illges123*

Author Affiliations

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

2 Biotechnology Institute Thurgau, Tägerwilen, Switzerland

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

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

Published: 16 May 2005


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.