The role of the complement and the FcγR system in the pathogenesis of arthritis
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
Arthritis Research & Therapy 2005, 7:129-135 doi:10.1186/ar1761Published: 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.