Qian Chen

Personal Data:
Country of Origin: P. R. China
Start of PhD: 2010
Institution: HKI

PhD Project:
The Role of Complement in Autoimmune Disease

Supervisor(s): P.F. Zipfel (HKI), G. Wolf (UKJ)

Abstract:
The complement system is a crucial component of innate immunity and a central effective system to fight infections, microbes and to maintain cellular integrity and tissue homeostasis. The activated complement system avoids invading of microorganisms and mediates the elimination of dead or modified self cells, but the over-activation may also damage host tissues. To prevent this, several complement regulators act as either facilitators or cofactors to control the spontaneously activated complement cascade. Any disturbance in this self-mediated balance can result in damage of tissues and in autoimmune disease. Therefore, insights into the mechanisms of complement regulation are critical for understanding disease pathology and accelerate the development of therapies for complement –associated diseases. The complement-related disease Membranoproliferative glomerulonephritis type II is caused by a defective surface activation of the glomerular basement membrane and accumulation of debris, which induces rare kidney disorder leads to mesangial cell proliferation and structural changes in glomerular capillary walls. MPGN is associated with inappropriate complement regulation, such as functional inactivation or absence of the regulator Factor H, the presence of autoantibodies against Factor H or to the C3 convertase. The goal of my project is to identify additional pathological identifications of MPGN, and I hypothesize that Factor H related proteins or C3 convertase components are relevant for pathology. They will update the current knowledge of such kinds of diseases and will define to the mechanisms of complement regulation.