[FG] Trendelenburg Marten

Systemic Lupus Erythematosus (SLE) is the archetype of an autoimmune disease and can involve any organ system eventually leading to comorbidities that can also be observed independently of underlying SLE. The complex pathogenic mechanisms leading to and being involved in this autoimmune-inflammatory syndrome are not well understood. However, complement C1q, the first component of the classical pathway, seems to play a central role. By analysing the role of C1q as well as it’s interaction with autoantibodies targeting C1q (anti-C1q) in SLE, we aim at elucidating 1) mechanisms being involved in the initiation of autoimmunity, 2) mechanisms of secondary acceleration of inflammation, and 3) processes being associated with atherosclerosis and thromboembolism.