Complement-mediated pathogenic mechanisms in Systemic Lupus Erythematosus (SLE)
Being primarily a medical doctor with clinical responsibilities (Deputy Head of the Division of Internal Medicine), my research is situated at the interface between basic experimental and clinical projects in systemic autoimmunity (translational research).
In my experimental studies, the major goal is to understand pathogenic mechanisms in Systemic Lupus Erythematosus (SLE). The complex pathogenic mechanisms leading to and being involved in this autoimmune-inflammatory syndrome are not well understood, but complement C1q, the first component of the classical pathway, seems to play a central role. Studying the origin and consequences of autoantibodies against C1q (anti-C1q) offers the exceptional opportunity to elucidate the interplay of complement C1q, phagocytes, apoptosis, Epstein-Barr-Virus (EBV) and the hemostatic system, all having been implicated in the pathogenesis of SLE. More specifically, in the current projects my group is i) investigating whether anti-C1q induced by an EBV-derived antigen can accelerate SLE in vivo, ii) trying to identify epitopes of anti-C1q, iii) studying the interference of C1q with anti-C1q and vWF in a microfluidic vessel model and iv) aiming at the identification of C1q receptors on macrophages that might be blocked by the presence of anti-C1q.
On the clinical side, I have regular contact with patients with SLE and founded (together with other colleagues in Switzerland) the Swiss SLE Cohort Study (SSCS) of which I am currently the president. Thus, in addition to my clinical expertise in judging on disease activity and other parameters being of importance for the interpretation of biomarkers in this disease, I also have access to a large number of patient samples (beyond those that we are collecting in Basel). In addition, in own projects I am studying the role of complement in SLE patients and I am involved in a number of clinical/translational projects.