The primary aim of our research group is to understand the molecular mechanisms underlying inflammatory diseases. Closely related to this, we also study the function and intracellular signaling of various cell types of hematopoietic origin. Our experiments contribute to a better understanding of these diseases and the identification of new potential therapeutic targets.
Inflammatory diseases affect a significant part of the population and are often chronic diseases with limited therapeutic options. They include joint diseases such as rheumatoid arthritis and gout, as well as numerous inflammatory skin and kidney diseases. Regardless of the origin of the inflammation process (e.g., autoimmunity or autoinflammation), tissue damage is mostly mediated by cells of the innate immune system.
We use transgenic approaches in in vivo model systems to study the molecular mechanisms of rheumatoid arthritis, gout, certain autoimmune blistering skin diseases and inflammatory kidney diseases (e.g. glomerulonephritis). We also examine the function and intracellular signaling of immune cells primarily responsible for tissue damage, such as neutrophils, macrophages and osteoclasts. We invest significant effort in developing new experimental methods, including human model systems and CRISPR/Cas9-based genetic deletions.
We have identified the role of several intracellular signaling molecules, including Src-family kinases, the Syk tyrosine kinase, the PLCγ2 phospholipase, and the CARD9 adaptor protein, in various autoimmune and autoinflammatory diseases. Inhibiting these signaling processes may facilitate the development of novel therapeutic strategies.