Our unit studies the mechanisms of inflammation and associated tissue damage (cartilage/bone) in musculoskeletal diseases, particularly spondyloarthritis (SpA), osteoarthritis and rheumatoid arthritis using a translational research approach.

Specifically gut inflammation is investigated as a driver of joint inflammation in SpA: about 50% of patients with SpA have subclinical, microscopical bowel inflammation. Mesenchymal cells are crucial effector cells in the gut-joint axis in SpA. Regulatory cells by contrast, particularly invariant natural killer T (iNKT) cells, have a marked anti-inflammatory effect.

We have a longstanding interest in the biology of iNKT cells under steady state conditions and in arthritic disease. In studying how regulatory feedback mechanisms fail in arthritic disease, we have uncovered an important functional interaction between Treg cells and iNKT cells.

Another common pathogenic principle for musculoskeletal disorders is mechanical strain. In a mouse model of SpA characterized by enhanced TNF mRNA stability and spontaneous development of enthesitis, unloading inhibits enthesitis development entirely.

We are also looking for new therapeutical opportunities to modulate cartilage and bone metabolism. Over the past years, we have established several new modes to influence human chondrocyte metabolism. We also study osteoclast formation under conditions of chronic inflammation, a particularly high risk factor for inflammation induced bone loss