Background

Inflammatory rheumatic diseases constitute a major burden to the German society. They affect about 1.5 million adults, causing severe disability, chronic pain and premature mortality. The socioeconomic impact is estimated to be about 5 billion Euro per year, 1 billion through early retirements and 4 billion through treatment costs (Quelle: Krankheitskostenrechnung des Statis- tischen Bundesamtes 2002 und 2006, Sonderauswertung). Currently available treatment options ameliorate the disease but are not curative, treatment is expensive, requires chronic application, has considerable side effects and many patients do not respond. Genetic predisposition and environmental triggers, e.g. smoking of tobacco, have been shown to be involved in the etiology and pathogenesis of such diseases. Despite intensive research efforts, the triggers of inflammation have not been identified yet and key events in the pathogenesis of inflammatory rheumatic diseases are not understood. One such unknown key event is the transition of acute inflammation into chronic inflammation, and the resistance of chronic inflammation to endogenous mechanisms of regulation and therapeutic suppression. This lack of knowledge hampers the development of causative and, in perspective, curative therapeutic strategies.

In recent years, research on inflammatory rheumatic diseases has largely focused on cytokine regulation. Here, we suggest to analyze in molecular detail the interactions and the functional imprinting of the cells driving and regulating chronic rheumatic inflammation. This includes not only cells of the adaptive and innate immune response but also mesenchymal cells resident within the joints. Together, we aim to develop advanced diagnostic tools and curative therapies for chronic inflammatory rheumatic diseases.