I am working on the development of strategies for prevention and treatment of acute intestinal graft-versus-host-disease (GVHD) after hematopoietic stem cell transplantation (HSCT). An interesting novel therapeutic concept with potential simultaneous impact on tumor growth and inflammatory processes, such as acute GVHD, is the inhibition of the formation of new blood vessels (neo-vascularization). Both angiogenesis, the sprouting of resident tissue endothelial cells (ECs), and vasculogenesis, the recruitment of bone marrow (BM)-derived circulating endothelial progenitor cells (EPCs), are thought to participate in this process. Neo-vascularization has been implicated in a number of inflammatory diseases as well as tumor growth, making neo-vasculature an attractive therapeutic target in patients undergoing HSCT for malignant tumors. I am currently studying neo-vascularization and the therapeutic potential of the specific inhibition of vasculogenesis during GVHD and tumor growth in well-characterized murine models of HSCT.

My second focus is to improve our understanding about the molecular mechanisms in the initiation phase of GVHD. Several insights into inflammatory processes have been gained from recent research, which show that interactions between microbial associated molecules (pathogen associated molecular patterns, PAMPs) and innate immune receptors (pathogen recognition receptors, PRRs) control adaptive immune responses in inflammatory disorders. To identify important mechanisms on how GVHD is induced by the interplay of microbial molecules and innate immunity I am currently working on the role of one of those PRRs (NOD2) in mouse models of GVHD. Clinical data, showing that patients with mutations in the NOD2 gene have a higher risk of GVHD, suggest an important function of NOD2 receptors in the pathophysiology of GVHD.