Using state of the art mouse models to uncover principles of cell death and cancerogenesis
Inflammatory responses protect the body from microbial infections and promote wound healing and tissue regeneration. However, excessive or prolonged inflammation causes tissue damage and is involved in the pathogenesis of many diseases. We are studying the mechanisms regulating inflammation and the development of inflammatory diseases. Our research revealed the important role of cell death as a trigger for inflammation in epithelial tissues such as the skin and the intestine. Our long-term goal is to understand the mechanisms that control inflammation and contribute to the pathogenesis of chronic inflammatory diseases.
Our research: Healthy tissue homeostasis is maintained by balanced interactions between epithelial, stromal and immune cells with the commensal microbes that normally reside on the surface of our barrier tissues such as the gut and the skin. Disruption of tissue homeostasis can cause chronic inflammatory diseases and in some cases also cancer. Despite recent progress in identifying factors that contribute to tissue damage and chronic disease, the causes that initiate pathogenic inflammatory responses remain unknown. As a consequence, currently available therapies mainly target the symptoms and aim to achieve stable suppression of the inflammatory response, which requires chronic treatment that causes side effects and increases costs. Our group studies the mechanisms that regulate immune responses, with particular interest on identifying molecules and pathways that are responsible for causing chronic inflammatory diseases. We have a long-standing interest on understanding how NF-κB signalling contributes to disease pathogenesis.
More recently, we have been interested in studying how different pathways of regulated cell death, such as apoptosis or necroptosis, may contribute to inflammation and the patho-genesis of inflammatory diseases.