Our research aims to understand the in vivo mechanisms by which chronic inflammation drives (autoimmune) pathology. One major focus concerns the molecular mechanisms by which the transcription factor NF-kB and the inflammasome signaling complex control inflammatory and cytotoxic responses. For these studies we use transgenic mice as a model to study gene function in vivo, both through Cre/LoxP-mediated gene targeting allowing tissue-specific gene deletion, and through CRISPR/Cas technology to introduce specific gene mutations. Our transgenic mouse lines are studied in several mouse models of chronic inflammatory pathology (including models for inflammatory bowel disease, rheumatoid arthritis, hepatitis, multiple sclerosis, infectious diseases and auto-inflammatory disorders) and models of inflammation-associated cancer, in order to identify and clarify the role of a specific gene or pathway in disease development.