Our research team focuses on the study of the molecular mechanisms regulating cell death and inflammation, two interconnected cellular processes. Inflammation, the first response of the immune system to infection or tissue injury, is of crucial importance to protect the human body against these insults. Nevertheless, inflammation needs tight regulation as it can turn into a maladaptive response at the origin of various human diseases (such as septic shock, inflammatory bowel disease, psoriasis, cancer, …) when not properly controlled. On the other hand, cell death is an essential cellular process during development and for homeostasis, and is also known to drive inflammation during sterile injury or to amplify inflammation during infection. Gaining a better understanding of the molecular mechanisms that regulate cell death, the type of cell death modality induced, and how dead cells drive inflammation therefore has important implications for our understanding and treatment of inflammatory diseases.

Cell death and innate immunity are ancient evolutionary conserved processes that use a great number of related molecular effectors and parallel signal transduction mechanisms. In our research group, we study regulation of the signalling pathways activated downstream of innate immune Pattern Recognition Receptors (PRRs), and members of the Tumor Necrosis Factor Receptor (TNFR) family. We aim at understanding the molecular nature of the checkpoints that regulate the different cellular outcomes, namely cell survival, cell death (mainly apoptosis and necroptosis) and inflammation. We have a particular interest in the receptor interacting protein kinases (RIPKs) and in their regulation by post-translational modifications. Our studies are conducted at the biochemical, cellular and in vivo levels.