Hepatitis & Liver Diseases

Biography

Michel Samson has got his PhD in 1993 at University of Paris XI (France). He studied as postdoctoral scientist at Université Libre de Bruxelles (Brussels, Belgium) supported by prestigious fellowships (EMBO, European Community, etc..). He passed two years as visiting scientist at Genentech (California, USA). He is now team leader and director of research of Inserm at University of Rennes (France) in UMR 1085 Inserm, vice-director of Institut de Recherche en Santé, Environnement et Travail. He studies the inflammation, cell death and fibrosis in liver pathologies. He has published more than 90 papers in reputed journals (Nature, Cell, J Exp Med, Hepatology, J Hepatol., etc...), with already more than 8400 citations and H-index 37.

Research Interest

Liver pathologies due to infectious agents including mainly hepatitis B and C viruses, use of some drugs or metabolic syndrome constitute real public health problems. During liver injury, cytokines play a central role in the orientation of the immune response to an effective response or not and in the establishment and maintenance of the inflammatory response, which when it becomes chronic is at the origin of dysfunctions of the liver. Our team's work focuses on studying the role of new cytokines or immunomodulatory factors (chemokines, IL-33, soluble HLA-G, etc.) and of their associated receptors in liver pathologies. We are also interested in the type of death of hepatocytes induce by cytokines such as TNF, FASL or TRAIL. We recently showed, by the use of RIPK1 kinase dead mice (Ripk1K45A) or a RIPK1 kinase activity inhibitor (Nec-1s) that blockade of RIPK1 kinase activity reduced hepatolysis during immuno-dependent hepatitis. Furthermore, using conditionally deficient mice for RIPK1 in hepatic parenchymal cells (Ripk1LPC-KO), we observed an increase in the susceptibility of mice to ConA-induced hepatitis or to the administration of PAMPs (LPS or CpG-unmethylated DNA). We have demonstrated that this hepatocyte death is apoptotic and is dependent on TNF-α produced mainly by activated macrophages. FasL alone or the IFNγ plus TRAIL combination also sensitizes the hepatocytes of Ripk1LPC-KO mice to apoptotic death. This project is currently underway to show the role of RIPK1 in infectious hepatitis, in nonalcoholic steatohepatitis (NASH) or in drug-induced liver injury.