CV Science

Mathias Faure Autophagy Infection Immunity

Course and current status

I have got my B. Sc. (1993) and M. Sc. (1994) in Cellular Biology and Physiology at the University of Grenoble 1. During my M. Sc., I spent several month at the University of Montreal where I worked on persistent infection of fibroblasts by reovirus (G. Lemay's lab). I then obtained my Master-2 Research (1995) and my Ph.D. (1999) in Immunology from the University of Paris 6. I worked at the Pasteur Institute of Paris on a model of T cell tolerance (P.-A. Cazenave's lab) with Dr. Rueff-Juy. I pursued my formation with a post-doctoral training at the National Institutes of Health (NIH, NIAID, Rockville, USA, 1999-2002), focused on Natural Killer cells biology (E.O. Long's lab). During a second postdoc in Grenoble (INSERM U548, CEA-Grenoble, 2002-2004), I studied some characteristics of dendritic cells (P.N. Marche's lab). In 2004, I have got a permanent position as an associate professor at the University of Lyon 1, executing research in the unit INSERM U851 (C. Rabourdin-Combe's lab). I was nominated Full Professor at the University of Lyon 1 in 2013. I am the PI of a team focusing on the role of autophagy in infection and inflammatory bowel diseases at CIRI, international center of infectious diseases (INSERM U1111 / CNRS UMR 5308 / ENS de Lyon / University Lyon 1).

Scientific summary

Our research project aim at studying the role of macroautophagy in the immune system, especially in the context of infections. Macroautophagy, referred to as autophagy, is a lysosomal catabolic pathway. It allows the sequestration of large portions of the cytoplasm within double-membraned vesicles called autophagosomes. Subsequently to the fusion of autophagosomes with lysosomes, the cytoplasmic content is degraded within autolysosomes. In mammalian cells, regulation of autophagy involves dozens of proteins including those of the ATG (AuTphaGy-related) family. Essential for the maintenance of cellular homeostasis, disruption of autophagy is associated with many human diseases such as neurodegenerative diseases, cancer, inflammatory diseases or infectious diseases. Indeed, autophagy is a cell-autonomous defense mechanism that allows each cell to fight intracellular pathogens (viruses, bacteria or parasites), by targeting them towards a lysosomal degradation. In addition, autophagy contributes to the regulation of innate (type I interferon synthesis, inflammation, cell death…) and adaptive (peptide presentation on major histocompatibility molecules) immune responses, by facilitating their development in response to an infection. Thus, autophagy appears to be central for the establishment of an immediate as well as a long-term immune response against infectious agents. However, many pathogens have evolved molecular strategies in order to escape or hijack autophagy to facilitate their replication. Our work aims at understanding how autophagy contributes to the pathogen control, and how some pathogens manipulate autophagy. We translate our knowledge to better understand how disregulated autophagy could contribute to inflammatory bowel disease, especially Crohn disease, and to severe and rare monogenic diseases.