Prof. Michele SWANSON
Department of Microbiology & Immunology University of Michigan Medical School Ann Arbor, Michigan, USA
To investigate how the innate immune system detects and responds to infection, we exploit Legionella pnuemophila, an intracellular pathogen of amoebae and macrophages that causes Legionnaires’ disease, an opportunistic pneumonia that afflicts the elderly and smokers. Our genetic and cell biological studies of primary mouse macrophages establish that, in response to cytosolic contamination with flagellin or other microbial products, NOD-‐like receptor and caspase-‐1 proteins equip macrophages either to induce autophagy, a disposal pathway, or to commit pyroptosis, a failsafe caspase-‐1-‐dependent pro-‐inflammatory cell death. Indeed, mutations to either NOD-‐like receptor proteins or the autophagy component Atg16L1 put humans at risk for Crohn’s disease, an inflammatory bowel syndrome.
Thus, modulation of the autophagy pathway appears to offer an excellent strategy for the development of novel
therapeutic paradigms to treat a wide range of diseases.
Host: Brian B. RUDKIN
Public concerné : chercheurs
Type d'évenement : conference