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