Innate Immunity in infectious and autoimmune diseases

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General interests

We are interested in deciphering cellular and molecular mechanisms underlying innate immunity. We study how innate responses are initiated and the crosstalk between myeloid cells and innate lymphocytes such as Natural Killer (NK) cells at early phases of immune responses. We try to understand the mechanisms that prime NK cells to efficiently respond and kill pathogen-infected cells or tumoral cells. We also study how chronic infections, cancer cells or cancer microenvironment negatively impact on innate sensors and NK cell functions, both in mouse and human. Moreover, we study genetic causes of autoimmunity or autoinflammatory disorders in pediatric patients. In many cases, these diseases are caused by mutations in genes encoding innate sensors, cytokines or regulatory mechanisms that reduce inflammation. Our approach therefore combines the fundamental study of immune networks in mouse models with a translational study of human immunological disorders. This multi-scale approach allows cross-fertilization between topics, disciplines and lab members. Our research could also lead to therapeutic applications as strategies to restore immune function are increasingly used to treat cancer, chronic infections, and novel ways to reduce inflammation without adverse effects are crucially needed to treat patients with autoimmunity.

Main achievements

  • Identification of mTOR as an essential checkpoint in NK cell development and activation (2014)
  • Identification of a new phenotype caused by DNA-PKCS variants in human (2014)
  • Identification of molecular mechanisms of HPV-induced TLR9 down regulation


inserm, erc, university, anr, league, finovi

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