Taking advantage of our expertise on mouse models and interactions with several clinical departments, our research focuses on the role of adaptive and innate immune cells in type 1 (T1D) and type 2 (T2D) diabetes/obesity and genetics of diabetes. Our projects serve to understand disease mechanisms, discover biomarkers and develop therapeutic strategies.

The specific objectives are:
- Determine the role of innate T lymphocytes in the regulation of T1D. NKT and MAIT cells are unconventional T cells that act as sensors of metabolic abnormalities. These innate-like T cells can regulate both innate and adaptive immunity. Our data demonstrated the efficiency of NKT and MAIT cells in preventing T1D.
- Determine the role of innate T lymphocytes in the regulation of T2D, obesity and non-alcoholic fatty liver disease. We have shown that in patients and mouse models, T2D and obesity induce alterations in MAIT cells, and high levels of inflammatory cytokines in adipose tissue. With our collaborators, we have shown that MAIT cells are profibrogenic in the liver of cirrhotic patients associated with non-alcoholic steatohepatitis (NASH).
- Develop "humanized" murine models that more closely mimic human T1D and understand the role of co-stimulation pathways in autoimmune activation against a given self-tissue. Such models are crucial for the initiation of clinical trials exploring vaccination strategies with cell antigens aimed at restoring immune tolerance.
- Identify genetic factors  involved in the diversity of juvenile-onset diabetes, ranging from multifactorial T1D to monogenic forms of diabetes whose clinical presentation may be atypical or not.