Lay summary
Our research focuses on the mechanisms regulating beta-cell (the cell that produces insulin) adaptation to metabolic stress in type 2 diabetes. We have described a specific inflammatory process responsible for the failure of beta-cells in type 2 diabetes. In the present project, we hypothesise that islet inflammation is initially an attempt of the islet to adapt and repair itself in response to metabolic stress. If this initially physiological response is short-lived, it may be beneficial. If the response is sustained over a prolonged period of time at a high level of activity it will eventually become deleterious. Therefore, remodelling this response may promote survival and regeneration. Our overall goal is to characterize the putative physiological role of islet-derived cytokines and chemokines as well as of some immune cells in islet regeneration. It may open the door to therapeutic strategies aiming at remodeling this response. Several drugs enabling modulation of cytokines and chemokines are in clinical trials for the treatment of other diseases, e.g. rheumatic arthritis. Therefore, timely clinical evaluation is a realistic goal of this project.