Growing evidence suggests inflammation as a major underlying mechanism in the pathogenesis of type 2 diabetes mellitus (T2DM). Supporting the involvement of the immune system in T2DM, cross-sectional and prospective studies have associated elevated circulating levels of acute-phase proteins. Furthermore, clinical studies have demonstrated that anti-inflammatory drugs may improve glycaemia. Morphological and therapeutic intervention studies have uncovered an inflammatory process in islets of patients with type 2 diabetes characterized by the presence of cytokines, macrophages, β cell apoptosis, amyloid deposits, and fibrosis. However, the immune cells involved in pancreatic islet inflammation during T2D are insufficiently described. In human tissue samples, only CD68 positive macrophages have been documented. The level of activity of these cells as well as the occurrence and role of other immune cell types remain to be investigated.

Using the pancreatic tissue samples supplied by nPOD, we plan on investigating the presence of innate and adaptive immune cells within or around the islets of T2DM patients versus healthy donors. Defining the inflammatory milieu within the islets of T2DM patients will help us target further inflammatory treatments.