Role of macrophages in diabetes
Type 1 diabetes is an autoimmune condition caused by the destruction of pancreatic beta cells. Affected individuals produce insufficient or no insulin and as a result cannot regulate blood sugar levels. Disease management usually entails monitoring of glucose levels and lifelong injections of insulin. Nonetheless, serious neuronal and vascular long-term complications can still ensue. Mechanistic insight into the immune-mediated decay of insulin-producing cells has long supported a role for T cells. At the same time, innate immunity and macrophages in particular have attracted very little attention. Data from recent clinical trials, however, indicate that induction of peripheral T cell tolerance is not a valid therapeutic strategy. The EU-funded MACROPHAGES IN T1D (Functional profiling and therapeutic tolerization of macrophages in type 1 diabetes) project set out to investigate the role of macrophages in diabetes. For this purpose, they utilised the NOD mouse model that develops diabetes around 20-30 weeks after birth. Researchers performed immunohistochemistry and flow cytometric analysis of islet-infiltrating macrophages before and at the onset of disease. Compared to normal mice, they found fewer resident and more inflammatory macrophages in the pancreatic islets around the time of diabetes onset in the NOD model. This data clearly indicates that macrophages are somehow implicated in diabetes although further work is required to delineate the precise mechanism. Taken together, the MACROPHAGES IN T1D findings disclose an unknown role for innate immunity in the development of diabetes. This opens up a new avenue for therapeutic exploitation through manipulation of the innate immune system.
Keywords
Macrophages, Diabetes, pancreatic beta cells, immune system, T cells
