Shifting the paradigm of islet inflammation—good guy or bad guy?

The main theme for the Servier-IGIS Meetings, which have been held annually since 2000, is β-cell biology and insulin secretion. The 14th IGIS symposium in March 2013 focused on islet inflammation and its impact on islet function. It has been long known that type 1 diabetes (T1D) is associated with immune attacks on the β-cells and therefore that the immune system with its inflammatory components is a key player in this disease. In recent years, however, this knowledge has been widened so that metabolic disorders have now also been established as associated with both the innate and the adaptive immune system. This also includes the islet dysfunction in type 2 diabetes (T2D). This came about with the progressive characterization of the islet of Langerhans as a complex structure in which endocrine cells are interspersed with resident immune cells, and of β-cells as being able to express chemokines, cytokines and genes encoding innate immune receptors. Altogether this ensures close interactions with immune resident cells, and, more broadly, with the external environment of the islet of Langerhans. During the last decade it has also become apparent that the immune system plays a more subtle role in local and systemic metabolism, a topic now called immunometabolism. Immunometabolism is therefore highly relevant for obesity and T2D.