Fig. 2.

The possible role of iNKT cells in the pathophysiology of type 2 diabetes. iNKT cells are present in lean adipose tissue and produce IL-4. This could favor the M2 anti-inflammatory phenotype of resident macrophages. During obesity, macrophages accumulate in the adipose tissue and iNKT cell frequency is reduced. The lack of IL-4, among other mechanisms, could participate in the switch of macrophages toward M1 pro-inflammatory phenotype that induces insulin resistance. In pancreatic islets, the increased concentration of glucose and fatty acids induces local inflammation and the production of IL-1β. This cytokine could activate iNKT cells, preferentially the iNKT17 cell subset, which then contribute to β-cell destruction.