Insulitis in type 2 diabetes

Abstract

Islets of patients with type 2 diabetes have the feature of an inflammatory process reflected by the presence of cytokines, immune cells, β-cell apoptosis, amyloid deposits and fibrosis. Indeed, β-cells from patients with type 2 diabetes display inflammatory markers, including increased interleukin (IL)-1β expression. Furthermore, increased islet-associated macrophages are observed in human type 2 diabetic patients and in most animal models of diabetes. Importantly, increased numbers of macrophages are detectable very early in high fat-fed mice islets, before the onset of diabetes. These immune cells are most likely attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1β. It follows that modulation of intra-islet inflammatory mediators, in particular IL-1β, may prevent insulitis in type 2 diabetes and therefore presents itself as a possible causal therapy with disease-modifying potential. © 2008 The Authors Journal Compilation © 2008 Blackwell Publishing Ltd.