Pathological changes in human islets.

Purpose of review: This paper reviews the most recent articles on human islet inflammation in type 1 and type 2 diabetes, in recurrent autoimmunity and alloimmunity, which can result in pancreatic graft failure. Finally, we examine data supporting the hypothesis that islet destruction is accompanied by regenerative phenomena aimed at restoring beta cell mass. Recent findings: Type 1 diabetes: Application of high-resolution magnetic resonance imaging and fluorescence of long circulating nanoparticles was successfully used in evaluating islet inflammation in animal models of autoimmune diabetes. Among environmental factors in type 1 diabetes, enteroviral beta-cell infection was reported in some Finnish type 1 diabetic patients. Finally, a family of modulators of cytokine signaling was reported to occur in human islets. Pancreatic islet transplantation: Several observations suggested that (a) interventions to activate, amplify, or sustain intra-islet endothelial cells may facilitate islet revascularization; and (b) the development of strategies aimed at preventing upregulation of proinflammatory molecules can improve islet transplantation. Type 2 diabetes: Multiple factors such as proinflammatory cytokines, high glucose and free fatty acids can contribute to islet inflammation in type 2 diabetes. Accordingly, type 2 diabetic islets show increased apoptotic phenomena and a series of functional defects. Beta-cell regeneration: A number of reports observed beta-cell neogenesis in rodent and in human pancreas. Newly formed beta-cells likely derive either from ductal cells or as results of proliferation phenomena from pre-existing beta cells. Summary: Increasing evidence supports the hypothesis that islet inflammation together with beta-cell dysfunction is a common feature to both type 1 and type 2 diabetes