Islet inflammation in type 2 diabetes and physiology
Kosei Eguchi, Ryozo Nagai
Kosei Eguchi, Ryozo Nagai
Published January 3, 2017
Citation Information: J Clin Invest. 2017;127(1):14-23. https://doi.org/10.1172/JCI88877.
View: Text | PDF
Review Series

Islet inflammation in type 2 diabetes and physiology

Abstract

The finding of islet inflammation in type 2 diabetes (T2D) and its involvement in β cell dysfunction has further highlighted the significance of inflammation in metabolic diseases. The number of intra-islet macrophages is increased in T2D, and these cells are the main source of proinflammatory cytokines within islets. Multiple human studies of T2D have shown that targeting islet inflammation has the potential to be an effective therapeutic strategy. In this Review we provide an overview of the cellular and molecular mechanisms by which islet inflammation develops and causes β cell dysfunction. We also emphasize the regulation and roles of macrophage polarity shift within islets in the context of T2D pathology and β cell health, which may have broad translational implications for therapeutics aimed at improving islet function.

Authors

Kosei Eguchi, Ryozo Nagai

×

Figure 2

M2-like polarization of islet macrophages plays key roles in the proliferation and physiologic maintenance of β cells.

Options: View larger image (or click on image) Download as PowerPoint
M2-like polarization of islet macrophages plays key roles in the prolife...
Multiple cytokines (e.g., TGF-β1, VEGFA, and CSF1) secreted from multiple cell types within islets (e.g., macrophages, β cells, and endothelial cells) form networks that contribute to a microenvironment that promotes M2-like polarization of islet macrophages. CSF1 signaling is a common mediator that maintains and promotes M2-like activation of both islet-resident and recruited macrophages. M2-like macrophages play an indispensable role in the establishment of the microenvironment necessary for β cell health. CSF1R, CSF1 receptor.