Eguchi Kosei, Nagai Ryozo
J Clin Invest. 2017 Jan 3;127(1):14-23. doi: 10.1172/JCI88877.
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.
2型糖尿病（T2D）中胰岛炎症的发现及其与β细胞功能障碍的关联，进一步凸显了炎症在代谢性疾病中的重要性。T2D患者胰岛内巨噬细胞数量增加，这些细胞是胰岛内促炎细胞因子的主要来源。多项针对T2D的人体研究表明，针对胰岛炎症可能是一种有效的治疗策略。在本综述中，我们概述了胰岛炎症发生并导致β细胞功能障碍的细胞和分子机制。我们还强调了在T2D病理和β细胞健康背景下，胰岛内巨噬细胞极性转变的调节及其作用，这可能对旨在改善胰岛功能的治疗方法具有广泛的转化意义。
