The islet of Langerhans produces endocrine hormones to regulate glucose homeostasis. The normal function of the islet relies on the homeostatic regulations of cellular composition and cell–cell interactions within the islet microenvironment. Immune cells populate the islet during embryonic development and participate in islet organogenesis and function. In obesity, a low-grade inflammation manifests in multiple organs, including pancreatic islets. Obesity-associated islet inflammation is evident in both animal models and humans, characterized by the accumulation of immune cells and elevated production of inflammatory cytokines/chemokines and metabolic mediators. Myeloid lineage cells (monocytes and macrophages) are the dominant types of immune cells in islet inflammation during the development of obesity and type 2 diabetes mellitus (T2DM). In this review, we will discuss the role of the immune system in islet homeostasis and inflammation and summarize recent findings of the cellular and molecular factors that alter islet microenvironment and β cell function in obesity and T2DM.

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胰岛稳态和适应的免疫调节

朗格汉斯胰岛产生内分泌激素来调节葡萄糖稳态。胰岛的正常功能依赖于胰岛微环境中细胞组成和细胞间相互作用的稳态调节。免疫细胞在胚胎发育过程中填充胰岛并参与胰岛器官发生和功能。在肥胖症中，包括胰岛在内的多个器官出现轻度炎症。肥胖相关的胰岛炎症在动物模型和人类中都很明显，其特征是免疫细胞的积累和炎性细胞因子/趋化因子和代谢介质的产生增加。在肥胖和 2 型糖尿病 (T2DM) 的发展过程中，髓系细胞（单核细胞和巨噬细胞）是胰岛炎症中免疫细胞的主要类型。