Clinic of Endocrinology and Diabetes, Center for Integrated Human Physiology, University Hospital of Zurich, 8091 Zurich, Switzerland.
Trends Endocrinol Metab. 2010 May;21(5):261-7. doi: 10.1016/j.tem.2009.12.010. Epub 2010 Jan 22.
Islets produce a variety of cytokines and chemokines in response to physiologic and pathologic stimulation by nutrients. The cellular source of these inflammatory mediators includes alpha-, beta-, endothelial-, ductal- and recruited immune cells. Islet-derived cytokines promote alpha- and beta-cell adaptation and repair in the short term. Eventually, chronic metabolic stress can induce a deleterious autoinflammatory process in islets leading to insulin secretion failure and type 2 diabetes. Understanding the specific role of islet derived cytokines and chemokines has opened the door to targeted clinical interventions aimed at remodeling islet inflammation from destruction to adaptation. In this article, we review the islet cellular origin of various cytokines and chemokines and describe their regulation and respective roles in physiology and diabetes.
胰岛在受到营养物质的生理和病理刺激时会产生多种细胞因子和趋化因子。这些炎症介质的细胞来源包括α细胞、β细胞、内皮细胞、导管细胞和募集的免疫细胞。胰岛来源的细胞因子在短期内促进α细胞和β细胞的适应和修复。然而，慢性代谢应激可导致胰岛中有害的自身炎症过程，导致胰岛素分泌失败和 2 型糖尿病。了解胰岛来源的细胞因子和趋化因子的特定作用为靶向临床干预开辟了道路，旨在将胰岛炎症从破坏重塑为适应。本文综述了各种细胞因子和趋化因子的胰岛细胞来源，并描述了它们在生理和糖尿病中的调节及其各自作用。
