促炎细胞因子
炎症
小岛
胰岛
生物
分泌物
先天免疫系统
免疫系统
细胞因子
免疫学
受体
胰岛素
内分泌学
生物化学
作者
Masamichi Fujita,Takashi Miyazawa,Kei Uchida,Naohiro Uchida,Shojiro Haji,Shunsuke Yano,Norifusa Iwahashi,Tomoko Hatayama,Shunsuke Katsuhara,Shintaro Nakamura,Yukina Takeichi,Maki Yokomoto‐Umakoshi,Yukihisa Miyachi,Ryuichi Sakamoto,Yoichiro Iwakura,Yoshihiro Ogawa
出处
期刊:Endocrinology
[The Endocrine Society]
日期:2023-11-20
卷期号:165 (1)
标识
DOI:10.1210/endocr/bqad181
摘要
Abstract Pancreatic islet inflammation plays a crucial role in the etiology of type 2 diabetes (T2D). Macrophages residing in pancreatic islets have emerged as key players in islet inflammation. Macrophages express a plethora of innate immune receptors that bind to environmental and metabolic cues and integrate these signals to trigger an inflammatory response that contributes to the development of islet inflammation. One such receptor, Dectin-2, has been identified within pancreatic islets; however, its role in glucose metabolism remains largely unknown. Here we have demonstrated that mice lacking Dectin-2 exhibit local inflammation within islets, along with impaired insulin secretion and β-cell dysfunction. Our findings indicate that these effects are mediated by proinflammatory cytokines, such as interleukin (IL)-1α and IL-6, which are secreted by macrophages that have acquired an inflammatory phenotype because of the loss of Dectin-2. This study provides novel insights into the mechanisms underlying the role of Dectin-2 in the development of islet inflammation.
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