Macrophages, cytokines and β-cell death in Type 2 diabetes
Macrophages, cytokines and β-cell death in Type 2 diabetes
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DOI：
10.1042/bst0360340
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发表时间：
2008-06-01
影响因子：
3.9
通讯作者：
Donath, Marc Y.
中科院分区：
文献类型：
--
作者：
Ehses, Jan A.;Boeni-Schnetzler, Marianne;Donath, Marc Y.
2型糖尿病患者胰岛的病理表现为炎症过程，其特征是免疫细胞浸润、细胞因子、凋亡细胞、淀粉样蛋白沉积，最终导致纤维化。事实上，对2型糖尿病患者的β细胞的分析显示，IL-1β(白细胞介素1β)的表达增加。此外，在人类2型糖尿病患者和大多数糖尿病动物模型中观察到胰岛相关巨噬细胞的增加。重要的是，在糖尿病发作之前，高脂饮食的小鼠的胰岛中就可以很早地检测到巨噬细胞数量的增加。这些免疫细胞可能被胰岛衍生的趋化因子所吸引，这些趋化因子是在新陈代谢压力下产生的，并受IL-1β的控制。因此，胰岛内炎症介质的调节，特别是白介素1β，可以预防2型糖尿病的胰岛炎症，因此成为一种有前途的治疗方法。
The pathology of islets from patients with Type 2 diabetes displays an inflammatory process characterized by the presence of immune cell infiltration, cytokines, apoptotic cells, amyloid deposits and, eventually, fibrosis. indeed, analysis of beta-cells from patients with Type 2 diabetes displays increased IL-1 beta (interleukin 1 beta) expression. Furthermore, increased islet-associated macrophages are observed in human Type 2 diabetic patients and in most animal models of diabetes. importantly, increased numbers of macrophages are detectable very early in high-fat-fed mice islets, before the onset of diabetes. These immune cells are probably attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1 beta. It follows that modulation of intra-islet inflammatory mediators, particularly interleukin-1 beta, may prevent islet inflammation in Type 2 diabetes and therefore presents itself as a promising therapeutic approach.