Inflammatory mechanisms in diabetes: lessons from the beta-cell.

H E Hohmeier, V V Tran, G Chen, R Gasa, C B Newgard
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引用次数: 50

Abstract

Inflammation plays an important role in the destruction of pancreatic islet beta-cells that leads to type I diabetes. This involves infiltration of T-cells and macrophages into the islets and local production of inflammatory cytokines such as interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. Our laboratory has developed several strategies for protecting beta-cells against oxidative stress and cytokine-induced cytotoxicity. These include a cytokine selection strategy that results in cell lines that are resistant to the combined effects of IL-1 beta+IFN-gamma. More recently, we have combined the cytokine selection procedure with overexpression of the antiapoptotic gene bcl-2, resulting in cell lines with greater resistance to oxidative stress and cytokine-induced damage than achieved with either procedure alone. This article summarizes this work and the remarkably divergent mechanisms by which protection is achieved in the different model systems. We also discuss the potential relevance of insights gained from these approaches for enhancing islet cell survival and function in both major forms of diabetes.

糖尿病的炎症机制:来自β细胞的教训。
炎症在胰岛β细胞的破坏中起着重要作用,导致I型糖尿病。这包括t细胞和巨噬细胞浸润到胰岛和局部产生炎性细胞因子,如白细胞介素(IL)-1 β、肿瘤坏死因子(TNF)- α和干扰素(IFN)- γ。我们的实验室已经开发了几种策略来保护β细胞免受氧化应激和细胞因子诱导的细胞毒性。其中包括细胞因子选择策略,该策略导致细胞系能够抵抗IL-1 β + ifn - γ的联合作用。最近,我们将细胞因子选择过程与抗凋亡基因bcl-2的过度表达结合起来,使细胞系对氧化应激和细胞因子诱导的损伤具有更强的抵抗力,而不是单独使用任何一种方法。本文总结了这项工作以及在不同模型系统中实现保护的显著不同机制。我们还讨论了从这些方法中获得的见解对提高两种主要糖尿病形式的胰岛细胞存活和功能的潜在相关性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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