The role of inflammation in insulitis and β-cell loss in type 1 diabetes
The role of inflammation in insulitis and β-cell loss in type 1 diabetes
复制标题
DOI：
10.1038/nrendo.2009.21
复制
发表时间：
2009-04-01
影响因子：
40.5
通讯作者：
Ortis, Fernanda
中科院分区：
文献类型：
--
作者：
Eizirik, Decio L.;Colli, Maikel L.;Ortis, Fernanda
1 型糖尿病 (T1DM) 是一种具有强烈炎症成分的慢性自身免疫性疾病。最新研究表明，先天免疫和炎症介质在 T1DM 中的作用比最初假设的要广泛得多。炎症可能有助于早期诱导和放大针对胰腺β细胞的免疫攻击，并在后期有助于稳定和维持胰岛炎。炎症介质可能有助于抑制 β 细胞功能和随后的细胞凋亡；它们还可能抑制或刺激β细胞再生，并可能导致外周胰岛素抵抗。炎症的不同影响发生在 T1DM 病程的不同阶段，应在入侵免疫细胞与目标 β 细胞之间的“对话”背景下予以考虑。这种对话由β细胞和免疫细胞释放的细胞因子和趋化因子以及死亡的β细胞传递的推定免疫原性信号介导。在这篇综述中，我们将炎症在 T1DM 中的作用分为三个任意阶段：胰岛炎的诱导、放大和维持或消退。这些阶段及其进展或解决可能取决于患者的遗传背景，这会导致疾病异质性。
Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease with a strong inflammatory component. The latest studies indicate that innate immunity and inflammatory mediators have a much broader role in T1DM than initially assumed. inflammation might contribute to early induction and amplification of the immune assault against pancreatic beta cells and, at later stages, to the stabilization and maintenance of insulitis. inflammatory mediators probably contribute to the suppression of beta-cell function and subsequent apoptosis; they may also inhibit or stimulate beta-cell regeneration and might cause peripheral insulin resistance. The different effects of inflammation take place in different phases of the course of T1DM, and should be considered in the context of a 'dialog' between invading immune cells and the target beta cells. This dialog is mediated both by cytokines and chemokines that are released by beta cells and immune cells, and by putative, immunogenic signals that are delivered by dying beta cells. in this review, we divided the role of inflammation in T1DM into three arbitrary stages: induction, amplification and maintenance or resolution of insulitis. These stages, and their progression or resolution, might depend on a patient's genetic background, which contributes to disease heterogeneity.