人类1型糖尿病的胰腺病理。

A. Foulis
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引用次数: 26

摘要

在1型自身免疫性糖尿病中,胰岛素分泌β细胞被选择性破坏。在临床表现前后,大多数病例存在胰岛素炎,一种慢性炎症浸润胰岛,主要影响含胰岛素的胰岛。炎性浸润主要由T淋巴细胞组成;CD8细胞多于CD4细胞,B淋巴细胞较少,巨噬细胞相对稀少。β细胞死亡可能涉及Fas凋亡途径,因为它们已被证明表达Fas,浸润性T淋巴细胞表达Fas- l和凋亡的β细胞已被描述。在许多含胰岛素的胰岛中,所有内分泌细胞高表达I类MHC是一种公认的现象,是本病的特征。有人认为,这是一个比胰岛内的胰岛素炎更早的事件,似乎是由于胰岛内的β细胞分泌干扰素α。最近的一项研究发现,在新近发病的1型糖尿病患者的6例胰腺中,有3例的β细胞感染柯萨奇病毒。已知柯萨奇病毒诱导β细胞分泌α干扰素,这可能引发一系列事件,最终导致自身免疫破坏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pancreatic pathology in type 1 diabetes in human.
In type 1 autoimmune diabetes there is a selective destruction of insulin-secreting beta cells. Around the time of clinical presentation, insulitis, a chronic inflammatory infiltrate of the islets affecting primarily insulin containing islets, is present in the majority of cases. The inflammatory infiltrate consists primarily of T lymphocytes; CD8 cells outnumber CD4 cells, there are fewer B lymphocytes and macrophages are relatively scarce. beta cell death may involve the Fas apoptotic pathway since they have been shown to express Fas, infiltrating T lymphocytes express Fas-L and apoptotic beta cells have been described. Hyperexpression of class I MHC by all the endocrine cells in many insulin-containing islets is a well recognized phenomenon, characteristic of the disease. It has been argued that this is an earlier event than insulitis within a given islet and appears to be due to secretion of interferon alpha by beta cells within that islet. A recent study has found evidence of Coxsackie virus infection in beta cells in three out of six pancreases of patients with recent-onset type 1 diabetes. Coxsackie viruses are known to induce interferon alpha secretion by beta cells and this could initiate the sequence of events that culminates in their autoimmune destruction.
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