Department of Pathology, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium.
Diabetologia. 2011 Sep;54(9):2220-2. doi: 10.1007/s00125-011-2224-3. Epub 2011 Jun 24.
Defining the role of viruses in the aetiopathogenesis of human type 1 diabetes has been an elusive goal for more than 40 years, although indirect evidence is mounting that viruses have an important modulatory role in the development of the disease through their interaction with the innate immune system. In this issue of Diabetologia, Willcox et al. provide histopathological evidence that the islets of Langerhans in seven young patients with recent-onset disease expressed the enteroviral protein VP1 and report that this marker is preferentially present in islets that show signs of enhanced replicative activity. They suggest that insulitis may be the common factor linking beta cell replication and VP1 positivity, with persistent virus infection leading to chemokine secretion, infiltration of immune cells (insulitis) and pro-inflammatory cytokine-induced beta cell replication.
四十多年来,明确病毒在人类 1 型糖尿病发病机制中的作用一直是一个难以实现的目标,尽管越来越多的间接证据表明,病毒通过与先天免疫系统相互作用,在疾病的发展中具有重要的调节作用。在本期《糖尿病学》中,Willcox 等人提供了组织病理学证据,表明七名近期发病的年轻患者的胰岛中表达了肠病毒蛋白 VP1,并报告称该标志物主要存在于显示增强复制活性的胰岛中。他们认为,胰岛炎可能是将β细胞复制与 VP1 阳性联系起来的共同因素,持续的病毒感染导致趋化因子分泌、免疫细胞浸润(胰岛炎)和促炎细胞因子诱导的β细胞复制。