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首页> 外文期刊>Diabetologia >The role of viruses in Type I diabetes: two distinct cellular and molecular pathogenic mechanisms of virus-induced diabetes in animals
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The role of viruses in Type I diabetes: two distinct cellular and molecular pathogenic mechanisms of virus-induced diabetes in animals

机译：病毒在I型糖尿病中的作用：动物诱发病毒的糖尿病的两种不同的细胞和分子致病机制

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Type I (insulin-dependent) diabetes mellitus results from the progressive loss of pancreatic beta cells. Environmental factors are believed to play an important part in the development of Type I diabetes by influencing the penetrance of diabetes susceptibility genes. As one environmental factor, the virus has long been considered to play a part in this disease. To date 13 different viruses have been reported to be associated with the development of Type I diabetes in humans and in various animal models. The most clear and unequivocal evidence that a virus induces diabetes in animals comes from studies on the d variant of the encephalomyocarditis (EMC-D) virus in mice and the Kilham rat virus (KRV) in rats. The infection of genetically susceptible strains of mice with a high titre of EMC-D virus results in the development of diabetes within 3 days. This is largely due to the rapid destruction of beta cells by the replication of the virus within the beta cells. In contrast, the infection of mice with a low titre of EMC-D virus results in a limited replication of the virus before the induction of neutralizing anti-virus antibody and the subsequent recruitment of activated macrophages. The Src kinases, particularly hck, play an important part in the activation of macrophages and the subsequent production of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and nitric oxide (NO), leading to the destruction of beta cells which results in the development of diabetes. The Kilham rat virus causes autoimmune diabetes in diabetes resistant (DR)-BB rats without infection of beta cells. The infection of DR-BB rats with KRV results in the disruption of the finely tuned immune balance of Th1-like CD45RC+CD4+ and Th2-like CD45RC-CD4+ T cells, leading to the selective activation of beta-cell-cytotoxic effector T cells. [Diabetologia (2001) 44: 271–285]
机译：I型（胰岛素依赖型）糖尿病是由胰腺β细胞的逐渐丧失引起的。人们认为，环境因素通过影响糖尿病易感基因的渗透性，在I型糖尿病的发展中起着重要作用。作为一种环境因素，长期以来人们一直认为该病毒在这种疾病中起作用。迄今为止，已经报道了13种不同的病毒与人类和各种动物模型中I型糖尿病的发生有关。病毒在动物中诱发糖尿病的最明确和明确的证据来自对小鼠脑心肌炎（EMC-D）病毒的d变体和大鼠Kilham大鼠病毒（KRV）的研究。高滴度的EMC-D病毒感染遗传易感品系的小鼠导致3天内患上糖尿病。这主要是由于病毒在β细胞内的复制而迅速破坏了β细胞。相反，以低滴度的EMC-D病毒感染小鼠会导致病毒复制受限，然后诱导中和性抗病毒抗体并随后募集活化的巨噬细胞。 Src激酶，特别是hck，在巨噬细胞的活化以及随后的肿瘤坏死因子（TNF）-α，白介素（IL）-1β和一氧化氮（NO）的产生中起重要作用，导致β细胞的破坏导致糖尿病的发展。 Kilham大鼠病毒可在没有感染β细胞的情况下在抗糖尿病（DR）-BB大鼠中引起自身免疫性糖尿病。 DR-BB大鼠感染KRV导致Th1类CD45RC + CD4 + 和Th2类CD45RC- CD4 + T细胞的微调免疫平衡受到破坏，导致选择性激活β细胞的细胞毒性效应T细胞。 [糖尿病（2001）44：271–285]

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