Institute of Biomedical & Clinical Science, University of Exeter Medical School, Exeter, Devon, UK.
Curr Opin Pharmacol. 2018 Dec;43:11-19. doi: 10.1016/j.coph.2018.07.006. Epub 2018 Jul 29.
The development of islet autoimmunity and type 1 diabetes has long been linked with enteroviral infection but a causal relationship has proven hard to establish. This is partly because much of the epidemiological evidence derives from studies of neutralising antibody generation in blood samples while less attention has been paid to the pancreatic beta cell as a site of infection. Nevertheless, recent studies have revealed that beta cells express specific enteroviral receptors and that they can sustain a productive enteroviral infection. Importantly, they can also mount antiviral responses which attenuate viral replication and may favour the establishment of a persistent enteroviral infection. Together, these responses combine to create the Trojan horse by which enteroviruses might precipitate islet autoimmunity.
胰岛自身免疫和 1 型糖尿病的发展长期以来一直与肠道病毒感染有关,但因果关系很难确定。这在一定程度上是因为,大部分流行病学证据来自于血液样本中中和抗体生成的研究,而对胰腺β细胞作为感染部位的关注较少。然而,最近的研究表明,β细胞表达特定的肠道病毒受体,并且可以维持有效的肠道病毒感染。重要的是,它们还可以产生抗病毒反应,从而抑制病毒复制,并可能有利于建立持续的肠道病毒感染。这些反应共同构成了特洛伊木马,肠道病毒可能通过它引发胰岛自身免疫。