Virus infection, antiviral immunity, and autoimmunity.
Virus infection, antiviral immunity, and autoimmunity.
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DOI：
10.1111/imr.12091
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发表时间：
2013-09
影响因子：
8.7
通讯作者：
Miller SD
中科院分区：
文献类型：
--
作者：
Getts DR;Chastain EM;Terry RL;Miller SD
作为一组疾病，自身免疫性疾病在西方世界中是发病率和死亡率的第三大最普遍原因。然而，大多数自身免疫性疾病的病因仍然未知。虽然遗传连锁研究支持遗传学的关键作用，但这些疾病的地理分布以及单卵双胞胎的低一致率表明，包括环境因素在内的其他因素也参与其中。病毒感染是引发自身免疫性疾病的主要因素。感染引发了一个强大的，通常协调良好的免疫反应，这是病毒清除的关键。然而，在某些情况下，免疫调节机制可能会动摇，最终导致自身耐受性的崩溃，导致针对病毒和自身抗原的免疫介导的攻击。传统上，交叉反应性T细胞识别，称为分子模拟，以及旁观者T细胞活化，最终在表位扩散，已阐明的主要机制，通过感染可能最终在T细胞介导的自身免疫反应。然而，包括病毒诱导的免疫系统诱饵在内的其他假设也值得讨论它们触发自身免疫的潜力。本文就病毒感染和抗病毒免疫在自身免疫中的作用机制作一综述。
As a group of disorders, autoimmunity ranks as the third most prevalent cause of morbidity and mortality in the Western World. However, the etiology of most autoimmune diseases remains unknown. Although genetic linkage studies support a critical underlying role for genetics, the geographic distribution of these disorders as well as the low concordance rates in monozygotic twins suggest that a combination of other factors including environmental ones are involved. Virus infection is a primary factor that has been implicated in the initiation of autoimmune disease. Infection triggers a robust and usually well-coordinated immune response that is critical for viral clearance. However, in some instances, immune regulatory mechanisms may falter, culminating in the breakdown of self-tolerance, resulting in immune-mediated attack directed against both viral and self-antigens. Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as bystander T-cell activation, culminating in epitope spreading, have been the predominant mechanisms elucidated through which infection may culminate in an T-cell-mediated autoimmune response. However, other hypotheses including virus-induced decoy of the immune system also warrant discussion in regard to their potential for triggering autoimmunity. In this review, we discuss the mechanisms by which virus infection and antiviral immunity contribute to the development of autoimmunity.
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DOI：
10.1016/j.bbadis.2010.07.008
发表时间：
2011-02
影响因子：
6.2
作者：
Chastain, Emily M. L.;Duncan, D'Anne S.;Rodgers, Jane M.;Miller, Stephen D.
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影响因子：
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10.1084/jem.192.3.393
发表时间：
2000-08-07
期刊：
The Journal of experimental medicine
影响因子：
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Rajewsky K
DOI：
10.1038/nrmicro2071
发表时间：
2009-02
期刊：
Nature reviews. Microbiology
影响因子：
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