Department of Mathematics, University of Sussex, Falmer, Brighton BN1 9QH, UK.
J Theor Biol. 2012 Sep 7;308:45-55. doi: 10.1016/j.jtbi.2012.05.019. Epub 2012 May 31.
It has been known for some time that human autoimmune diseases can be triggered by viral infections. Several possible mechanisms of interactions between a virus and immune system have been analysed, with a prevailing opinion being that the onset of autoimmunity can in many cases be attributed to "molecular mimicry", where linear peptide epitopes, processed from viral proteins, mimic normal host self-proteins, thus leading to a cross-reaction of immune response against virus with host cells. In this paper we present a mathematical model for the dynamics of an immune response to a viral infection and autoimmunity, which takes into account T cells with different activation thresholds. We show how the infection can be cleared by the immune system, as well as how it can lead to a chronic infection or recurrent infection with relapses and remissions. Numerical simulations of the model are performed to illustrate various dynamical regimes, as well as to analyse the potential impact of treatment of autoimmune disease in the chronic and recurrent states. The results provide good qualitative agreement with available data on immune responses to viral infections and progression of autoimmune diseases.
一段时间以来，人们已经知道人类自身免疫性疾病可能由病毒感染引发。人们已经分析了病毒和免疫系统之间相互作用的几种可能机制，一种主流观点认为，在许多情况下，自身免疫的发作可以归因于“分子模拟”，即来自病毒蛋白的线性肽表位模拟正常宿主自身蛋白，从而导致针对病毒的免疫反应与宿主细胞发生交叉反应。在本文中，我们提出了一个针对病毒感染和自身免疫的免疫反应动力学的数学模型，该模型考虑了具有不同激活阈值的 T 细胞。我们展示了免疫系统如何清除感染，以及它如何导致慢性感染或反复感染，伴有复发和缓解。对模型进行数值模拟，以说明各种动态状态，并分析在慢性和反复状态下治疗自身免疫性疾病的潜在影响。结果与关于病毒感染的免疫反应和自身免疫性疾病进展的现有数据具有很好的定性一致性。
