Iwami Shingo, Takeuchi Yasuhiro, Iwamoto Kentaro, Naruo Yoshimi, Yasukawa Masahiro
Graduate School of Science and Technology, Shizuoka University, Japan.
J Theor Biol. 2009 Feb 7;256(3):382-92. doi: 10.1016/j.jtbi.2008.09.038. Epub 2008 Oct 19.
Viruses have been implicated in the initiation, progression, and exacerbation of several human autoimmune diseases. Evidence also exists that viruses can protect against autoimmune disease. Several proposed mechanisms explain the viral effects. One mechanism is "molecular mimicry" which represents a shared immunologic epitope with a microbe and the host. We consider, using a simple mathematical model, whether and how a viral infection with molecular mimicry can be beneficial or detrimental for autoimmune disease. Furthermore, we consider the possibility of development of a vector therapeutic vaccine that can relieve autoimmune disease symptoms. Our findings demonstrate that vaccine therapy success necessitates (i) appropriate immune response function, (ii) appropriate affinities with self and non-self antigen, and (iii) a replicative vector vaccine. Moreover, the model shows that the viral infection can cause autoimmune relapses.
病毒与多种人类自身免疫性疾病的起始、进展和恶化有关。也有证据表明病毒可以预防自身免疫性疾病。有几种提出的机制可以解释病毒的作用。一种机制是“分子模拟”,即微生物与宿主具有共同的免疫表位。我们使用一个简单的数学模型来考虑,具有分子模拟的病毒感染对自身免疫性疾病是否有益以及如何有益或有害。此外,我们考虑开发一种可以缓解自身免疫性疾病症状的载体治疗性疫苗的可能性。我们的研究结果表明,疫苗治疗成功需要(i)适当的免疫反应功能,(ii)与自身和非自身抗原的适当亲和力,以及(iii)一种复制性载体疫苗。此外,该模型表明病毒感染可导致自身免疫复发。