von Herrath M G, Holz A, Homann D, Oldstone M B
Department of Neuropharmacology, Scripps Research Institute, La Jolla, CA 92037, USA.
Semin Immunol. 1998 Feb;10(1):87-100. doi: 10.1006/smim.1997.0108.
Viral infections frequently elicit strong cellular and humoral immune responses. This bears the inherent danger of co-activating autoreactive lymphocytes, either through bystander activation by cytokines or through direct sharing of conformational determinants between self and virus (mimicry). Autoimmune diseases could then result, even after clearance of the viral infection, if enough autoreactive cells are activated. Alternatively, viral infection of antigen presenting cells can locally enhance inflammation and drive autoreactive lymphocytes. Evidence for these mechanisms, as well as emerging therapeutic concepts, will be discussed.
病毒感染常常引发强烈的细胞免疫和体液免疫反应。这存在共同激活自身反应性淋巴细胞的内在风险，其途径要么是通过细胞因子的旁观者激活，要么是通过自身与病毒之间构象决定簇的直接共享（模拟）。如果激活了足够多的自身反应性细胞，那么即使在病毒感染清除后也可能引发自身免疫性疾病。另外，抗原呈递细胞的病毒感染可局部增强炎症并驱动自身反应性淋巴细胞。将讨论这些机制的证据以及新出现的治疗理念。
