Krone Bernd, Grange John M
Institute of Virology, Centre for Hygiene and Human Genetics, University of Göttingen, Kreuzbergring 57, 37075 Göttingen, Germany.
Autoimmune Dis. 2010 Dec 20;2011:708750. doi: 10.4061/2011/708750.
The immunological background of multiple sclerosis (MS) manifests as an altered reactivity against a diverse range of infections, particularly with the Epstein-Barr virus. Although this could be only an epiphenomenon of a more generalised dysfunction of the immune system in MS, it is also possible that a complex infectious background forms the basis of a specific immune dysregulation finally causing the disease. It is thus suggested that the complex infectious background bears the key for an understanding of the immune pathogenesis of the disease. It appears probable that improved standards of hygiene cause regulatory defects in the immune system, allowing the abnormal expression of human endogenous retroviral (HERV) genes. On the basis of epidemiological observations we describe how a failure of expansion or an eclipse of a subfraction of self-antigen-specific CD8(+) T cells mediating immune repair, and a deleterious mode of action of HERV gene products, could underlie the pathogenesis of MS.
多发性硬化症（MS）的免疫学背景表现为对多种感染的反应性改变，尤其是对爱泼斯坦-巴尔病毒的反应。虽然这可能只是MS中免疫系统更广泛功能障碍的一种附带现象，但也有可能复杂的感染背景构成了特定免疫失调的基础，最终导致了该疾病。因此，有人提出复杂的感染背景是理解该疾病免疫发病机制的关键。卫生标准的提高似乎可能导致免疫系统的调节缺陷，从而使人类内源性逆转录病毒（HERV）基因异常表达。基于流行病学观察，我们描述了介导免疫修复的自身抗原特异性CD8(+) T细胞亚群的扩增失败或缺失，以及HERV基因产物的有害作用模式，如何可能是MS发病机制的基础。
