Stys Peter K
Department of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary 3330 Hospital Dr. NW, Calgary T2N 4N1 Canada.
F1000Prime Rep. 2013 Jun 3;5:20. doi: 10.12703/P5-20. Print 2013.
Despite a century of intensive investigation, the underlying cause of multiple sclerosis has eluded us. It is clear that there exists a prominent progressive degenerative phenotype together with an important autoimmune inflammatory component, and careful histopathological examination always shows, to a greater or lesser degree, concomitant degeneration/demyelination and adaptive T cell-dependent immune responses. Given this picture, it is difficult, if not impossible, to definitively say whether degeneration or autoimmunity is the initiator of the disease. In this review, I put forward the evidence for and against both models and speculate that, in contrast to the accepted view, it is equally likely that multiple sclerosis may be a degenerative disease that secondarily elicits an autoimmune response, and suggest how this might influence therapeutic approaches.
尽管经过了一个世纪的深入研究,我们仍未找到多发性硬化症的根本病因。很明显,该病存在显著的进行性退行性表型以及重要的自身免疫炎症成分,仔细的组织病理学检查总是或多或少地显示出伴随的变性/脱髓鞘以及适应性T细胞依赖性免疫反应。鉴于此情况,很难(甚至不可能)明确断定变性或自身免疫是该疾病的起始因素。在这篇综述中,我提出了支持和反对这两种模型的证据,并推测,与普遍观点相反,多发性硬化症同样有可能是一种继发性引发自身免疫反应的退行性疾病,并提出这可能如何影响治疗方法。