Virus-mediated autoimmunity in Multiple Sclerosis.

Nikolaos Grigoriadis, Georgios M Hadjigeorgiou
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引用次数: 48

Abstract

Epidemiological data suggest the notion that in Multiple Sclerosis (MS) is an acquired autoimmune disease and the cause may be an environmental factor(s), probably infectious, in genetically susceptible individuals. Several cases of viral induced demyelinatimg encephalomyelitis in human beings and in experimental models as well as the presence of IgG oligoclonal bands in the cerebrospinal fluid indicate that the infectious factor may be viral. However, the absence of a specific virus identification in MS central nervous system may hardly support this notion. On the other hand, the partial response of patients with MS to immunosuppressive and immunomodulatory therapy support the evidence of an autoimmune etiology for MS. However, the autoimmune hypothesis shares the same criticism with the infectious one in that no autoantigen(s) specific to and causative for MS has ever been identified. Nevertheless, the absence of identifiable infectious agent, especially viral does not rule out its presence at a certain time--point and the concomitant long term triggering of an autoimmune cascade of events thereafter. Several concepts have emerged in an attempt to explain the autoimmune mechanisms and ongoing neurodegeneration in MS on the basis of the infectious--viral hypothesis.

Abstract Image

多发性硬化症病毒介导的自身免疫
流行病学数据表明,多发性硬化症(MS)是一种获得性自身免疫性疾病,其病因可能是环境因素,可能是遗传易感个体的传染性因素。在人类和实验模型中出现的几例病毒诱导的脱髓鞘性脑脊髓炎以及脑脊液中IgG寡克隆带的存在表明,感染因素可能是病毒。然而,在MS中枢神经系统中缺乏特异性的病毒鉴定可能很难支持这一观点。另一方面,多发性硬化症患者对免疫抑制和免疫调节治疗的部分反应支持了多发性硬化症的自身免疫性病因的证据。然而,自身免疫性假说与感染性假说同样受到批评,因为没有发现多发性硬化症特异性和致病性的自身抗原。然而,没有可识别的感染因子,特别是病毒,并不排除它在某个时间点的存在,以及随之而来的长期自身免疫级联事件的触发。在感染病毒假说的基础上,出现了几个概念,试图解释多发性硬化症的自身免疫机制和正在进行的神经退行性变。
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