Department of Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, Rome 00161, Italy.
Department of Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, Rome 00161, Italy.
Mult Scler Relat Disord. 2022 Oct;66:104069. doi: 10.1016/j.msard.2022.104069. Epub 2022 Jul 22.
The EBV as the 'gluten of MS' hypothesis discussed by Drosu et al. in a recent Editorial envisages the existence of similar mechanisms leading to celiac disease and multiple sclerosis, such as induction of immunity against an ubiquitous exogenous antigen - gluten and EBV, respectively - and subsequent development of autoimmunity that is maintained by persistence of the initial trigger. While this hypothesis provides the rationale for treating MS with antivirals to lower EBV load, it can be misleading when trying to translate concepts of T cell-B cell interaction and autoimmunity development in celiac disease to multiple sclerosis. Here, we propose that EBV might act as the driver of multiple sclerosis without involving autoimmunity.
多瘤病毒(EBV)作为 Drosu 等人在最近的社论中讨论的“多发性硬化症的谷蛋白”假说,设想存在类似的机制导致乳糜泻和多发性硬化症,例如分别针对无处不在的外源性抗原-谷蛋白和 EBV 产生免疫,以及随后由最初触发因素持续存在维持的自身免疫的发展。虽然该假说为用抗病毒药物降低 EBV 载量治疗多发性硬化症提供了依据,但在试图将乳糜泻中 T 细胞-B 细胞相互作用和自身免疫发展的概念转化为多发性硬化症时,可能会产生误导。在这里,我们提出 EBV 可能在不涉及自身免疫的情况下作为多发性硬化症的驱动因素。