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Trends Mol Med. 2009 Jun;15(6):235-44. doi: 10.1016/j.molmed.2009.04.001. Epub 2009 May 18.

Multiple sclerosis - a response-to-damage model.

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Department of Immunobiology, Biomedical Primate Research Center, Lange Kleiweg 139, 2288 GJ Rijswijk, The Netherlands.


According to a widely supported but unproven concept, the autoimmune mechanisms that drive neuroinflammation in multiple sclerosis (MS) are triggered by virus infection. However, a direct viral trigger of MS has not been identified. MS models in non-human primates suggest that lifelong asymptomatic infection with certain herpesviruses (e.g. cytomegalovirus) creates a repertoire of potentially autoreactive memory T cells. When these are exposed to antigens released after central nervous system injury as a consequence of an unknown pathogenic event, they are reactivated and induce autoimmune neurological disease. This response-to-damage of antiviral memory cells can take place years after the initiating infection. Consequently, elucidating the anti-herpesvirus T-cell repertoire might provide new targets for preventive diagnosis and therapy.

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