Multiple sclerosis - a response-to-damage model.
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.
't Hart
Bert A
BA
Department of Immunobiology, Biomedical Primate Research Center, Lange Kleiweg 139, 2288 GJ Rijswijk, The Netherlands. hart@bprc.nl
Hintzen
Rogier Q
RQ
Laman
Jon D
JD
D000818:Animals; D002490:Central Nervous System / Q000276:immunology / Q000473:pathology / Q000821:virology; D006564:Herpesviridae / Q000502:physiology; D006801:Humans; D009103:Multiple Sclerosis / Q000276:immunology* / Q000473:pathology / Q000628:therapy / Q000821:virology