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.
|Persistent URL||dx.doi.org/10.1016/j.molmed.2009.04.001, hdl.handle.net/1765/24474|
|Journal||Trends in Molecular Medicine|
't Hart, B.A, Hintzen, R.Q, & Laman, J.D. (2009). Multiple sclerosis - a response-to-damage model. Trends in Molecular Medicine, 15(6), 235–244. doi:10.1016/j.molmed.2009.04.001