Key result
Human T-lymphotrophic viruses (HTLVs) and other enveloped viruses are hypothesized to induce autoimmunity in multiple sclerosis by triggering class II antigen expression on brain cells.
The paper proposes a hypothesis that HTLVs and other enveloped viruses may trigger autoimmunity in multiple sclerosis by causing expression of class II antigens on brain cells.
Should not change MS practice; leaves open whether HTLVs trigger autoimmunity via class II antigen expression.
A virally induced autoimmune reaction may be important in the pathogenesis of multiple sclerosis. The role that glycolipids and myelin basic protein presented to the virus may play in this process is considered. The most likely cells to be the source of autoantigens are neurons, myelin and oligodendrocytes. Viral infection of class II-expressing cells and association of the viral envelope autoantigens and the class II molecules could trigger an autoimmune reaction. It is suggested that for MS to develop following a virus infection the virus will need to cause expression of class II antigens on brain cells as well as fulfill the same role as an antigen presenting cell. The part which T-lymphotrophic viruses (HTLVs) and other enveloped viruses may play in this phenomenon is discussed.
No takes yet. Share an insight, caveat, or question.
Dalgleish et al. (1987) conducted a review in Multiple sclerosis. Human T-lymphotrophic viruses (HTLVs) and other enveloped viruses was evaluated. Human T-lymphotrophic viruses (HTLVs) and other enveloped viruses are hypothesized to induce autoimmunity in multiple sclerosis by triggering class II antigen expression on brain cells.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: