The etiology of MS is not known but there is ample evidence that MS has an immunopathogenic basis and that both genetic and environmental factors contribute to the pathogenesis of the disease.
Most direct evidence to support the influence of genetic factors comes from family studies and from the comparison of concordance in monozygotic (MZ) and dizygotic (DZ) twins. A higher concordance rate (30%) has been found consistently in MZ twins. Furthermore, magnetic resonance imaging (MRI) studies showed lesions in 40% of 'clinically normal' monozygotic twins of individuals with MS. Although the disease is not genetically determined, genetic factors such as the HLA class II alleles within the MHC consistently seem to influence the susceptibility to develop MS. The development of the disorder is believed to be the consequence of multiple genes plus an environmental factor. Different HLA-DR specificities are associated with MS in different ethnic groups and the MHC association with MS appears to be less important than that seen in other autoimmune diseases such as rheumatoid arthritis and type I diabetes, suggesting that other loci contribute to the genetic susceptibility.
Evidence for environmental factors is largely derived from epidemiological studies. The epidemiological data indicate that MS is related to an infectious agent encountered during childhood. Over the years, more than ten different viruses have been implicated in the etiology of MS, but thus far, no single agent related to the disease has been confirmed. MBP-specific lymphocytes belong to the 'normal' T cell repertoire and it is possible that these cells are expanded by myelin release during MS or virus infection. It is also possible that self-reactive T cells are activated by the recognition of epitopes shared by virus and auto-antigen (molecular mimicry).
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