作者: Gerald L. Stoner
DOI: 10.1111/J.1750-3639.1993.TB00748.X
关键词: Myelin 、 Progressive multifocal leukoencephalopathy 、 Demyelinating disease 、 Pathogenesis 、 Molecular mimicry 、 Biology 、 Multiple sclerosis 、 Immunology 、 Autoimmunity 、 JC virus
摘要: Multiple sclerosis (MS) is generally considered to be an autoimmune disorder with myelin as the target and several unidentified viruses playing ancillary roles, possibly through molecular mimicry. Although this paradigm has led important progress on potential mechanisms of loss, neither a antigen in nor triggering mechanism yet been identified, leaving etiology MS still unknown. Animal models viral demyelination studies showing that JC virus (JCV), polyomavirus which causes progressive multifocal leukoencephalopathy (PML), may latent some normal human brains suggest another possibility. A host immune response targeting proteins expressed at low levels from DNA central nervous system (CNS) might underlie focal demyelinating disease such MS. shift autoimmunity latent-virus model not trivial substitution antigens. This would expand search for definitive laboratory test could lead improved therapeutic preventive approaches.