作者: Pierre J. Talbot , Annie Boucher , Pierre Duquette , Edith Gruslin
关键词: Immunology 、 Immune system 、 Proteolipid protein 1 、 T cell 、 Biology 、 Molecular mimicry 、 Myelin 、 Antigen 、 Autoimmune disease 、 Multiple sclerosis
摘要: Multiple sclerosis (MS) is an autoimmune disease in which autoreactive T cells specific to central nervous system (CNS) myelin antigens are activated. Although etiology remains unknown, coronaviruses suspected be involved MS pathology. Molecular mimicry, the recognition of two by a single immune cell, could mechanism explaining link between viral infection and through activation myelin-reactive virus genetically predisposed individual. Evidence supporting this hypothesis humans has been accumulated our laboratory. Human coronavirus (HCoV) — cross-reactive T-cell lines (TCL) were predominantly found patients compared with other neurological or inflammatory diseases, healthy controls. Moreover, virus-myelin cell cross-reactivity was confirmed at clonal level. mimicry infectious pathogens such as ubiquitous human respiratory could, susceptible individuals, play role leading development MS. Together possible mechanisms bystander effects, epitope spreading even superantigenic activities, pathogen-associated induction maintaining broadening response associated