The immunopathogenesis of multiple sclerosis.
The aetiology of multiple sclerosis (MS) remains unknown. Evidence from clinical and animal studies strongly supports MS as an organ-specific autoimmune disease mediated by T helper 1 CD4+ autoreactive T cells. This chapter will review the evidence in favour of this theory, discuss central nervous system autoimmune hypotheses and outline the important inflammatory mechanisms involved in the immunopathogenesis of MS. The immunology applicable to the acute or isolated MS lesion is presented. Relevant clinical aspects of the disease are discussed to support and highlight potential inconsistencies in current thinking. Hypotheses are presented where parts of the immunopathogenic jigsaw puzzle remain incomplete, for example the mechanisms responsible for disease evolution. Where necessary, supportive evidence from the animal model experimental allergic encephalomyelitis is presented.
Giovannoni
G
G
Institute of Neurology, London, UK.
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000503:physiopathology; D015551:Autoimmunity / Q000187:drug effects / Q000235:genetics; D016207:Cytokines / Q000502:physiology; D003711:Demyelinating Diseases / Q000276:immunology; D018450:Disease Progression; D006801:Humans; D007156:Immunologic Memory; D008213:Lymphocyte Activation; D009103:Multiple Sclerosis / Q000276:immunology* / Q000503:physiopathology; D009410:Nerve Degeneration / Q000276:immunology / Q000503:physiopathology; D012008:Recurrence; D012075:Remission, Spontaneous; D013601:T-Lymphocytes / Q000502:physiology; D013997:Time Factors
D016207:Cytokines