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The close similarities existing between experimental allergic neuritis and the Guillain-Barré syndrome constitute the main argument in favour of the immune nature of the syndrome. The studies devoted to the identification of antigenic determinants of myelin in the peripheral nervous system are reviewed. Whether the immune mechanisms involved are humoral or cellular remains under discussion, and the data in favour of one or the other in both the experimental and the clinical disease are presented. It must be noted that while the Guillain-Barré syndrome most probably results from an immune reaction, the antigen against which it is directed has not yet been determined. Contrary to the commonly held view, the Guillain-Barré syndrome may leave sequelae which are unpredictable, save for the fact that the plateau phase is significantly longer in such cases. Therapeutically, the ineffectiveness of corticosteroid treatment has been established; controlled study aimed at assessing the value of plasmapheresis are under way.

Autoimmune diseases are experimental models of human demyelinating diseases such as multiple sclerosis and idiopathic polyneuritis: experimental auto-immune encephalomyelitis (EAE) and experimental autoimmune neuritis. Demyelinating lesions occurring in chronic EAE could be due to the action of autoantibodies rather than to a cellular action involving lymphokines. An antibody-dependent cellular myelinotoxicity could also be the mechanism responsible for demyelination; these mechanisms are suggested by in vitro and in vivo demyelination experiments and by the presence of demyelinating autoantibodies against component(s) of myelin in EAE area. The demyelinating mechanisms could be the same in multiple sclerosis. However, they have not been proven so far.