Abstract
Experimental allergic encephalomyelitis (EAE) is considered a model of autoimmune disease. The development of cellular immunity of delayed hypersensitivity type in the pathogenesis of this disease seems established (1, 2). Less well defined are the relative contributions of humoral events in this process. Bornstein (3) and Appel and Bornstein (3, 4) demonstrated specific antimyelin antibody activity in this disease in tissue culture, while Sherwin et al. (5) showed by immunofluorescence the presence of specific antibody in rabbit central nervous system (CNS) in EAE. More recently, Oldstone and Dixon found that the earliest microscopic change in the CNS of Lewis rats with developing EAE is the appearance of C3, IgG. and fibrinogen in the vessel walls; and IgG and C3 around neurons in the parenchyma itself (6). These deposits seemed to be specific since they were present only in the brain among a number of organs studied and were shown not to reflect more general deposition of serum proteins. Thus, presence...
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