[Electron microscopic study of experimental allergic encephalomyelitis in dogs. II. Relationship between ultrastructural changes in the central nervous system and the severity of the course. Mechanism of allergic demyelination]

Abstract

It is determined that in grave forms of experimental allergic encephalomyelitis (EAE) demyelination and inflammatory infiltration are spread widely, whereas in easy forms only demyelination is observed. A conclusion is made that disturbances in the vascular permeability, activation of lysosomes and degeneration of synapses are of pathogenic value. Important role of a glia in phagocytizing myelin is emphasized. Significance of the role of immunological humoral factors and of biologic active substances in the pathogenesis of EAE is discussed.