Abstract

The histopathology of the ordinary form of experimental allergic encephalomyelitis (EAE) is subject to considerable variation, depending on the duration and severity of the disease as well as on the age and species of the animal subject. In addition there are four distinct varieties that are characterized according to manner of production, location in the central nervous system (CNS) and histopathology. Localized EAE differs from ordinary EAE primarily in its topographic restriction to the environs of a CNS injury. Hyperacute EAE is produced with the aid of pertussis vaccine as sole or ancillary adjuvant; the histopathology features exudation of fibrin, edema fluid and polymorphonuclear neutrophils. The same process occurs in localized hyperacute EAE, but lesions are restricted to the perimeter of a CNS injury. All these forms of EAE can be produced by active immunization with CNS antigen and adjuvants, or by passive immunization with living lymphoid cells taken from actively immunized donors. Neutrophilic EAE has been described only after passive immunization inasmuch as it requires the transfer of encephalitogenic cells from a donor to a recipient with a drug-induced relative neutrophilia. The lesions of neutrophilic EAE contain a remarkable number of neutrophils, but fibrin and edema are not conspicuous. The technique of passive immunization has made it possible to produce this unique variant of EAE, and it has also facilitated studies of the evolution of lesions, the role of nonspecific cells, the effects of multiple attacks, and the effects of therapeutic modalities in all the forms of EAE.

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