Relapsing experimental allergic encephalomyelitis an autoimmune model of multiple sclerosis
Open Access
- 1 August 1985
- journal article
- Published by Springer Nature in Springer Seminars in Immunopathology
- Vol. 8 (3), 197-208
- https://doi.org/10.1007/bf00197296
Abstract
R-EAE is a valuable model for human MS. Table 2 outlines the similarities between R-EAE and MS. The clinical course and pathologic changes seen in this model accurately reflect the pattern of MS. The immunologic changes seen in animals with R-EAE also are similar to those seen in MS. Therefore, the clinicopathologic features of MS can be duplicated with a purely autoimmune model. Although this is of considerable pathogenic significance in understanding MS, we do not know what the inciting event is in MS that would be the equivalent of immunizing an animal with neural antigen. Despite this, R-EAE has and should continue to provide experimental data of considerable importance to an understanding of the mechanisms involved in the evolution of inflammatory demyelination. Other important models of MS utilize viral-induced demyelination. Although the clinical picture of most of the chronic demyelinating viral infections does not show as clear a relapsing or remitting pattern as seen in R-EAE, viral etiologies better fit the epidemiology of MS [16]. Several studies have demonstrated development of an acute EAE-like disease with sensitization to neural antigens following viral infection [12, 30, 56]. Thus, one can hypothesize an initial viral illness causing sensitization of the host to a neural antigen (?MBP) with a subsequent immunopathogenic course similar to that seen in R-EAE. Whether this will in fact be the case remains unproven as yet. Our understanding of the immunopathogenic mechanisms underlying inflammatory demyelination has been enlarged through studies of R-EAE. It is now clear that the minimal myelin antigen necessary for production of the disease is MBP, although this may differ in some species. The relapsing nature of this disorder is mediated in part through lymphocytes, as demonstrated in transfer studies, and thus does not require persistent antigenic depots. There is a genetic susceptibility to development of the CNS autoimmune state, and we speculate that an as yet unidentified perturbation of the host immune system allows for the occurrence of relapsing disease (Table 3).Keywords
This publication has 59 references indexed in Scilit:
- Adoptive transfer of murine relapsing experimental allergic encephalomyelitisAnnals of Neurology, 1985
- Contamination of proteolipid protein with basic proteinAnnals of Neurology, 1984
- Experimental autoimmune encephalomyelitis mediated by T-cell lineClinical Immunology and Immunopathology, 1984
- Measles Encephalomyelitis — Clinical and Immunologic StudiesNew England Journal of Medicine, 1984
- Multiple sclerosis☆Distribution of T cells, T cell subsets and Ia-positive macrophages in lesions of different agesJournal of Neuroimmunology, 1983
- THE DEVELOPMENT OF PERIVENTRICULAR LESIONS IN CHRONIC RELAPSING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN GUINEA-PIGS: A LIGHT AND SCANNING ELECTRON MICROSCOPIC STUDYNeuropathology and Applied Neurobiology, 1981
- A latent-relapsing neuroautoimmune disease in Syrian hamstersClinical Immunology and Immunopathology, 1980
- Structural variability of demyelinating lesions in different models of subacute and chronic experimental allergic encephalomyelitisActa Neuropathologica, 1980
- Chronic relapsing experimental allergic encephalomyelitis: An experimental model of multiple sclerosisAnnals of Neurology, 1977
- T cell necessity in the pathogenesis of experimental autoimmune encephalomyelitis in miceEuropean Journal of Immunology, 1976