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American Journal of Pathology, Vol 130, 443-454, Copyright © 1988 by American Society for Investigative Pathology
REGULAR ARTICLES |
C Linington, M Bradl, H Lassmann, C Brunner and K Vass
Neurological Institute, University of Vienna, Austria.
In this study the authors have developed a model with which can be studied directly the influence of circulating anti-myelin antibody on the clinical and pathologic course of inflammatory T-cell-mediated experimental allergic encephalomyelitis (EAE) in the rat. EAE was induced by passive transfer of either myelin basic protein (MBP)- activated spleen cells derived from sensitized donors or long-term- cultured MBP-specific T-cell lines. At the onset of the disease, monoclonal antibodies against a myelin/oligodendrocyte glycoprotein (MOG) were injected intravenously. This antigen is exposed on the surface of central nervous system myelin and oligodendrocytes. Intravenous injection of the antibody in the course of T-cell-mediated transfer EAE augmented the severity and duration of clinical signs and resulted in the formation of large, confluent demyelinated plaques.
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