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Abstract
The leukocyte integrin receptor, alpha sub 4 beta sub 1, and its endothelial cell ligand, vascular cell adhesion molecule 1, appear to be of critical importance in the leukocyte trafficking that accompanies CNS damage in experimental allergic encephalomyelitis (EAE).In this study, the persistence of the role for alpha4 beta1/VCAM-1 in EAE was established by observing antibody-mediated disease reversal up to 1 month following disease onset. Limited treatment with a monoclonal antibody against alpha4 integrin, GG5/3, resulted in a significant decrease in both clinical and histopathologic signs. This was not observed in isotype control experiments. In the latter phase of progressive disease, widespread demyelination occurred in the animals that did not respond to 6 days of anti-alpha4 treatment. These results demonstrate an essential role for alpha4 beta1 interactions throughout active EAE and illustrate the difference between reversible clinical deficits caused by edema and irreversible deficits associated with demyelination.
NEUROLOGY 1996;47: 1053-1059
- Copyright 1996 by Advanstar Communications Inc.
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