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Treatment of experimental encephalomyelitis with a peptide analogue of myelin basic protein

An Erratum to this article was published on 09 April 1998

Abstract

FOLLOWING induction of experimental encephalomyelitis with a T-cell clone, L10C1, that is specific for the myelin basic protein epitope p87–99, the inflammatory infiltrate in the central nervous system contains a diverse collection of T cells with heterogeneous receptors. We show here that when clone L10C1 is tolerized in vivo with an analogue of p87–99, established paralysis is reversed, inflammatory infiltrates regress, and the heterogeneous T-cell infiltrate disappears from the brain, with only the T-cell clones that incited disease remaining in the original lesions. We found that antibody raised against inter-leukin-4 reversed the tolerance induced by the altered peptide ligand. Treatment with this altered peptide ligand selectively silences pathogenic T cells and actively signals for the efflux of other T cells recruited to the site of disease as a result of the production of interleukin-4 and the reduction of tumour-necrosis factor-α in the lesion.

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Brocke, S., Gijbels, K., Allegretta, M. et al. Treatment of experimental encephalomyelitis with a peptide analogue of myelin basic protein. Nature 379, 343–346 (1996). https://doi.org/10.1038/379343a0

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