TREATMENT OF EXPERIMENTAL ENCEPHALOMYELITIS WITH A PEPTIDE ANALOG OF MYELIN BASIC-PROTEIN

FOLLOWING induction of experimental encephalomyelitis with a T-cell cl one, 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 p 87-99, established paralysis is reversed, inflammatory infiltrates reg ress, and the heterogeneous T-cell infiltrate disappears from the brai n, with only the T-cell clones that incited disease remaining in the o riginal lesions. We found that antibody raised against interleukin-4 r eversed the tolerance induced by the altered peptide ligand. Treatment ,vith this altered peptide ligand selectively silences pathogenic T ce lls 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-alpha in the lesion.