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

Nature. 1996 Jan 25;379(6563):343-6. doi: 10.1038/379343a0.


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 interleukin-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-alpha in the lesion.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Brain / immunology
  • Encephalomyelitis / drug therapy*
  • Encephalomyelitis / immunology
  • Epitopes
  • Immune Tolerance
  • Interleukin-4 / immunology
  • Mice
  • Molecular Sequence Data
  • Myelin Basic Protein / immunology
  • Myelin Basic Protein / therapeutic use*
  • Paralysis / immunology
  • Peptide Fragments / therapeutic use
  • T-Lymphocytes / immunology


  • Epitopes
  • Myelin Basic Protein
  • Peptide Fragments
  • Interleukin-4