Epitope spread is not critical for the relapse and progression of MOG 8-21 induced EAE in Biozzi ABH mice

Paul A Smith, Margaret Morris-Downes, Nicole Heijmans, Gareth Pryce, Elizabeth Arter, Janet K O'Neill, Bert 't Hart, David Baker, Sandra Amor

Research output: Contribution to journalArticleAcademicpeer-review

31 Citations (Scopus)


Emerging autoimmunity (epitope-spreading) generated as a consequence of myelin damage is suggested to underlie the relapses in multiple sclerosis (MS). Myelin oligodendrocyte glycoprotein (MOG 8-21) induces relapsing EAE in ABH mice characterized by broadening of the autoimmune reportoire. Despite epitope spreading tolerance to the priming antigen, but not emerging epitope reactivities, resulted in long-term inhibition of clinical relapse. In contrast, spinal cord homogenate induced EAE was dominated by a proteolipid protein (PLP 56-70) autoreactivity despite the plethora of CNS antigens in the immunogen. This data suggests that during relapsing-remitting demyelinating disease the pathogenic process is dominated by the initiating antigen, with only a minor role played by emerging T-cell populations. These findings may have important implications for the efficacy of antigen-based immune therapies in autoimmune disorders.

Original languageEnglish
Pages (from-to)76-84
Number of pages9
JournalJournal of Neuroimmunology
Issue number1-2
Publication statusPublished - Jul 2005


  • Animals
  • Apoproteins
  • Cell Proliferation
  • Comparative Study
  • Cytokines
  • Disease Progression
  • Encephalomyelitis, Autoimmune, Experimental
  • Enzyme-Linked Immunosorbent Assay
  • Epitopes
  • Journal Article
  • Lymphocyte Activation
  • Mice
  • Mice, Biozzi
  • Mice, Inbred C57BL
  • Myelin Proteins
  • Myelin Proteolipid Protein
  • Myelin-Associated Glycoprotein
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments
  • Recurrence
  • Research Support, Non-U.S. Gov't
  • Statistics, Nonparametric
  • T-Lymphocytes
  • Time Factors

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