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

Abstract

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
Volume164
Issue number1-2
DOIs
Publication statusPublished - Jul 2005

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