EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model

Bert Hart, 't, Yolanda S. Kap, Elena Morandi, Jon D. Laman, Bruno Gran

Research output: Contribution to journalReview articlepeer-review

28 Citations (Scopus)

Abstract

Multiple sclerosis (MS) is thought to be initiated by the interaction of genetic and environmental factors, eliciting an autoimmune attack on the central nervous system. Epstein-Barr virus (EBV) is the strongest infectious risk factor, but an explanation for the paradox between high infection prevalence and low MS incidence remains elusive. We discuss new data using marmosets with experimental autoimmune encephalomyelitis (EAE)- a valid primate model of MS. The findings may help to explain how a common infection can contribute to the pathogenesis of MS. We propose that EBV infection induces citrullination of peptides in conjunction with autophagy during antigen processing, endowing B cells with the capacity to cross-present autoantigen to CD8+CD56+ T cells, thereby leading to MS progression.

Original languageEnglish
Pages (from-to)1012-1024
Number of pages13
JournalTRENDS IN MOLECULAR MEDICINE
Volume22
Issue number12
DOIs
Publication statusPublished - Dec-2016

Keywords

  • EPSTEIN-BARR-VIRUS
  • EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
  • ANTIGEN-PRESENTING CELLS
  • MYELIN OLIGODENDROCYTE GLYCOPROTEIN
  • ENVIRONMENTAL RISK-FACTORS
  • COMMON MARMOSET
  • NONHUMAN PRIMATE
  • IMMUNE-SYSTEM
  • EAE MODEL
  • T-CELLS

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