EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model

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

Onderzoeksoutput: Review articlepeer review

29 Citaten (Scopus)


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.

Originele taal-2English
Pagina's (van-tot)1012-1024
Aantal pagina's13
Nummer van het tijdschrift12
StatusPublished - dec-2016

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