EBV Infection and Multiple Sclerosis: Lessons from a Marmoset ModelHart, 't, B., Kap, Y. S., Morandi, E., Laman, J. D. & Gran, B., Dec-2016, In : TRENDS IN MOLECULAR MEDICINE. 22, 12, p. 1012-1024 13 p.
Research output: Contribution to journal › Review article › Academic › peer-review
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.
|Number of pages||13|
|Journal||TRENDS IN MOLECULAR MEDICINE|
|Publication status||Published - Dec-2016|
- 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