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Author Spotlight: Marmoset Research - Scope and Challenges
Published on: June 9, 2023
EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model
Bert A 'tHart1, Yolanda S Kap2, Elena Morandi3
1Department of Immunobiology, Biomedical Primate Research Centre (BPRC), Rijswijk, The Netherlands; University of Groningen, University Medical Center, Department of Neuroscience, Groningen, The Netherlands.
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.
Insights
Epstein-Barr virus (EBV) infection may trigger multiple sclerosis (MS) by altering how the immune system processes antigens. This mechanism explains how a common virus contributes to this autoimmune disease.
Area of Science:
- Neuroimmunology
- Virology
- Autoimmunity
Background:
- Multiple sclerosis (MS) pathogenesis involves genetic and environmental factors.
- Epstein-Barr virus (EBV) is a significant infectious risk factor for MS.
- The link between high EBV prevalence and low MS incidence requires explanation.
Purpose of the Study:
- To investigate the mechanism by which EBV infection may contribute to MS pathogenesis.
- To explore the role of EBV in initiating autoimmune responses in the central nervous system.
Main Methods:
- Utilized marmosets with experimental autoimmune encephalomyelitis (EAE), a primate model for MS.
- Analyzed the interaction between EBV infection, antigen processing, and immune cell activation.
Main Results:
- EBV infection induces peptide citrullination and autophagy during antigen processing.
- This process enables B cells to cross-present autoantigen to specific T cells.
Conclusions:
- EBV infection can equip B cells to initiate an autoimmune attack on the central nervous system.
- This mechanism provides a potential explanation for EBV's role in MS progression.
