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Analysis of the cross‐talk of Epstein–Barr virus‐infected B cells with T cells in the marmoset
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Analysis of the cross‐talk of Epstein–Barr virus‐infected B cells with T cells in the marmoset
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Journal Article
Analysis of the cross‐talk of Epstein–Barr virus‐infected B cells with T cells in the marmoset
2017
Overview
Despite the well‐known association of Epstein–Barr virus (EBV), a lymphocryptovirus (LCV), with multiple sclerosis, a clear pathogenic role for disease progression has not been established. The translationally relevant experimental autoimmune encephalomyelitis (EAE) model in marmoset monkeys revealed that LCV‐infected B cells have a central pathogenic role in the activation of T cells that drive EAE progression. We hypothesized that LCV‐infected B cells induce T‐cell functions relevant for EAE progression. In the current study, we examined the ex vivo cross‐talk between lymph node mononuclear cells (MNCs) from EAE marmosets and (semi‐) autologous EBV‐infected B‐lymphoblastoid cell lines (B‐LCLs). Results presented here demonstrate that infection with EBV B95‐8 has a strong impact on gene expression profile of marmoset B cells, particularly those involved with antigen processing and presentation or co‐stimulation to T cells. At the cellular level, we observed that MNC co‐culture with B‐LCLs induced decrease of CCR7 expression on T cells from EAE responder marmosets, but not in EAE monkeys without clinically evident disease. B‐LCL interaction with T cells also resulted in significant loss of CD27 expression and reduced expression of IL‐23R and CCR6, which coincided with enhanced IL‐17A production. These results highlight the profound impact that EBV‐infected B‐LCL cells can have on second and third co‐stimulatory signals involved in (autoreactive) T‐cell activation. Multiple sclerosis: Understanding how a virus evades immune responses Research on marmoset white blood cells is helping to elaborate the link between a herpes virus and multiple sclerosis (MS). Yolanda Kap of the Biomedical Primate Research Centre, Rijswijk, The Netherlands and colleagues examined the mechanisms behind a poorly understood but well supported association between MS and Epstein‐Barr virus (EBV). This common virus causes infectious mononucleosis, among other diseases. They examined signalling between T cells and EBV‐infected B cells derived from marmosets with an induced autoimmune inflammation of the brain and spinal cord that resembles MS in humans. The results show EBV‐infected B cells may escape immune defences by causing alterations in T cells and by affecting their activation. EBV infection of B cells increased the expression of nearly 3,000 genes and decreased the expression of more than 2,500 others.
Publisher
Nature Publishing Group,John Wiley & Sons, Inc
Subject
