ArticleFrontiers in immunology2022
Epstein-Barr virus, interleukin-10 and multiple sclerosis: A ménage à trois.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The Role of Selected Interleukins in the Development and Progression of Multiple Sclerosis-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Selected Cytokines and Matrix Metalloproteinases in Pathogenesis and Treatment of Multiple Sclerosis.International journal of molecular sciences · 2026Review
- Diagnostic value of combined flow cytometry-based detection of peripheral blood lymphocyte subsets and cytokines for pediatric infectious mononucleosis.Frontiers in pediatrics · 2026Article
- Epstein-Barr Virus Central Nervous System Infections and Mortality Risk in Patients Presenting With Suspected Meningitis: Results From the Botswana National Meningitis Survey and the Harare Meningitis Aetiology Study.Open forum infectious diseases · 2025Article
- Latent EBV enhances the efficacy of anti-CD3 mAb in Type 1 diabetes.Nature communications · 2025Article
- Fibrinaloid Microclots and Atrial Fibrillation.Biomedicines · 2024Review
- Review
- Single-Cell Sequencing Combined with Transcriptome Sequencing Constructs a Predictive Model of Key Genes in Multiple Sclerosis and Explores Molecular Mechanisms Related to Cellular Communication.Journal of inflammation research · 2024Article
- Editorial: Immune evasion mechanisms and their role in the pathogenesis of autoimmune disorders.Frontiers in immunology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple Sclerosis (MS) is an autoimmune disease that is characterized by inflammation and demyelination of nerve cells. There is strong evidence that Epstein-Barr virus (EBV), a human herpesvirus infecting B cells, greatly increases the risk of subsequent MS. Intriguingly, EBV not only induces human interleukin-10 but also encodes a homologue of this molecule, which is a key anti-inflammatory cytokine of the immune system. Although EBV-encoded IL-10 (ebvIL-10) has a high amino acid identity with its cellular counterpart (cIL-10), it shows more restricted and partially weaker functionality. We propose that both EBV-induced cIL-10 and ebvIL-10 act in a temporally and functionally coordinated manner helping the pathogen to establish latency in B cells and, at the same time, to balance the function of antiviral T cells. As a result, the EBV load persisting in the immune system is kept at a constant but individually different level (set point). During this immunological tug of war between virus and host, however, MS can be induced as collateral damage if the set point is too high. Here, we discuss a possible role of ebvIL-10 and EBV-induced cIL-10 in EBV-driven pathogenesis of MS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.