ArticleProceedings of the National Academy of Sciences of the United States of America2024
Expanded T lymphocytes in the cerebrospinal fluid of multiple sclerosis patients are specific for Epstein-Barr-virus-infected B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Dynamics of Myelin-Specific T-Cell Repertoires Mirror Disease Activity and Central Nervous System Trafficking in Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Epstein-Barr Virus and Multiple Sclerosis: Mechanistic Insights into Virus-Driven Autoimmunity.Microorganisms · 2026Review
- CD4Science translational medicine · 2026Article
- Infectious Agents in Multiple Sclerosis: Viral Triggers, Antibody-Mediated Autoimmunity, and Parasitic Immunomodulation.Biomolecules · 2026Review
- Central Nervous System T-cell immune architecture, and not HIV burden, tracks with cognition under long-term viral suppression.PLoS pathogens · 2026Article
- Neuroinflammation as a result of non-neurotropic herpesvirus infection.Immunology and cell biology · 2026Review
- Antigen specificity of clonally enriched CD8Nature immunology · 2026Article
- De novo identification of the specificities of recurrently identified human T cell receptors.Science advances · 2026Article
- Detection of Human Brain Cancers using Genomic and Immune Cell Characterization of Cerebrospinal Fluid through CSF-BAM.Cancer discovery · 2025Article
- Article
- Epstein-Barr virus pathogenesis and emerging control strategies.Nature reviews. Microbiology · 2025Review
- The case for targeting latent and lytic Epstein-Barr virus infection in multiple sclerosis.Brain : a journal of neurology · 2025Review
- Targeting pyruvate metabolism generates distinct CD8+ T cell responses to gammaherpesvirus and B lymphoma.JCI insight · 2025Article
- Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Antibody reactivity against EBNA1 and GlialCAM differentiates multiple sclerosis patients from healthy controls.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Single-cell transcriptomics for immune profiling of cerebrospinal fluid in neurological diseases.Frontiers in immunology · 2025Review
- Short-term exposure to particulate matter triggers a selective alteration of plasma extracellular vesicle-packaged miRNAs in a mouse model of multiple sclerosis.Frontiers in immunology · 2025Article
- Connecting the dots: Presentation of EBV antigens on HLA class II risk alleles connects the two main risk factors of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Choroid Plexus as a Mediator of CNS Inflammation in Multiple Sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) infection has long been associated with multiple sclerosis (MS), but the role of EBV in the pathogenesis of MS is not clear. Our hypothesis is that a major fraction of the expanded clones of T lymphocytes in the cerebrospinal fluid (CSF) are specific for autologous EBV-infected B cells. We obtained blood and CSF samples from eight relapsing-remitting patients in the process of diagnosis. We stimulated cells from the blood with autologous EBV-infected lymphoblastoid cell lines (LCL), EBV, varicella zoster virus, influenza, and candida and sorted the responding cells with flow cytometry after 6 d. We sequenced the RNA for T cell receptors (TCR) from CSF, unselected blood cells, and the antigen-specific cells. We used the TCR Vβ CDR3 sequences from the antigen-specific cells to assign antigen specificity to the sequences from the CSF and blood. LCL-specific cells comprised 13.0 ± 4.3% (mean ± SD) of the total reads present in CSF and 13.3 ± 7.5% of the reads present in blood. The next most abundant antigen specificity was flu, which was 4.7 ± 1.7% of the reads in the CSF and 9.3 ± 6.6% in the blood. The prominence of LCL-specific reads was even more marked in the top 1% most abundant CSF clones with statistically significant 47% mean overlap with LCL. We conclude that LCL-specific sequences form a major portion of the TCR repertoire in both CSF and blood and that expanded clones specific for LCL are present in MS CSF. This has important implications for the pathogenesis of MS.
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