ArticleImmunology2013
Epstein-Barr virus infection transforms CD25+ B cells into antibody-secreting cells in rheumatoid arthritis patients.
Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Anti-citrullinated protein antibody response after primary EBV infection in kidney transplant patients.PloS one · 2018Trial
- The causal relationship between immune cells and knee osteoarthritis: Mendelian randomization study.BMC musculoskeletal disorders · 2025Article
- Changes in immune subsets during chemotherapy as prognosis biomarkers for multiple myeloma patients by longitudinal monitoring.Immunologic research · 2024Article
- Mechanisms ofOpen medicine (Warsaw, Poland) · 2024Article
- Pro-inflammatory, IL-17 pathways dominate the architecture of the immunome in pediatric refractory epilepsy.JCI insight · 2019Article
- Low levels of antibodies against common viruses associate with anti-citrullinated protein antibody-positive rheumatoid arthritis; implications for disease aetiology.Arthritis research & therapy · 2017Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Epstein-Barr virus (EBV) infection may initiate production of autoantibodies and development of cancer and autoimmune diseases. Here we outline phenotypic and functional changes in B cells of patients with rheumatoid arthritis (RA) related to EBV infection. The B-cell phenotype was analysed in blood and bone marrow (BM) of RA patients who had EBV transcripts in BM (EBV(+) , n = 13) and in EBV(-) (n = 22) patients with RA. The functional effect of EBV was studied in the sorted CD25(+) and CD25(-) peripheral B cells of RA patients (n = 18) and healthy controls (n = 9). Rituximab treatment results in enrichment of CD25(+) B cells in peripheral blood (PB) of EBV(+) RA patients. The CD25(+) B-cell subset displayed a more mature phenotype accumulating IgG-expressing cells. It was also enriched with CD27(+) and CD95(+) cells in PB and BM. EBV stimulation of the sorted CD25(+) B cells in vitro induced a polyclonal IgG and IgM secretion in RA patients, while CD25(+) B cells of healthy subjects did not respond to EBV stimulation. CD25(+) B cells were enriched in PB and synovial fluid of RA patients. EBV infection affects the B-cell phenotype in RA patients by increasing the CD25(+) subset and by inducing their immunoglobulin production. These findings clearly link CD25(+) B cells to the EBV-dependent sequence of reactions in the pathogenesis of RA.
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Registered trials
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