ArticleJournal of immunology (Baltimore, Md. : 1950)2003
EBV-encoded latent membrane protein 1 cooperates with BAFF/BLyS and APRIL to induce T cell-independent Ig heavy chain class switching.
Article in Journal of immunology (Baltimore, Md. : 1950), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.
- Pooled it
- The role of soluble mediators in the clinical course of EBV infection and B cell homeostasis after kidney transplantation.Scientific reports · 2020Trial
- Anti-citrullinated protein antibody response after primary EBV infection in kidney transplant patients.PloS one · 2018Trial
- Differential effects on BAFF and APRIL levels in rituximab-treated patients with systemic lupus erythematosus and rheumatoid arthritis.Arthritis research & therapy · 2006Trial
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- A tonsil organoid model reveals Epstein-Barr virus-infected germinal center B cell states during primary infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- IgA nephropathy: a novel pathway in immunopathogenesis dependent on the timing of Epstein-Barr virus infection.Frontiers in immunology · 2026Review
- Mechanisms of Epstein-Barr virus-associated autoimmunity: a comparative overview.Frontiers in immunology · 2026Review
- Epstein-Barr Virus in Multiple Sclerosis: Past, Present, and Future.Neurology(R) neuroimmunology & neuroinflammation · 2025Review
- Effectiveness and safety of telitacicept in IgA nephropathy: a propensity score matching analysis with a 6-month follow-up.BMC nephrology · 2025Article
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- Pathophysiology of Congenital High Production of IgE and Its Consequences: A Narrative Review Uncovering a Neglected Setting of Disorders.Life (Basel, Switzerland) · 2024Review
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- A PRoliferation-Inducing Ligand (APRIL) in the Pathogenesis of Immunoglobulin A Nephropathy: A Review of the Evidence.Journal of clinical medicine · 2023Review
- Review
- Epstein-Barr virus as a leading cause of multiple sclerosis: mechanisms and implications.Nature reviews. Neurology · 2023Review
- When AHR signaling pathways meet viral infections.Cell communication and signaling : CCS · 2023Review
- Integrated signaling and transcriptome analysis reveals Src family kinase individualities and novel pathways controlled by their constitutive activity.Frontiers in immunology · 2023Article
- The impact of Epstein-Barr virus latent membrane protein 2A on the production of B cell activating factor of the tumor necrosis factor family (BAFF), APRIL and their receptors.Immunity, inflammation and disease · 2022Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
By substituting the H chain C region of IgM with that of IgG, IgA, or IgE, class switching enables Abs to acquire new effector functions that are crucial for the neutralization of invading pathogens. Class switching occurs through class switch DNA recombination (CSR) and usually requires engagement of CD40 on B cells by CD40 ligand on Ag-activated CD4(+) T cells. CSR must be tightly regulated because abnormal IgG and IgA production favors the onset of autoimmunity, whereas increased switching to IgE leads to atopy. These inflammatory disorders can be triggered or exacerbated by EBV infection. In this study, we show that EBV induces CD40-independent CSR from C( micro ) to multiple downstream C(gamma), C(alpha), and C(epsilon) genes through latent membrane protein 1 (LMP1), a CD40-like viral protein that signals in a ligand-independent fashion. LMP1-induced CSR is associated with transcriptional activation of germline C(gamma), C(alpha), and C(epsilon) genes and triggers the up-regulation of activation-induced cytidine deaminase, a crucial component of the CSR machinery. In addition, LMP1 induces B cells to express B cell-activating factor of the TNF family and a proliferation-inducing ligand, two molecules that mediate B cell survival and T cell-independent Ab production. B cell-activating factor of the TNF family and a proliferation-inducing ligand cooperate with LMP1 to induce Ig class switching because their neutralization by appropriate soluble decoy receptors attenuates CSR in LMP1-expressing B cells. By showing that LMP1 triggers T cell-independent CSR, our findings suggest that EBV could play an important role in the pathogenesis of disorders with aberrant IgG, IgA, and/or IgE production.
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What OpenQuestion holds
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.