ArticlePLoS pathogens2021
NK cells eliminate Epstein-Barr virus bound to B cells through a specific antibody-mediated uptake.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Acyclovir and ganciclovir exposure and short-term outcomes in hospitalized children with EBV-associated mononucleosis-like illness: a retrospective cohort study using inverse probability of treatment weighting.Translational pediatrics · 2026Article
- Immune surveillance interrupted: how cancer exploits trogocytosis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Review
- The Similarities and Differences between the Effects of Testosterone and DHEA on the Innate and Adaptive Immune Response.Biomolecules · 2022Review
- Trogocytosis in innate immunity to cancer is an intimate relationship with unexpected outcomes.iScience · 2022Article
- FcγR-Mediated Trogocytosis 2.0: Revisiting History Gives Rise to a Unifying Hypothesis.Antibodies (Basel, Switzerland) · 2022Review
- Epstein-Barr Virus Genome Deletions in Epstein-Barr Virus-Positive T/NK Cell Lymphoproliferative Diseases.Journal of virology · 2022Article
- Article
- Bryostatin Activates CAR T-Cell Antigen-Non-Specific Killing (CTAK), and CAR-T NK-Like Killing for Pre-B ALL, While Blocking Cytolysis of a Burkitt Lymphoma Cell Line.Frontiers in immunology · 2022Article
- How Does Epstein-Barr Virus Interact With Other Microbiomes in EBV-Driven Cancers?Frontiers in cellular and infection microbiology · 2022Review
- Do Epstein-Barr Virus Mutations and Natural Genome Sequence Variations Contribute to Disease?Biomolecules · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein Barr virus (EBV) causes a highly prevalent and lifelong infection contributing to the development of some malignancies. In addition to the key role played by T cells in controlling this pathogen, NK cells mediate cytotoxicity and IFNγ production in response to EBV-infected B cells in lytic cycle, both directly and through antibody (Ab)-dependent activation. We recently described that EBV-specific Ab-dependent NK cell interaction with viral particles (VP) bound to B cells triggered degranulation and TNFα secretion but not B cell lysis nor IFNγ production. In this report we show that NK cell activation under these conditions reduced B cell transformation by EBV. NK cells eliminated VP from the surface of B cells through a specific and active process which required tyrosine kinase activation, actin polymerization and Ca2+, being independent of proteolysis and perforin. VP were displayed at the NK cell surface before being internalized and partially shuttled to early endosomes and lysosomes. VP transfer was encompassed by a trogocytosis process including the EBV receptor CD21, together with CD19 and CD20. Our study reveals a novel facet of the antibody-dependent NK cell mediated response to this viral infection.
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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.