Open AccessNK cells eliminate Epstein-Barr virus bound to B cells through a specific antibody-mediated uptake
Author(s) -
Elisenda Alari-Pahissa,
Michelle Ataya,
Ilias Moraitis,
Miriam Campos-Ruiz,
Mireia Altadill,
Aura Muntasell,
Anna Moles,
Miguel LópezBotet
Publication year - 2021
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1009868
Subject(s) - biology , janus kinase 3 , lytic cycle , epstein–barr virus , degranulation , microbiology and biotechnology , interleukin 21 , t cell , virus , virology , receptor , immune system , immunology , biochemistry
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.