Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism

Fredrik B. Thorén, Rebecca E. Riise, Jenny Ousbäck, Mariella Della Chiesa, Mikael Alsterholm, Emanuela Marcenaro, Silvia Pesce, Carola Prato, Claudia Cantoni, Johan Bylund, Lorenzo Moretta, Alessandro Moretta

Research output: Contribution to journalArticlepeer-review


Polymorphonuclear neutrophils (PMN) are potent inflammatory effector cells essential to host defense, but at the same time they may cause significant tissue damage. Thus, timely induction of neutrophil apoptosis is crucial to avoid tissue damage and induce resolution of inflammation. NK cells have been reported to influence innate and adaptive immune responses by multiple mechanisms including cytotoxicity against other immune cells. In this study, we analyzed the effect of the interaction between NK cells and neutrophils. Coculture experiments revealed that human NK cells could trigger caspase-dependent neutrophil apoptosis in vitro. This event was dependent on cell-cell contact, and experiments using blocking Abs indicated that the effect was mediated by the activating NK cell receptor NKp46 and the Fas pathway. CD56-depleted lymphocytes had minimal effects on neutrophil survival, suggesting that the ability to induce neutrophil apoptosis is specific to NK cells. Our findings provide evidence that NK cells may accelerate neutrophil apoptosis, and that this interaction may be involved in the resolution of acute inflammation. Copyright

Original languageEnglish
Pages (from-to)1668-1674
Number of pages7
JournalJournal of Immunology
Issue number4
Publication statusPublished - Feb 15 2012

ASJC Scopus subject areas

  • Immunology

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