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 journalArticle

47 Citations (Scopus)

Abstract

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
Volume188
Issue number4
DOIs
Publication statusPublished - Feb 15 2012

Fingerprint

Natural Killer Cells
Neutrophils
Apoptosis
Natural Killer Cell Receptors
Inflammation
Adaptive Immunity
Caspases
Coculture Techniques
Innate Immunity
Lymphocytes

ASJC Scopus subject areas

  • Immunology

Cite this

Thorén, F. B., Riise, R. E., Ousbäck, J., Della Chiesa, M., Alsterholm, M., Marcenaro, E., ... Moretta, A. (2012). Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism. Journal of Immunology, 188(4), 1668-1674. https://doi.org/10.4049/jimmunol.1102002

Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism. / Thorén, Fredrik B.; Riise, Rebecca E.; Ousbäck, Jenny; Della Chiesa, Mariella; Alsterholm, Mikael; Marcenaro, Emanuela; Pesce, Silvia; Prato, Carola; Cantoni, Claudia; Bylund, Johan; Moretta, Lorenzo; Moretta, Alessandro.

In: Journal of Immunology, Vol. 188, No. 4, 15.02.2012, p. 1668-1674.

Research output: Contribution to journalArticle

Thorén, FB, Riise, RE, Ousbäck, J, Della Chiesa, M, Alsterholm, M, Marcenaro, E, Pesce, S, Prato, C, Cantoni, C, Bylund, J, Moretta, L & Moretta, A 2012, 'Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism', Journal of Immunology, vol. 188, no. 4, pp. 1668-1674. https://doi.org/10.4049/jimmunol.1102002
Thorén FB, Riise RE, Ousbäck J, Della Chiesa M, Alsterholm M, Marcenaro E et al. Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism. Journal of Immunology. 2012 Feb 15;188(4):1668-1674. https://doi.org/10.4049/jimmunol.1102002
Thorén, Fredrik B. ; Riise, Rebecca E. ; Ousbäck, Jenny ; Della Chiesa, Mariella ; Alsterholm, Mikael ; Marcenaro, Emanuela ; Pesce, Silvia ; Prato, Carola ; Cantoni, Claudia ; Bylund, Johan ; Moretta, Lorenzo ; Moretta, Alessandro. / Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism. In: Journal of Immunology. 2012 ; Vol. 188, No. 4. pp. 1668-1674.
@article{1c51729256b240f79e47796e95bf3b20,
title = "Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism",
abstract = "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",
author = "Thor{\'e}n, {Fredrik B.} and Riise, {Rebecca E.} and Jenny Ousb{\"a}ck and {Della Chiesa}, Mariella and Mikael Alsterholm and Emanuela Marcenaro and Silvia Pesce and Carola Prato and Claudia Cantoni and Johan Bylund and Lorenzo Moretta and Alessandro Moretta",
year = "2012",
month = "2",
day = "15",
doi = "10.4049/jimmunol.1102002",
language = "English",
volume = "188",
pages = "1668--1674",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "4",

}

TY - JOUR

T1 - Human NK cells induce neutrophil apoptosis via an NKp46- and fas-dependent mechanism

AU - Thorén, Fredrik B.

AU - Riise, Rebecca E.

AU - Ousbäck, Jenny

AU - Della Chiesa, Mariella

AU - Alsterholm, Mikael

AU - Marcenaro, Emanuela

AU - Pesce, Silvia

AU - Prato, Carola

AU - Cantoni, Claudia

AU - Bylund, Johan

AU - Moretta, Lorenzo

AU - Moretta, Alessandro

PY - 2012/2/15

Y1 - 2012/2/15

N2 - 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

AB - 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

UR - http://www.scopus.com/inward/record.url?scp=84856876954&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84856876954&partnerID=8YFLogxK

U2 - 10.4049/jimmunol.1102002

DO - 10.4049/jimmunol.1102002

M3 - Article

VL - 188

SP - 1668

EP - 1674

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 4

ER -