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Downregulation of HLA Class I Renders Inflammatory Neutrophils More Susceptible to NK Cell-Induced Apoptosis

Journal article
Authors Elin Bernson
Karin Christenson
Silvia Pesce
Malin Pasanen
E. Marcenaro
S. Sivori
Fredrik Bergh Thorén
Published in Frontiers in Immunology
Volume 10
Pages 11
ISSN 1664-3224
Publication year 2019
Published at Sahlgrenska Cancer Center
Institute of Biomedicine
Institute of Biomedicine, Department of Infectious Medicine
Pages 11
Language en
Keywords neutrophil, NK cell, HLA class I, immunoregulation, neutrophil apoptosis, natural-killer-cells, open conformers, receptor nkp30, ligand, b7-h6, recognition, activation, leukocytes, infection, proteins, Immunology
Subject categories Immunology in the medical area


Neutrophils are potent effector cells and contain a battery of harmful substances and degrading enzymes. A silent neutrophil death, i.e., apoptosis, is therefore of importance to avoid damage to the surrounding tissue and to enable termination of the acute inflammatory process. There is a pile of evidence supporting the role for pro-inflammatory cytokines in extending the life-span of neutrophils, but relatively few studies have been devoted to mechanisms actively driving apoptosis induction in neutrophils. We have previously demonstrated that natural killer (NK) cells can promote apoptosis in healthy neutrophils. In this study, we set out to investigate how neutrophil sensitivity to NK cell-mediated cytotoxicity is regulated under inflammatory conditions. Using in vitro-activated neutrophils and a human skin chamber model that allowed collection of in vivo-transmigrated neutrophils, we performed a comprehensive characterization of neutrophil expression of ligands to NK cell receptors. These studies revealed a dramatic downregulation of HLA class I molecules in inflammatory neutrophils, which was associated with an enhanced susceptibility to NK cell cytotoxicity. Collectively, our data shed light on the complex regulation of interactions between NK cells and neutrophils during an inflammatory response and provide further support for a role of NK cells in the resolution phase of inflammation.

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