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

Artikel i vetenskaplig tidskrift
Författare Elin Bernson
Karin Christenson
Silvia Pesce
Malin Pasanen
E. Marcenaro
S. Sivori
Fredrik Bergh Thorén
Publicerad i Frontiers in Immunology
Volym 10
Sidor 11
ISSN 1664-3224
Publiceringsår 2019
Publicerad vid Sahlgrenska Cancer Center
Institutionen för biomedicin
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 11
Språk en
Länkar dx.doi.org/10.3389/fimmu.2019.02444
Ämnesord 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
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

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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