Expression of the Pseudorabies Virus gB Glycoprotein Triggers NK Cell Cytotoxicity and Increases Binding of the Activating NK Cell Receptor PILRβ.
Animals
Cell Line
Glycoproteins
/ immunology
Herpesvirus 1, Suid
/ immunology
Humans
Kidney
/ virology
Killer Cells, Natural
/ immunology
Membrane Glycoproteins
/ immunology
Mice
Pseudorabies
/ immunology
Rabbits
Receptors, Natural Killer Cell
/ immunology
Swine
Viral Proteins
/ immunology
Virus Internalization
NK cells
PILRβ
glycoprotein gB
herpes
natural killer cells
pseudorabies virus
Journal
Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724
Informations de publication
Date de publication:
01 04 2019
01 04 2019
Historique:
received:
26
11
2018
accepted:
17
01
2019
pubmed:
1
2
2019
medline:
19
11
2019
entrez:
1
2
2019
Statut:
epublish
Résumé
Natural killer (NK) cells are components of the innate immunity and are key players in the defense against virus-infected and malignant cells. NK cells are particularly important in the innate defense against herpesviruses, including alphaherpesviruses. Aggravated and life-threatening alphaherpesvirus-induced disease has been reported in patients with NK cell deficiencies. NK cells are regulated by a diversity of activating and inhibitory cell surface receptors that recognize specific ligands on the plasma membrane of virus-infected or malignant target cells. Although alphaherpesviruses have developed several evasion strategies against NK cell-mediated attack, alphaherpesvirus-infected cells are still readily recognized and killed by NK cells. However, the (viral) factors that trigger NK cell activation against alphaherpesvirus-infected cells are largely unknown. In this study, we show that expression of the gB glycoprotein of the alphaherpesvirus pseudorabies virus (PRV) triggers NK cell-mediated cytotoxicity, both in PRV-infected and in gB-transfected cells. In addition, we report that, like their human and murine counterpart, porcine NK cells express the activating receptor paired immunoglobulin-like type 2 receptor beta (PILRβ), and we show that gB expression triggers increased binding of recombinant porcine PILRβ to the surfaces of PRV-infected cells and gB-transfected cells.
Identifiants
pubmed: 30700600
pii: JVI.02107-18
doi: 10.1128/JVI.02107-18
pmc: PMC6430535
pii:
doi:
Substances chimiques
Glycoproteins
0
Membrane Glycoproteins
0
Receptors, Natural Killer Cell
0
Viral Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2019 American Society for Microbiology.
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