Engagement of TRAIL triggers degranulation and IFNγ production in human natural killer cells.
HIV-1
NK cell
TRAIL
death receptor
degranulation
Journal
EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049
Informations de publication
Date de publication:
03 08 2022
03 08 2022
Historique:
revised:
16
05
2022
received:
10
10
2021
accepted:
23
05
2022
pubmed:
28
6
2022
medline:
5
8
2022
entrez:
27
6
2022
Statut:
ppublish
Résumé
NK cells utilize a large array of receptors to screen their surroundings for aberrant or virus-infected cells. Given the vast diversity of receptors expressed on NK cells we seek to identify receptors involved in the recognition of HIV-1-infected cells. By combining an unbiased large-scale screening approach with a functional assay, we identify TRAIL to be associated with NK cell degranulation against HIV-1-infected target cells. Further investigating the underlying mechanisms, we demonstrate that TRAIL is able to elicit multiple effector functions in human NK cells independent of receptor-mediated induction of apoptosis. Direct engagement of TRAIL not only results in degranulation but also IFNγ production. Moreover, TRAIL-mediated NK cell activation is not limited to its cognate death receptors but also decoy receptor I, adding a new perspective to the perceived regulatory role of decoy receptors in TRAIL-mediated cytotoxicity. Based on these findings, we propose that TRAIL not only contributes to the anti-HIV-1 activity of NK cells but also possesses a multifunctional role beyond receptor-mediated induction of apoptosis, acting as a regulator for the induction of different effector functions.
Identifiants
pubmed: 35758160
doi: 10.15252/embr.202154133
pmc: PMC9346491
doi:
Substances chimiques
TNF-Related Apoptosis-Inducing Ligand
0
TNFSF10 protein, human
0
Interferon-gamma
82115-62-6
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e54133Informations de copyright
© 2022 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
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