IL-4, IL-13 and IFN-γ -induced genes in highly purified human neutrophils.
Allergy
IL-13
IL-4
Neutrophil
Signal transduction
Transcriptome
Type 2 immune response
Journal
Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353
Informations de publication
Date de publication:
04 2023
04 2023
Historique:
received:
29
11
2022
revised:
27
01
2023
accepted:
10
02
2023
pubmed:
23
2
2023
medline:
17
3
2023
entrez:
22
2
2023
Statut:
ppublish
Résumé
Interleukin (IL)-4 and IL-13 are related cytokines with well-known specific roles in type 2 immune response. However, their effects on neutrophils are not completely understood. For this, we studied human primary neutrophil responses to IL-4 and IL-13. Neutrophils are dose-dependently responsive to both IL-4 and IL-13 as indicated by signal transducer and activator of transcription 6 (STAT6) phosphorylation upon stimulation, with IL-4 being more potent inducer of STAT6. IL-4-, IL-13- and Interferon (IFN)-γ-stimulated gene expression in highly purified human neutrophils induced both overlapping and unique gene expression in highly purified human neutrophils. IL-4 and IL-13 specifically regulate several immune-related genes, including IL-10, tumor necrosis factor (TNF) and leukemia inhibitory factor (LIF), while type1 immune response-related IFN-γ induced gene expression related for example, to intracellular infections. In analysis of neutrophil metabolic responses, oxygen independent glycolysis was specifically regulated by IL-4, but not by IL-13 or IFN-γ, suggesting specific role for type I IL-4 receptor in this process. Our results provide a comprehensive analysis of IL-4, IL-13 and IFN-γ -induced gene expression in neutrophils while also addressing cytokine-mediated metabolic changes in neutrophils.
Identifiants
pubmed: 36809715
pii: S1043-4666(23)00037-6
doi: 10.1016/j.cyto.2023.156159
pmc: PMC10331420
mid: NIHMS1908116
pii:
doi:
Substances chimiques
Cytokines
0
Interferon-gamma
82115-62-6
Interleukin-13
0
Interleukin-4
207137-56-2
Tumor Necrosis Factor-alpha
0
IL4 protein, human
0
IL13 protein, human
0
IFNG protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
156159Subventions
Organisme : Intramural NIH HHS
ID : ZIA BC009283
Pays : United States
Informations de copyright
Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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