HIF1α-regulated glycolysis promotes activation-induced cell death and IFN-γ induction in hypoxic T cells.
Animals
Hypoxia-Inducible Factor 1, alpha Subunit
/ metabolism
Glycolysis
Interferon-gamma
/ metabolism
Humans
Mice
T-Lymphocytes
/ immunology
Mice, Knockout
Tumor Microenvironment
/ immunology
Von Hippel-Lindau Tumor Suppressor Protein
/ metabolism
Cell Hypoxia
/ immunology
Mice, Inbred C57BL
Cell Line, Tumor
Cell Death
Immune Checkpoint Inhibitors
/ pharmacology
Lymphocyte Activation
/ immunology
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
30 Oct 2024
30 Oct 2024
Historique:
received:
04
01
2024
accepted:
14
10
2024
medline:
31
10
2024
pubmed:
31
10
2024
entrez:
31
10
2024
Statut:
epublish
Résumé
Hypoxia is a common feature in various pathophysiological contexts, including tumor microenvironment, and IFN-γ is instrumental for anti-tumor immunity. HIF1α has long been known as a primary regulator of cellular adaptive responses to hypoxia, but its role in IFN-γ induction in hypoxic T cells is unknown. Here, we show that the HIF1α-glycolysis axis controls IFN-γ induction in both human and mouse T cells, activated under hypoxia. Specific deletion of HIF1α in T cells (Hif1α
Identifiants
pubmed: 39477954
doi: 10.1038/s41467-024-53593-8
pii: 10.1038/s41467-024-53593-8
doi:
Substances chimiques
Hypoxia-Inducible Factor 1, alpha Subunit
0
Interferon-gamma
82115-62-6
Hif1a protein, mouse
0
Von Hippel-Lindau Tumor Suppressor Protein
EC 2.3.2.27
HIF1A protein, human
0
Immune Checkpoint Inhibitors
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
9394Subventions
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : 1R21CA230475-01A1
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : 1R21CA259721-01A1
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : 1R01CA279849-01A1
Organisme : U.S. Department of Defense (United States Department of Defense)
ID : ME210108
Organisme : V Foundation for Cancer Research (V Foundation)
ID : V2018-023
Organisme : Cancer Research Institute (CRI)
ID : CRI4342
Organisme : UAB | School of Medicine, University of Alabama at Birmingham (UAB School of Medicine)
ID : O'Neal Invests Pre-R01 Award
Informations de copyright
© 2024. The Author(s).
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