ArticleBlood advances2022
IFNγ regulates NAD+ metabolism to promote the respiratory burst in human monocytes.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 15 citations in OpenAlex.
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- Metabolic reprogramming of myeloid cells in cancer: from lactate-NAMPT axis to AI-guided therapeutics.Experimental & molecular medicine · 2026Review
- A STAT1/ETC/GBP1 axis represents a potential therapeutic target for noncommunicable granulomatous skin disease.Science advances · 2026Article
- Bi-directional regulation between NAD/NAMPT and IFN-γ/PD-L1 axes via BRD4/IRF1 and mitochondrial respiration in metastatic cutaneous melanoma.Journal of experimental & clinical cancer research : CR · 2026Article
- A metabolic constraint in de novo NAD+ synthesis drives mucosal inflammation in IBD.Journal of Crohn's & colitis · 2026Article
- Octreotide Counteracts IFN-γ-Induced Endothelial Inflammation.Journal of biochemical and molecular toxicology · 2026Article
- Integrated multi-omics analysis reveals shared IFN-γ-associated monocyte signatures in primary Sjögren's syndrome and Alzheimer's disease.Frontiers in immunology · 2026Article
- Interferon gamma rebalances immunopathological signatures in chronic granulomatous disease through metabolic rewiring.Blood advances · 2025Article
- APOL1 risk variants induce metabolic reprogramming of podocytes in patient-derived kidney organoids.Stem cell reports · 2025Article
- Five CGD-Linked CYBB Mutations in Chinese Patients: Insights Into Predicting IFN-γ Treatment Efficacy.Journal of clinical immunology · 2025Article
- Article
- Derivation of novel metabolic pathway score identifies alanine metabolism as a targetable influencer of TNF-alpha signaling.Heliyon · 2024Article
- Parasite-induced IFN-γ regulates host defense via CD115 and mTOR-dependent mechanism of tissue-resident macrophage death.PLoS pathogens · 2024Article
- Neutrophil extracellular trap formation and gene programs distinguish TST/IGRA sensitization outcomes among Mycobacterium tuberculosis exposed persons living with HIV.PLoS genetics · 2023Article
- Article
- Identification and Verification of Biomarkers and Immune Infiltration in Obesity-Related Atrial Fibrillation.Biology · 2023Article
- Rapid glycolytic activation accompanying innate immune responses: mechanisms and function.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Interferon γ (IFNγ) is an essential and pleiotropic activator of human monocytes, but little is known about the changes in cellular metabolism required for IFNγ-induced activation. We sought to elucidate the mechanisms by which IFNγ reprograms monocyte metabolism to support its immunologic activities. We found that IFNγ increased oxygen consumption rates (OCR) in monocytes, indicative of reactive oxygen species generation by both mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Transcriptional profiling revealed that this oxidative phenotype was driven by IFNγ-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively. Consistent with this pathway, monocytes from patients with gain-of-function mutations in STAT1 demonstrated higher-than-normal OCR, whereas chemical or genetic disruption of mitochondrial complex I (rotenone treatment or Leigh syndrome patient monocytes) or NADPH oxidase (diphenyleneiodonium treatment or chronic granulomatous disease [CGD] patient monocytes) reduced OCR. Interestingly, inhibition of NAMPT in healthy monocytes completely abrogated the IFNγ-induced oxygen consumption, comparable to levels observed in CGD monocytes. These data identify an IFNγ-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNγ activation of human monocytes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.