ArticleeLife2021
Mitochondrial respiration contributes to the interferon gamma response in antigen-presenting cells.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed.
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Ubiquitylation by the GID/CTLH complex regulates the metabolic and innate immune response of macrophages to infection by Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- Differential activation of NF-Κβ and HIF-1α between fetal liver-derived and myeloid-derived macrophages drives inflammatory differences followingInfection and immunity · 2026Article
- Vancomycin disrupts mitochondrial morphology and function and impairs macrophage fungal killing.mBio · 2026Article
- Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis.Precision clinical 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
- Review
- High-throughput screening to engineer optimal T cell therapies: current knowledge and future prospects.Frontiers in oncology · 2026Review
- Evaluating CAR-T cells from neurofibromatosis type 1 (NF1) patients for targeting AXL in malignant peripheral nerve sheath tumors associated with NF1.British journal of cancer · 2025Article
- Interferon gamma rebalances immunopathological signatures in chronic granulomatous disease through metabolic rewiring.Blood advances · 2025Article
- Incorporation of macrophage immune stresses into an intracellular assay of drug tolerance inAntimicrobial agents and chemotherapy · 2025Article
- Using host and bacterial genetic approaches to define virulence strategies and protective immunity duringmSphere · 2025Review
- Papaverine Targets STAT Signaling: A Dual-Action Therapy Option Against SARS-CoV-2.Journal of medical virology · 2025Article
- Impaired fatty acid import or catabolism in macrophages restricts intracellular growth ofeLife · 2025Article
- Impaired fatty acid import or catabolism in macrophages restricts intracellular growth ofbioRxiv : the preprint server for biology · 2025Article
- Article
- Mitochondrial unfolded protein response in regulatory T cell function: a protective mechanism in immune aging.Frontiers in immunology · 2025Review
- Chronic Low-Level IFN-γ Expression Disrupts Mitochondrial Complex I Activity in Renal Macrophages: An Early Mechanistic Driver of Lupus Nephritis Pathogenesis.International journal of molecular sciences · 2024Article
- Chronological Dynamics of Neuroinflammatory Responses in a High-Fat Diet Mouse Model.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The immunological synapse allows antigen-presenting cells (APCs) to convey a wide array of functionally distinct signals to T cells, which ultimately shape the immune response. The relative effect of stimulatory and inhibitory signals is influenced by the activation state of the APC, which is determined by an interplay between signal transduction and metabolic pathways. While pathways downstream of toll-like receptors rely on glycolytic metabolism for the proper expression of inflammatory mediators, little is known about the metabolic dependencies of other critical signals such as interferon gamma (IFNγ). Using CRISPR-Cas9, we performed a series of genome-wide knockout screens in murine macrophages to identify the regulators of IFNγ-inducible T cell stimulatory or inhibitory proteins MHCII, CD40, and PD-L1. Our multiscreen approach enabled us to identify novel pathways that preferentially control functionally distinct proteins. Further integration of these screening data implicated complex I of the mitochondrial respiratory chain in the expression of all three markers, and by extension the IFNγ signaling pathway. We report that the IFNγ response requires mitochondrial respiration, and APCs are unable to activate T cells upon genetic or chemical inhibition of complex I. These findings suggest a dichotomous metabolic dependency between IFNγ and toll-like receptor signaling, implicating mitochondrial function as a fulcrum of innate immunity.
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Registered trials
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.