ArticleScientific reports2016
Opposing regulation of the late phase TNF response by mTORC1-IL-10 signaling and hypoxia in human macrophages.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
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- Effect of Nutraceutical Supplementation and Mediterranean Hypocaloric Diet on Calculated Steatosis Indices and Inflammation: Clinical and In Vitro Evidences.Molecular nutrition & food research · 2025Article
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- Unconventional codon usage bias mediates mRNA translational dynamics in macrophages.PLoS biology · 2025Article
- mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025Review
- Indoximod Attenuates Inflammatory Responses in Acetic Acid-Induced Acute Colitis by Modulating Toll-like Receptor 4 (TLR4) Signaling and Proinflammatory Cytokines in Rats.Medicina (Kaunas, Lithuania) · 2025Article
- Multi-omic integration with human DRG proteomics highlights TNFα signalling as a relevant sexually dimorphic pathway.bioRxiv : the preprint server for biology · 2025Article
- In-depth proteomic profiling identifies potentiation of the LPS response by 7-ketocholesterol.Journal of molecular and cellular cardiology plus · 2025Article
- Case Report: Treating one autoimmune disease induces another: the paradox of TNF-alpha inhibitor therapies.Frontiers in immunology · 2025Article
- Angiotensin receptor blockers modulate the lupus CD4+ T cell epigenome characterized by TNF family-linked signaling.JCI insight · 2024Article
- Staphyloccocus aureus biofilm, in absence of planktonic bacteria, produces factors that activate counterbalancing inflammatory and immune-suppressive genes in human monocytes.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024Article
- Interleukin-10 induces TNF-driven apoptosis and ROS production in salivary gland cancer cells.Heliyon · 2024Article
- Nanobody-based pannexin1 channel inhibitors reduce inflammation in acute liver injury.Journal of nanobiotechnology · 2023Article
- Selective Inhibitors of Janus Kinase 3 Modify Responses to Lipopolysaccharides by Increasing the Interleukin-10-to-Tumor Necrosis Factor α Ratio.ACS pharmacology & translational science · 2023Article
- Vaginal epithelial dysfunction is mediated by the microbiome, metabolome, and mTOR signaling.Cell reports · 2023Article
- Do macrophages follow the beat of circadian rhythm in TIME (Tumor Immune Microenvironment)?F1000Research · 2023Review
- Prediction of six macrophage phenotypes and their IL-10 content based on single-cell morphology using artificial intelligence.Frontiers in immunology · 2023Article
- The IL-1β, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19.Cell reports. Medicine · 2022Article
- CXCL4 synergizes with TLR8 for TBK1-IRF5 activation, epigenomic remodeling and inflammatory response in human monocytes.Nature communications · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF) is best known for inducing a rapid but transient NF-κB-mediated inflammatory response. We investigated later phases of TNF signaling, after the initial transient induction of inflammatory genes has subsided, in primary human macrophages. TNF signaling induced expression of late response genes, including inhibitors of NF-κB and TLR signaling, with delayed and sustained kinetics 6-24 hr after TNF stimulation. A subset of late phase genes was expressed in rheumatoid arthritis synovial macrophages, confirming their expression under chronic inflammatory conditions in vivo. Expression of a subset of late phase genes was mediated by autocrine IL-10, which activated STAT3 with delayed kinetics. Hypoxia, which occurs at sites of infection or inflammation where TNF is expressed, suppressed this IL-10-STAT3 autocrine loop and expression of late phase genes. TNF-induced expression of IL-10 and downstream genes was also dependent on signaling by mTORC1, which senses the metabolic state of cells and is modulated by hypoxia. These results reveal an mTORC1-dependent IL-10-mediated late phase response to TNF by primary human macrophages, and identify suppression of IL-10 responses as a new mechanism by which hypoxia can promote inflammation. Thus, hypoxic and metabolic pathways may modulate TNF responses during chronic inflammation.
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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.