ArticleNature communications2019
IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate macrophage activation.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
92 citing papers in PubMed, 137 citations in OpenAlex.
- SM03, a non-depleting anti-CD22 antibody, modulates B cell activation and immune crosstalk to attenuate autoimmunity.Journal of translational autoimmunity · 2026Article
- A transcriptional cofactor GRIP1 drives PPARγ DNA binding and p300-dependent enhancer activity during homeostatic macrophage polarization.Science advances · 2026Article
- IL-17D reprograms CD93Cellular & molecular immunology · 2026Article
- Pan-cancer epigenetic landscape of human tumor-associated macrophages reveals crucial enhancers governing their heterogenous formation by Pol II pausing modulation.Journal of advanced research · 2026Article
- Dual-Targeted M1 Macrophage Extracellular Vesicles Reprogram the Tumor Microenvironment and Enhance Natural Killer Cell Immunotherapy in Breast Cancer.Journal of extracellular vesicles · 2026Article
- Antigen 85B ofVaccines · 2026Review
- Synergistic interaction between the macrophage polarizing signals IL-4 and IFNγ is controlled by the STAT6/STAT1/IRF1 axis.Nucleic acids research · 2026Article
- Metabolic-epigenetic crosstalk in innate immune cell plasticity within the tumor microenvironment.Experimental & molecular medicine · 2026Review
- A STAT1/ETC/GBP1 axis represents a potential therapeutic target for noncommunicable granulomatous skin disease.Science advances · 2026Article
- An in situ generated CAR-M with IFN-γ and negative dominance Sirpα isoform augments hepatocellular carcinoma immunotherapy.Journal of nanobiotechnology · 2026Article
- IFNγ-induced memory in human macrophages is sustained by the durability of cytokine signaling itself.The Journal of experimental medicine · 2026Article
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- Immune activation of primary human macrophages is suppressed by the coordinated action ofmBio · 2026Article
- Decoding Epigenetic Switches: How Histone Acetylation/Deacetylation Regulates Mononuclear/Macrophage Fate in Bone Disorders.International journal of biological sciences · 2026Review
- Integrated multi-omics analysis reveals shared IFN-γ-associated monocyte signatures in primary Sjögren's syndrome and Alzheimer's disease.Frontiers in immunology · 2026Article
- Gut bacteriophages induce specific-reprogramming of macrophages to generate a protective innate immunity response to lipopolysaccharide exposure.Gut microbes · 2025Article
- Trained Immunity in Health and Disease.MedComm · 2025Review
- Differential Responses of Human iPSC-Derived Microglia to Stimulation with Diverse Inflammogens.Cells · 2025Article
- Type 1 diabetes mellitus (T1DM) does not affect whole blood responses to alginate-based microspheres despite plasma lipid and glucose differences.Materials today. Bio · 2025Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Activation of macrophage proinflammatory and antimicrobial phenotypes is regulated by IFN-γ and LPS via synergistic induction of canonical, inflammatory NF-κB target genes. However, whether IFN-γ negatively regulates components of the LPS response, and how this may affect macrophage activation, is still unclear. Here we use combined transcriptomic and epigenomic approaches to find that IFN-γ selectively abrogates LPS-induced feedback and alters macrophage metabolic pathways by suppressing TLR4-mediated gene activation. In contrast to superinduction of inflammatory genes via enhancers that bind IRF1 and STAT1, IFN-γ represses target enhancers that bind STAT3. TLR4-activated but IFN-γ-suppressed enhancers comprise two subsets discernable by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin. Our findings thus show that IFN-γ suppresses feedback inhibitory and metabolic components of TLR responses to enhance macrophage activation; they also provide insights for IFN-γ-mediated selective inhibition of TLR4-induced transcription. Such inhibition can contribute to severe and sustained inflammatory responses.
Indexed as
Identifiers
What OpenQuestion holds
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.