ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Type I IFNs downregulate myeloid cell IFN-γ receptor by inducing recruitment of an early growth response 3/NGFI-A binding protein 1 complex that silences ifngr1 transcription.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- Genome-wide meta-analysis reveals shared newAnnals of the rheumatic diseases · 2019Pooled it
- Meta-analysis of Immunochip data of four autoimmune diseases reveals novel single-disease and cross-phenotype associations.Genome medicine · 2018Pooled it
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis.Nature communications · 2026Article
- Review
- Differential microRNA expression profiles and predicted miRNA-mRNA regulatory networks in human macrophage-like cells infected with Leishmania infantum.Scientific reports · 2026Article
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity tobioRxiv : the preprint server for biology · 2025Article
- Mendelian randomization study on the causal relationships among fasting blood glucose, plasma proteins, and squamous cell lung cancer.Discover oncology · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- PD-L1 and IFN-γ modulate Non-Small Cell Lung Cancer (NSCLC) cell plasticity associated to immune checkpoint inhibitor (ICI)-mediated hyperprogressive disease (HPD).Journal of translational medicine · 2025Article
- Deregulation of interferon-gamma receptor 1 expression and its implications for lung adenocarcinoma progression.World journal of clinical oncology · 2024Review
- The crucial regulatory role of type I interferon in inflammatory diseases.Cell & bioscience · 2023Review
- Genetics and epigenetics of primary Sjögren syndrome: implications for future therapies.Nature reviews. Rheumatology · 2023Review
- Gene expression of peripheral blood mononuclear cells and CD8Frontiers in immunology · 2023Article
- Immune cell-derived extracellular vesicular microRNAs induce pancreatic beta cell apoptosis.Heliyon · 2022Article
- Myeloid cell responsiveness to interferon-gamma is sufficient for initial resistance toCurrent research in immunology · 2020Article
- Pathogenic Biohacking: Induction, Modulation and Subversion of Host Transcriptional Responses byToxins · 2020Review
- IFNγ receptor down-regulation facilitates Legionella survival in alveolar macrophages.Journal of leukocyte biology · 2020Article
- Ligand-induced IFNGR1 down-regulation calibrates myeloid cell IFNγ responsiveness.Life science alliance · 2019Article
- Sequential conditioning-stimulation reveals distinct gene- and stimulus-specific effects of Type I and II IFN on human macrophage functions.Scientific reports · 2019Article
- Sources of Type I Interferons in Infectious Immunity: Plasmacytoid Dendritic Cells Not Always in the Driver's Seat.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The ability of type I IFNs to increase susceptibility to certain bacterial infections correlates with downregulation of myeloid cell surface IFNGR, the receptor for the type II IFN (IFN-γ), and reduced myeloid cell responsiveness to IFN-γ. In this study, we show that the rapid reductions in mouse and human myeloid cell surface IFNGR1 expression that occur in response to type I IFN treatment reflect a rapid silencing of new ifngr1 transcription by repressive transcriptional regulators. Treatment of macrophages with IFN-β reduced cellular abundance of ifngr1 transcripts as rapidly and effectively as actinomycin D treatment. IFN-β treatment also significantly reduced the amounts of activated RNA polymerase II (pol II) and acetylated histones H3 and H4 at the ifngr1 promoter and the activity of an IFNGR1-luc reporter construct in macrophages. The suppression of IFNGR1-luc activity required an intact early growth response factor (Egr) binding site in the proximal ifngr1 promoter. Three Egr proteins and two Egr/NGFI-A binding (Nab) proteins were found to be expressed in bone macrophages, but only Egr3 and Nab1 were recruited to the ifngr1 promoter upon IFN-β stimulation. Knockdown of Nab1 in a macrophage cell line prevented downregulation of IFNGR1 and prevented the loss of acetylated histones from the ifngr1 promoter. These data suggest that type I IFN stimulation induces a rapid recruitment of a repressive Egr3/Nab1 complex that silences transcription from the ifngr1 promoter. This mechanism of gene silencing may contribute to the anti-inflammatory effects of type I IFNs.
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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.