ArticleThe Journal of experimental medicine2020
The transcription factor NFAT5 limits infection-induced type I interferon responses.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Poorly perfused tumor regions harbor T cells with a glucose-dependent effector phenotype.EMBO reports · 2026Article
- Landscape of NFrontiers in microbiology · 2026Article
- HCMV encoded UL84 hijacks FHL2 to suppress type I interferon production and enhance viral replication.PLoS pathogens · 2026Article
- Review
- IRF4-regulated transcriptional and functional heterogeneity of lung-resident CD11b+ cDC2 subsets during influenza virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Characteristics of a CCL21 Gene-Modified Dendritic Cell Vaccine Utilized for a Clinical Trial in Non-Small Cell Lung Cancer.Molecular cancer therapeutics · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Heart-specific NFAT5 knockout suppresses type I interferon signaling and aggravates coxsackievirus-induced myocarditis.Basic research in cardiology · 2024Article
- NFAT5 counters long-term IFN-1 responses in hematopoietic stem cells to preserve reconstitution potential.Blood advances · 2024Article
- Article
- CRISPR/dCas9 DNA methylation editing is heritable during human hematopoiesis and shapes immune progeny.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- NFAT5 Restricts Bovine Herpesvirus 1 Productive Infection in MDBK Cell Cultures.Microbiology spectrum · 2023Article
- Regulation of IFNβ expression: focusing on the role of its promoter and transcription regulators.Frontiers in microbiology · 2023Review
- Immuno-metabolic signaling in leishmaniasis: insights gained from mathematical modeling.Bioinformatics advances · 2023Article
- Not enough by half: NFAT5 haploinsufficiency in two patients with Epstein-Barr virus susceptibility.Frontiers in immunology · 2022Review
- NFAT5 Amplifies Antipathogen Responses by Enhancing Chromatin Accessibility, H3K27 Demethylation, and Transcription Factor Recruitment.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- ceRNA analysis of SARS-CoV-2.Archives of virology · 2021Article
- Tumor-associated macrophages: potential therapeutic strategies and future prospects in cancer.Journal for immunotherapy of cancer · 2021Review
- Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-DependentViruses · 2020Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Type I interferon (IFN-I) provides effective antiviral immunity but can exacerbate harmful inflammatory reactions and cause hematopoietic stem cell (HSC) exhaustion; therefore, IFN-I expression must be tightly controlled. While signaling mechanisms that limit IFN-I induction and function have been extensively studied, less is known about transcriptional repressors acting directly on IFN-I regulatory regions. We show that NFAT5, an activator of macrophage pro-inflammatory responses, represses Toll-like receptor 3 and virus-induced expression of IFN-I in macrophages and dendritic cells. Mice lacking NFAT5 exhibit increased IFN-I production and better control of viral burden upon LCMV infection but show exacerbated HSC activation under systemic poly(I:C)-induced inflammation. We identify IFNβ as a primary target repressed by NFAT5, which opposes the master IFN-I inducer IRF3 by binding to an evolutionarily conserved sequence in the IFNB1 enhanceosome that overlaps a key IRF site. These findings illustrate how IFN-I responses are balanced by simultaneously opposing transcription factors.
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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.