ArticleJournal of innate immunity2020
Activation of Toll-Like Receptor 3 Induces Interleukin-1 Receptor Antagonist Expression by Activating the Interferon Regulatory Factor 3.
Article in Journal of innate immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 26 citations in OpenAlex.
- IRF3 in viral infections: more than just triggering the interferon response.Genes and immunity · 2025Review
- Exosome circ-CBLB promotes M1 macrophage polarization in rheumatoid arthritis through the TLR3/TRAF3 signaling axis.Frontiers in immunology · 2025Article
- Toll-like receptor 3 activation enhances antitumor immune response in lung adenocarcinoma through NF-κB signaling pathway.Frontiers in immunology · 2025Article
- Gut microbiota dysbiosis in inflammatory bowel disease: interaction with intestinal barriers and microbiota-targeted treatment options.Frontiers in cellular and infection microbiology · 2025Review
- Flotillins affect LPS-induced TLR4 signaling by modulating the trafficking and abundance of CD14.Cellular and molecular life sciences : CMLS · 2024Article
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Feline coronavirus influences the biogenesis and composition of extracellular vesicles derived from CRFK cells.Frontiers in veterinary science · 2024Article
- Heterogeneity of Phenotypic and Functional Changes to Porcine Monocyte-Derived Macrophages Triggered by Diverse Polarizing Factors In Vitro.International journal of molecular sciences · 2023Article
- Rintatolimod: a potential treatment in patients with pancreatic cancer expressing Toll-like receptor 3.American journal of cancer research · 2023Article
- Article
- Toll-like receptors in the mechanism of tributyltin-induced production of pro-inflammatory cytokines, IL-1β and IL-6.Toxicology · 2022Article
- Protective Efficacy of Novel Oral Biofilm Vaccines againstVaccines · 2022Article
- Grass Carp Mex3A Promotes Ubiquitination and Degradation of RIG-I to Inhibit Innate Immune Response.Frontiers in immunology · 2022Article
- Once Upon a Time.Journal of innate immunity · 2021Article
- Some Like It Hot.Journal of innate immunity · 2021Article
- Toll-like receptors (TLRs): An old family of immune receptors with a new face in cancer pathogenesis.Journal of cellular and molecular medicine · 2021Review
- The Road Not Taken: Commensal or Virulent Pathogen.Journal of innate immunity · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 3 (TLR3) is a sensor of endogenous cell necrosis during the process of acute inflammation. Interleukin (IL)-1 receptor antagonist (IL-1Ra) is an anti-inflammatory cytokine and can negatively regulate the pathogenesis of inflammation. However, whether and how activation of TLR3 can regulate IL-1Ra expression has not been clarified. Here, we show that poly(I:C) induces IL-1Ra expression in primarily cultured human fibroblast-like synoviocytes and other types of cells. Induction of IL-1Ra by poly(I:C) was dependent on TLR3, but was independent of melanoma differentiation--associated protein 5 or retinoic acid-inducible gene I. Interferon regulatory factor 3 (IRF3) directly binds to the IL-1Ra promoter and promotes IL-1Ra expression in response to poly(I:C) stimulation. Induction of IL-1Ra by poly(I:C) was abolished by the inhibition of the NF-κB signaling, attenuated by the inhibition of the PI3K-Akt signaling, enhanced by inhibition of the ERK1/2 or MSK1/2 activation, but was independent of the p38 MAPK signaling. Treatment with poly(I:C) or Sendai virus elevated the levels of serum IL-1Ra in wild-type, but not in TLR3-/- or IRF3-/- mice. Our findings may provide new insights into the intrinsic anti-inflammatory function of TLR3 and double-stranded RNA-induced IL-Ra expression by TLR3 and its regulation.
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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.