ArticleJournal of immunology (Baltimore, Md. : 1950)2016
IL-27 Is Essential for Suppression of Experimental Allergic Asthma by the TLR7/8 Agonist R848 (Resiquimod).
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Research status and future perspectives of IL‑27 in the treatment of stroke (Review).International journal of molecular medicine · 2025Review
- Antibody preparation and age-dependent distribution of TLR8 in Bactrian camel spleens.BMC veterinary research · 2023Article
- MAP3K19 Affects TWEAK-Induced Response in Cultured Bronchial Epithelial Cells and Regulates Allergic Airway Inflammation in an Asthma Murine Model.Current issues in molecular biology · 2023Article
- Interleukin‑27 ameliorates allergic asthma by alleviating the lung Th2 inflammatory environment.International journal of molecular medicine · 2022Article
- Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma.PloS one · 2021Article
- R848 or influenza virus can induce potent innate immune responses in the lungs of neonatal mice.Mucosal immunology · 2021Article
- TLR7 Ligation Inhibits TLR8 Responsiveness in IL-27-Primed Human THP-1 Monocytes and Macrophages.Journal of innate immunity · 2021Article
- Interleukin-27 and Its Diverse Effects on Bacterial Infections.Frontiers in immunology · 2021Review
- EGR3-HDAC6-IL-27 Axis Mediates Allergic Inflammation and Is Necessary for Tumorigenic Potential of Cancer Cells Enhanced by Allergic Inflammation-Promoted Cellular Interactions.Frontiers in immunology · 2021Article
- Regulation and Function of Interferon-Lambda (IFNλ) and Its Receptor in Asthma.Frontiers in immunology · 2021Review
- TLR9-IL-2 axis exacerbates allergic asthma by preventing IL-17A hyperproduction.Scientific reports · 2020Article
- IL‑27 suppresses airway inflammation, hyperresponsiveness and remodeling via the STAT1 and STAT3 pathways in mice with allergic asthma.International journal of molecular medicine · 2020Article
- Toll-Like Receptor Agonists as Adjuvants for Allergen Immunotherapy.Frontiers in immunology · 2020Review
- Eleven loci with new reproducible genetic associations with allergic disease risk.The Journal of allergy and clinical immunology · 2019Article
- Effects of interleukin-6 receptor blockade on allergen-induced airway responses in mild asthmatics.Clinical & translational immunology · 2019Article
- Costimulatory Molecules and Immune Checkpoints Are Differentially Expressed on Different Subsets of Dendritic Cells.Frontiers in immunology · 2019Article
- TLR-7 Stress Signaling in Differentiating and Mature Eosinophils Is Mediated by the Prolyl Isomerase Pin1.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- The Cell Research Trends of Asthma: A Stem Frequency Analysis of the Literature.Journal of healthcare engineering · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different models of experimental allergic asthma have shown that the TLR7/8 agonist resiquimod (R848) is a potential inhibitor of type 2 helper cell-driven inflammatory responses. However, the mechanisms mediating its therapeutic effects are not fully understood. Using a model of experimental allergic asthma, we show that induction of IL-27 by R848 is critical for the observed ameliorative effects. R848 significantly inhibited all hallmarks of experimental allergic asthma, including airway hyperreactivity, eosinophilic airway inflammation, mucus hypersecretion, and Ag-specific Ig production. Whereas R848 significantly reduced IL-5, IL-13, and IL-17, it induced IFN-γ and IL-27. Neutralization of IL-27 completely reversed the therapeutic effect of R848 in the experimental asthma model, demonstrating dependence of R848-mediated suppression on IL-27. In vitro, R848 induced production of IL-27 by murine alveolar macrophages and dendritic cells and enhanced expression of programmed death-ligand 1, whose expression on monocytes and dendritic cells has been shown to regulate peripheral tolerance in both murine and human studies. Moreover, in vitro IL-27 enhanced secretion of IFN-γ whereas it inhibited IL-5 and IL-13, demonstrating its direct effect on attenuating Th2 responses. Taken together, our study proves that R848-mediated suppression of experimental asthma is dependent on IL-27. These data provide evidence of a central role of IL-27 for the control of Th2-mediated allergic diseases.
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