ArticleAmerican journal of respiratory cell and molecular biology2021
TLR7 Agonist Suppresses Group 2 Innate Lymphoid Cell-mediated Inflammation via IL-27-Producing Interstitial Macrophages.
Article in American journal of respiratory cell and molecular biology, 2021. 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, 22 citations in OpenAlex.
- Breaking the bottleneck of asthma treatment: the future of omni-targeted therapy.Journal of advanced research · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- Regulation of macrophage polarization in chronic airway inflammatory diseases: immune interactions, metabolic reprogramming, and beyond.Frontiers in immunology · 2026Review
- The role of ILC2s in asthma combined with atopic dermatitis: bridging the gap from research to clinical practice.Frontiers in immunology · 2025Review
- Innate immune sensing and vaccine strategies against West Nile virus: role of Toll-like receptors and viral evasion mechanisms.Frontiers in microbiology · 2025Review
- Antiviral roles of eosinophils in asthma and respiratory viral infection.Frontiers in allergy · 2025Review
- Macrophages reprogramming improves immunotherapy of IL-33 in peritoneal metastasis of gastric cancer.EMBO molecular medicine · 2024Article
- Both Horatio and Polonius: Innate Lymphoid Cells in Tissue Homeostasis and Repair.ImmunoHorizons · 2023Article
- The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.Experimental & molecular medicine · 2023Review
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- Induced pluripotent and CD34+ stem cell derived myeloid cells display differential responses to particle and dust mite exposure.Scientific reports · 2023Article
- The Functional Role of Group 2 Innate Lymphoid Cells in Asthma.Biomolecules · 2023Review
- Innate Immune Responses by Respiratory Viruses, Including Rhinovirus, During Asthma Exacerbation.Frontiers in immunology · 2022Review
- Innate lymphoid cells: More than just immune cells.Frontiers in immunology · 2022Review
- The Therapeutic Potential for Targeting Group 2 Innate Lymphoid Cells in Asthma.Frontiers in immunology · 2022Review
- ILCs and Allergy.Advances in experimental medicine and biology · 2022Article
- Toward a More Precise Solution to Asthma Therapy.American journal of respiratory cell and molecular biology · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 2 innate lymphoid cells (ILC2s) play an important role in the pathophysiology of asthma via the robust production of type 2 cytokines. Recent studies have demonstrated that TLR7 (Toll-like receptor 7) signaling skews toward a type 1 inflammatory response in asthma, which may lead to the development of novel treatment strategies. However, the effect of TLR7 signaling on ILC2-dependent nonallergic eosinophilic inflammation remains unclear. In this study, we investigated the effects of R848, a TLR7 agonist, in a mouse model of IL-33-induced eosinophilic airway inflammation. Intranasal administration of R848 decreased infiltration of airway eosinophils and ILC2s, mucus production in epithelial cells, and type 2 cytokine production. Flow cytometric analysis identified an increased number of interstitial macrophages (IMs) expressing a high level of TLR7 in the lung upon IL-33 stimulation. IL-33-induced IMs also expressed high levels of alternatively activated (M2)-type genes and chemokines (CCL17 and CCL24). However, R848 stimulation modified these gene expressions and elicited the production of IL-27. Coculture experiments revealed that IL-33-induced IMs directly suppressed ILC2 activation in response to R848. In addition, the inhibitory effects of R848 on ILC2-induced type 2 inflammation were defective in WSX-1-deficient mice lacking the IL-27 receptor. Taken together, these findings indicate that R848 stimulates IL-33-induced IMs to suppress ILC2-mediated type 2 airway inflammation via IL-27. These findings highlight the therapeutic potential of TLR7 agonists and/or IL-27 cascades in nonallergic asthma.
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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.