ArticleJCI insight2020
IL-4Rα signaling in CD4+CD25+FoxP3+ T regulatory cells restrains airway inflammation via limiting local tissue IL-33.
Article in JCI insight, 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.
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
17 citing papers in PubMed, 21 citations in OpenAlex.
- Type 2 conventional dendritic cells and regulatory T cells form a barrier tissue circuit to control allergic inflammation.bioRxiv : the preprint server for biology · 2026Article
- Targeting the Epithelial Alarmin Axis with Biomedical Nanoparticles: A New Frontier in Allergic Asthma Therapy.International journal of nanomedicine · 2026Review
- From gut microbiota dysbiosis to immune dysregulation: pathogenic mechanisms and emerging therapeutic perspectives in pediatric asthma.Frontiers in immunology · 2026Review
- T Regulatory Mechanisms in Airway and Interstitial Lung Disease.Seminars in respiratory and critical care medicine · 2025Review
- Donor liver natural killer cells ameliorate liver allograft rejection via inducing apoptosis of alloreactive CD8Scientific reports · 2025Article
- Cell-Specific Contribution of IL-4 Receptor α Signaling Shapes the Overall Manifestation of Allergic Airway Disease.American journal of respiratory cell and molecular biology · 2024Article
- Deciphering the developmental trajectory of tissue-resident Foxp3Frontiers in immunology · 2024Review
- The divergent outcome of IL-4Rα signalling on Foxp3 T regulatory cells in listeriosis and tuberculosis.Frontiers in immunology · 2024Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- IL-4Rα signalling in B cells and T cells play differential roles in acute and chronic atopic dermatitis.Scientific reports · 2023Article
- Regulatory T cells in peripheral tissue tolerance and diseases.Frontiers in immunology · 2023Review
- Intestinal factors promoting the development of RORγtFrontiers in immunology · 2023Review
- Revisiting regulatory T cells as modulators of innate immune response and inflammatory diseases.Frontiers in immunology · 2023Review
- Protective role of tissue-resident Tregs in a murine model of beryllium-induced disease.JCI insight · 2022Article
- HDAC6/FOXP3/HNF4α axis promotes bile acids induced gastric intestinal metaplasia.American journal of cancer research · 2022Article
- The Mechanisms of Effector Th Cell Responses Contribute to Treg Cell Function: New Insights into Pathogenesis and Therapy of Asthma.Frontiers in immunology · 2022Review
- Neural Regulation of Interactions Between Group 2 Innate Lymphoid Cells and Pulmonary Immune Cells.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Impaired tolerance to innocuous particles during allergic asthma has been linked to increased plasticity of FoxP3+ regulatory T cells (Tregs) reprogramming into pathogenic effector cells, thus exacerbating airway disease. However, failure of tolerance mechanisms is driven by Th2 inflammatory signals. Therefore, the in vivo role of canonical IL-4 receptor α (IL-4Rα) signaling, an essential driver of Th2-type airway responses to allergens, on the regulatory function of FoxP3+ Tregs in allergic asthma was explored. Here, we used transgenic Foxp3cre IL-4Rα-/lox and littermate control mice to investigate the role of IL-4 and IL-13 signaling via Tregs in house dust mite-induced (HDM-induced) allergic airway disease. We sensitized mice intratracheally on day 0, challenged them on days 6-10, and analyzed airway hyperresponsiveness (AHR), airway inflammation, mucus production, and cellular profile on day 14. In the absence of IL-4Rα responsiveness on FoxP3+ Tregs, exacerbated AHR and airway inflammation were shown in HDM-sensitized mice. Interestingly, reduced induction of FoxP3+ Tregs accompanied increased IL-33 alarmin production and type 2 innate lymphoid cell activation in the lung, exacerbating airway hyperreactivity and lung eosinophilia. Taken together, our findings indicate that IL-4Rα-unresponsive FoxP3+ Tregs result in exaggerated innate Th2-type, IL-33-dependent airway inflammation and a break in tolerance during allergic 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.