ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2020
Involvement of the epidermal growth factor receptor in IL-13-mediated corticosteroid-resistant airway inflammation.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Examining the Interaction between Allergic Asthma and Air Pollution: a Potential Role for Trained Immunity.Current allergy and asthma reports · 2025Review
- Proteomics endotyping of infants with severe bronchiolitis and risk of childhood asthma.Allergy · 2022Article
- Possible selection bias limits the interpretation of single-cell transcriptomics data of steroid-resistant asthma exacerbation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Airway Epithelial Dysfunction in Asthma: Relevant to Epidermal Growth Factor Receptors and Airway Epithelial Cells.Journal of clinical medicine · 2020Review
- Involvement of the epidermal growth factor receptor in IL-13-mediated corticosteroid-resistant airway inflammation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEffective treatment for severe asthma is a significant unmet need. While eosinophilic inflammation caused by type 2 cytokines is responsive to corticosteroid and biologic therapies, many severe asthmatics exhibit corticosteroid-unresponsive mixed granulocytic inflammation.
objectiveHere, we tested the hypothesis that the pro-allergic cytokine, IL-13, can drive both corticosteroid-sensitive and corticosteroid-resistant responses.
resultsBy integration of in vivo and in vitro models of IL-13-driven inflammation, we identify a role for the epidermal growth factor receptor (EGFR/ERBB1) as a mediator of corticosteroid-unresponsive inflammation and bronchial hyperresponsiveness driven by IL-13. Topological data analysis using human epithelial transcriptomic data from the U-BIOPRED cohort identified severe asthma groups with features consistent with the presence of IL-13 and EGFR/ERBB activation, with involvement of distinct EGFR ligands. Our data suggest that IL-13 may play a dual role in severe asthma: on the one hand driving pathologic corticosteroid-refractory mixed granulocytic inflammation, but on the other hand underpinning beneficial epithelial repair responses, which may confound responses in clinical trials. CONCLUSION AND CLINICAL RELEVANCE: Detailed dissection of those molecular pathways that are downstream of IL-13 and utilize the ERBB receptor and ligand family to drive corticosteroid-refractory inflammation should enhance the development of new treatments that target this sub-phenotype(s) of severe asthma, where there is an unmet need.
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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.