ArticleAllergy2023
IL1RAP expression and the enrichment of IL-33 activation signatures in severe neutrophilic asthma.
Article in Allergy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- TIR domain proteins: regulatory mechanisms in the tumor immune microenvironment, clinical translation strategies, and prospects for precision therapy applications.Frontiers in immunology · 2025Pooled it
- The IL-33/ST2 pathway to modulate the inflammatory microenvironment: A new therapeutic target in chronic obstructive pulmonary disease.Biochemistry and biophysics reports · 2026Review
- Unknotting the nexus of asthma and neuroinflammation: from brain network alterations to therapeutic implications.Journal of neuroinflammation · 2026Review
- Current understanding and future directions in severe asthma through artificial intelligence-integrated multi-omic approaches.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Airway transcriptome networks for ozone and PMGenome medicine · 2025Article
- Lysosomal acidity and cathepsin L activate eosinophils via ARG1-mediated arginine metabolism in allergic airway inflammation.Nature communications · 2025Article
- Article
- Integrated multi-omics profiling reveals shared mechanistic pathways in asthma-allergic rhinitis comorbidity: A hybrid machine learning framework leveraging Mendelian randomization for precision diagnostics.The World Allergy Organization journal · 2025Article
- The Role of Alarmins in the Pathogenesis of Asthma.Biomolecules · 2025Review
- Integrated single-cell and transcriptome sequencing data reveal the value of IL1RAP in gastric cancer microenvironment and prognosis.Frontiers in oncology · 2025Article
- Article
- Induced Sputum Transcriptomics Profile and Serum C3 are Associated with Asthma Severity.Journal of asthma and allergy · 2025Article
- Exploring potential therapeutic targets for asthma: a proteome-wide Mendelian randomization analysis.Journal of translational medicine · 2024Article
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- From mesenchymal stem cells to their extracellular vesicles: Progress and prospects for asthma therapy.Asian journal of pharmaceutical sciences · 2024Review
- Inhibition of phosphoinositide 3-kinase activity attenuates neutrophilic airway inflammation and inhibits pyrin domain-containing 3 inflammasome activation in an ovalbumin-lipopolysaccharide-induced asthma murine model.Molecular biology reports · 2024Article
- New targets for type 2-low asthma.The Korean journal of internal medicine · 2024Review
- P2X7 Receptor-Induced Human Mast Cell Degranulation Is Enhanced by Interleukin 33.International journal of molecular sciences · 2024Article
- Role and regulators of NFrontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
Abstract
backgroundInterleukin (IL)-33 is an upstream regulator of type 2 (T2) eosinophilic inflammation and has been proposed as a key driver of some asthma phenotypes.
objectiveTo derive gene signatures from in vitro studies of IL-33-stimulated cells and use these to determine IL-33-associated enrichment patterns in asthma.
methodsSignatures downstream of IL-33 stimulation were derived from our in vitro study of human mast cells and from public datasets of in vitro stimulated human basophils, type 2 innate lymphoid cells (ILC2), regulatory T cells (Treg) and endothelial cells. Gene Set Variation Analysis (GSVA) was used to probe U-BIOPRED and ADEPT sputum transcriptomics to determine enrichment scores (ES) for each signature according to asthma severity, sputum granulocyte status and previously defined molecular phenotypes.
resultsIL-33-activated gene signatures were cell-specific with little gene overlap. Individual signatures, however, were associated with similar signalling pathways (TNF, NF-κB, IL-17 and JAK/STAT signalling) and immune cell differentiation pathways (Th17, Th1 and Th2 differentiation). ES for IL-33-activated gene signatures were significantly enriched in asthmatic sputum, particularly in patients with neutrophilic and mixed granulocytic phenotypes. IL-33 mRNA expression was not elevated in asthma whereas the expression of mRNA for IL1RL1, the IL-33 receptor, was up-regulated in the sputum of severe eosinophilic asthma. The mRNA expression for IL1RAP, the IL1RL1 co-receptor, was greatest in severe neutrophilic and mixed granulocytic asthma.
conclusionsIL-33-activated gene signatures are elevated in neutrophilic and mixed granulocytic asthma corresponding with IL1RAP co-receptor expression. This suggests incorporating T2-low asthma in anti-IL-33 trials.
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