ArticleThe Journal of allergy and clinical immunology2015
Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33.
Article in The Journal of allergy and clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers.
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Who cites it
177 citing papers in PubMed, 296 citations in OpenAlex.
- Pulmonary Innate Lymphoid Cell Responses during Rhinovirus-induced Asthma ExacerbationsAmerican journal of respiratory and critical care medicine · 2021Trial
- IL-33 as a boundary-tissue state-transfer signal: a Reader-Alarmin-Effector architecture linking CNS and skin.Brain, behavior, & immunity - health · 2026Review
- From Susceptibility to Severity: The Impact of Interleukin-33 rs1929992 Polymorphism on Asthma in a Taiwanese Population.Life (Basel, Switzerland) · 2026Article
- Aberrant mucin expression and keratinization distinguishing severe from mild asthma revealed by interpretable machine learning.JCI insight · 2026Article
- Metabolic Reprogramming and ILC2 Plasticity in Obesity-related Asthma.Clinical reviews in allergy & immunology · 2026Review
- Negative regulation of human IL-33 in endothelium during allergic airway inflammation.JCI insight · 2026Article
- Inflammatory memory: the core mechanism driving allergic asthma recurrence and chronicity.Journal of thoracic disease · 2026Review
- Sex Differences in Lung Immunity.Immunological reviews · 2026Review
- CBX7 functions as a methylation-dependent inducer of gene transcription and regulator of cytosolic signaling in lymphoid cells.Science advances · 2026Article
- The Expanding Role of ILC2s in Allergic Airways Disease.Allergy · 2026Review
- Neurogenic regulation of group 2 innate lymphoid cells in asthma.Frontiers in immunology · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- High-Dimensional Analysis of Type 2 Lymphocyte Dynamics During Mepolizumab or Dupilumab Treatment in Severe Asthma.Allergy · 2025Article
- In Asthmatic Patients, Sexual Dimorphism correlates With Androgen Receptor Expression in ILC2s at Single Cell-Resolution.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025Article
- The immunology of asthma and chronic rhinosinusitis.Nature reviews. Immunology · 2025Review
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.Journal of inflammation (London, England) · 2025Review
- Decoding innate lymphoid cells and innate-like lymphocytes in asthma: pathways to mechanisms and therapies.Journal of biomedical science · 2025Review
- Recurrence of acute allergic asthma depends on the role of ILC2 driven by Il1rl1 signaling.Cell communication and signaling : CCS · 2025Article
- Innate Immunity and Asthma Exacerbations: Insights From Human Models.Immunological reviews · 2025Review
117 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAsthma in a mouse model spontaneously resolves after cessation of allergen exposure. We developed a mouse model in which asthma features persisted for 6 months after cessation of allergen exposure.
objectiveWe sought to elucidate factors contributing to the persistence of asthma.
methodsWe used a combination of immunologic, genetic, microarray, and pharmacologic approaches to dissect the mechanism of asthma persistence.
resultsElimination of T cells though antibody-mediated depletion or lethal irradiation and transplantation of recombination-activating gene (Rag1)(-/-) bone marrow in mice with chronic asthma resulted in resolution of airway inflammation but not airway hyperreactivity or remodeling. Elimination of T cells and type 2 innate lymphoid cells (ILC2s) through lethal irradiation and transplantation of Rag2(-/-)γc(-/-) bone marrow or blockade of IL-33 resulted in resolution of airway inflammation and hyperreactivity. Persistence of asthma required multiple interconnected feedback and feed-forward circuits between ILC2s and epithelial cells. Epithelial IL-33 induced ILC2s, a rich source of IL-13. The latter directly induced epithelial IL-33, establishing a positive feedback circuit. IL-33 autoinduced, generating another feedback circuit. IL-13 upregulated IL-33 receptors and facilitated IL-33 autoinduction, thus establishing a feed-forward circuit. Elimination of any component of these circuits resulted in resolution of chronic asthma. In agreement with the foregoing, IL-33 and ILC2 levels were increased in the airways of asthmatic patients. IL-33 levels correlated with disease severity.
conclusionsWe present a critical network of feedback and feed-forward interactions between epithelial cells and ILC2s involved in maintaining chronic asthma. Although T cells contributed to the severity of chronic asthma, they were redundant in maintaining airway hyperreactivity and remodeling.
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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.