ArticleJCI insight2021
A role for IL-33-activated ILC2s in eosinophilic vasculitis.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Evidence-Based Guideline for the diagnosis and management of eosinophilic granulomatosis with polyangiitis.Nature reviews. Rheumatology · 2023Guideline
- Advances in the treatment of eosinophilic granulomatosis with polyangiitis.Nature reviews. Rheumatology · 2026Review
- Review
- Article
- Article
- Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis.Nature communications · 2026Article
- Eosinophilic Organ Complications Associated with Dupilumab Therapy - Narrative Review and Current Evidence.Journal of asthma and allergy · 2026Article
- Trained immunity in the lung.eLife · 2025Review
- Immunopathology of Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis.International journal of molecular sciences · 2025Review
- Comparative Insights on IL-5 Targeting with Mepolizumab and Benralizumab: Enhancing EGPA Treatment Strategies.Biomolecules · 2025Review
- Effect of anti-interleukin-5 antibody on development of vasculitis in an ovalbumin-induced eosinophilic vasculitis mouse model.Frontiers in pharmacology · 2025Article
- Biologics in Hypereosinophilic Syndrome and Eosinophilic Granulomatosis with Polyangiitis.Immunology and allergy clinics of North America · 2024Review
- Tezepelumab for refractory eosinophilic granulomatosis with polyangiitis-related asthma.Respiratory research · 2024Article
- Pathogenesis of Pulmonary Manifestations in ANCA-Associated Vasculitis and Goodpasture Syndrome.International journal of molecular sciences · 2024Review
- Eosinophilic Granulomatosis with Polyangiitis: Latest Findings and Updated Treatment Recommendations.Journal of clinical medicine · 2023Review
- CircRNA7632 down-regulation alleviates endothelial cell dysfunction in Kawasaki disease via regulating IL-33 expression.Cell stress & chaperones · 2023Article
- Long-term mepolizumab treatment reduces relapse rates in super-responders with eosinophilic granulomatosis with polyangiitis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023Article
- Pulmonary Fibrosis and Hypereosinophilia in TLR9Pathogens (Basel, Switzerland) · 2022Article
- Heterogeneity and individualized therapy for eosinophilic granulomatosis with polyangiitis.Therapeutic advances in respiratory diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare but serious disease with poorly understood mechanisms. Here, we report that patients with EGPA have elevated levels of TSLP, IL-25, and soluble ST2, which are well-characterized cytokine "alarmins" that activate or modulate type 2 innate lymphoid cells (ILC2s). Patients with active EGPA have a concurrent reduction in circulating ILC2s, suggesting a role for ILC2s in the pathogenesis of this disease. To explore the mechanism of these findings in patients, we established a model of EGPA in which active vasculitis and pulmonary hemorrhage were induced by IL-33 administration in predisposed, hypereosinophilic mice. In this model, induction of pulmonary hemorrhage and vasculitis was dependent on ILC2s and signaling through IL4Rα. In the absence of IL4Rα or STAT6, IL-33-treated mice had less vascular leak and pulmonary edema, less endothelial activation, and reduced eotaxin production, cumulatively leading to a reduction of pathologic eosinophil migration into the lung parenchyma. These results offer a mouse model for use in future mechanistic studies of EGPA, and they suggest that IL-33, ILC2s, and IL4Rα signaling may be potential targets for further study and therapeutic targeting in patients with EGPA.
Indexed as
Identifiers
What OpenQuestion holds
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.