ArticleJournal of immunology (Baltimore, Md. : 1950)2016
IL-33 Precedes IL-5 in Regulating Eosinophil Commitment and Is Required for Eosinophil Homeostasis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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Who cites it
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- Eosinophils and eosinophil-associated diseases: An update.The Journal of allergy and clinical immunology · 2018Pooled it
- Pharmacokinetics and pharmacodynamics of itepekimab in healthy adults and patients with asthma: Phase I first-in-human and first-in-patient trials.Clinical and translational science · 2022Trial
- From Susceptibility to Severity: The Impact of Interleukin-33 rs1929992 Polymorphism on Asthma in a Taiwanese Population.Life (Basel, Switzerland) · 2026Article
- Epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis: mechanistic roles and therapeutic implications.Molecular biology reports · 2026Review
- IL-33 Elicits LTCEuropean journal of immunology · 2026Article
- Distinguishing Features of ILC2s During Type 2 Immune Responses.European journal of immunology · 2026Review
- Constitutively high levels of endogenous soluble ST2 inhibit food allergic responses in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- IL-33 blockade attenuates vascular inflammation in a mouse model of Kawasaki disease vasculitis.Clinical and experimental immunology · 2026Article
- Biological functions and clinical efficacy of IL-5/IL-5Rα-targeted therapies across eosinophilia-associated diseases.Frontiers in immunology · 2026Review
- New perspectives in the treatment of chronic eosinophilic pneumonia in the era of targeted therapies.Frontiers in immunology · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- Exploration of miRNAs promoting eosinophilia and type 2 immunity.Frontiers in allergy · 2026Article
- Immunotherapy for asthma.Cellular & molecular immunology · 2025Review
- Review
- Guardians at the border: Peritumoral macrophages fight breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025Review
- Article
- Pathobiology and Regulation of Eosinophils, Mast Cells, and Basophils in Allergic Asthma.Immunological reviews · 2025Review
- The role of IL-33/ST2 axis in esophageal inflammatory diseases and cancers: implications for the immunopathogenesis and immunotherapeutic target?Therapeutic advances in gastroenterology · 2025Review
- Regulation of eosinophil recruitment and heterogeneity during allergic airway inflammation.Frontiers in allergy · 2025Review
44 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Eosinophils are important in the pathogenesis of many diseases, including asthma, eosinophilic esophagitis, and eczema. Whereas IL-5 is crucial for supporting mature eosinophils (EoMs), the signals that support earlier eosinophil lineage events are less defined. The IL-33R, ST2, is expressed on several inflammatory cells, including eosinophils, and is best characterized for its role during the initiation of allergic responses in peripheral tissues. Recently, ST2 expression was described on hematopoietic progenitor subsets, where its function remains controversial. Our findings demonstrate that IL-33 is required for basal eosinophil homeostasis, because both IL-33- and ST2-deficient mice exhibited diminished peripheral blood eosinophil numbers at baseline. Exogenous IL-33 administration increased EoMs in both the bone marrow and the periphery in wild-type and IL-33-deficient, but not ST2-deficient, mice. Systemic IL-5 was also increased under this treatment, and blocking IL-5 with a neutralizing Ab ablated the IL-33-induced EoM expansion. The homeostatic hypereosinophilia seen in IL-5-transgenic mice was significantly lower with ST2 deficiency despite similar elevations in systemic IL-5. Finally, in vitro treatment of bone marrow cells with IL-33, but not IL-5, led to specific early expansion of IL-5Rα-expressing precursor cells. In summary, our findings establish a basal defect in eosinophilopoiesis in IL-33- and ST2-deficient mice and a mechanism whereby IL-33 supports EoMs by driving both systemic IL-5 production and the expansion of IL-5Rα-expressing precursor cells.
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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.