ArticleJournal of immunology (Baltimore, Md. : 1950)2013
IL-33 markedly activates murine eosinophils by an NF-κB-dependent mechanism differentially dependent upon an IL-4-driven autoinflammatory loop.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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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
74 citing papers in PubMed, 101 citations in OpenAlex.
- The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation.Nature communications · 2018Trial
- Tissue adaptation of eosinophils.Journal of leukocyte biology · 2026Review
- The Immune Architecture of Eosinophilic Esophagitis: Mechanisms, Therapeutic Targets, and Precision Management.ImmunoTargets and therapy · 2026Review
- Interleukin-Mediated Macrophage Polarization in Allergic Rhinitis Inflammation: A Systematic Review.Journal of inflammation research · 2026Review
- Absence of BCAP in myeloid cells abrogates M2 macrophage differentiation and promotes anti-tumor immunity.iScience · 2025Article
- Unlocking IL-33: New Insights into Tumor Immunity.Immune network · 2025Review
- Regulation of eosinophil recruitment and heterogeneity during allergic airway inflammation.Frontiers in allergy · 2025Review
- Spatial adaptation of eosinophils and their emerging roles in homeostasis, infection and disease.Nature reviews. Immunology · 2024Review
- Advancing toward a unified eosinophil signature from transcriptional profiling.Journal of leukocyte biology · 2024Review
- Regulation of Airway Epithelial-Derived Alarmins in Asthma: Perspectives for Therapeutic Targets.Biomedicines · 2024Review
- Common and disparate clinical presentations and mechanisms in different eosinophilic gastrointestinal diseases.The Journal of allergy and clinical immunology · 2024Review
- Development and dysfunction of structural cells in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2024Review
- Female-specific enhancement of eosinophil recruitment and activation in a type 2 innate inflammation model in the lung.Clinical and experimental immunology · 2024Article
- Repeated sensitization of mice with microfilariae of Litomosoides sigmodontis induces pulmonary eosinophilia in an IL-33-dependent manner.PLoS pathogens · 2024Article
- Linking adipose tissue eosinophils, IL-4, and leptin in human obesity and insulin resistance.JCI insight · 2024Article
- Adenosine receptor A2b confers ovarian cancer survival and PARP inhibitor resistance through IL-6-STAT3 signalling.Journal of cellular and molecular medicine · 2023Article
- Morphological and histochemical identification of telocytes in adult yak epididymis.Scientific reports · 2023Article
- Review
- The IL-1 Family and Its Role in Atherosclerosis.International journal of molecular sciences · 2022Review
- RNA-sequencing reveals molecular and regional differences in the esophageal mucosa of achalasia patients.Scientific reports · 2022Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Eosinophils are major effector cells in type 2 inflammatory responses and become activated in response to IL-4 and IL-33, yet the molecular mechanisms and cooperative interaction between these cytokines remain unclear. Our objective was to investigate the molecular mechanism and cooperation of IL-4 and IL-33 in eosinophil activation. Eosinophils derived from bone marrow or isolated from Il5-transgenic mice were activated in the presence of IL-4 or IL-33 for 1 or 4 h, and the transcriptome was analyzed by RNA sequencing. The candidate genes were validated by quantitative PCR and ELISA. We demonstrated that murine-cultured eosinophils respond to IL-4 and IL-33 by phosphorylation of STAT-6 and NF-κB, respectively. RNA sequence analysis of murine-cultured eosinophils indicated that IL-33 induced 519 genes, whereas IL-4 induced only 28 genes, including 19 IL-33-regulated genes. Interestingly, IL-33 induced eosinophil activation via two distinct mechanisms, IL-4 independent and IL-4 secretion/autostimulation dependent. Anti-IL-4 or anti-IL-4Rα Ab-treated cultured and mature eosinophils, as well as Il4- or Stat6-deficient cultured eosinophils, had attenuated protein secretion of a subset of IL-33-induced genes, including Retnla and Ccl17. Additionally, IL-33 induced the rapid release of preformed IL-4 protein from eosinophils by a NF-κB-dependent mechanism. However, the induction of most IL-33-regulated transcripts (e.g., Il6 and Il13) was IL-4 independent and blocked by NF-κB inhibition. In conclusion, we have identified a novel activation pathway in murine eosinophils that is induced by IL-33 and differentially dependent upon an IL-4 auto-amplification loop.
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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.