ArticleJournal of immunology (Baltimore, Md. : 1950)2010
IL-13 induces esophageal remodeling and gene expression by an eosinophil-independent, IL-13R alpha 2-inhibited pathway.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
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Who cites it
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Replication and meta-analyses nominate numerous eosinophilic esophagitis risk genes.The Journal of allergy and clinical immunology · 2021Pooled it
- Latent Variable Indirect Response Modeling of Cendakimab Exposure-Response for Longitudinal Dysphagia Days Using a Combined Uniform-Binomial Likelihood Framework.CPT: pharmacometrics & systems pharmacology · 2026Trial
- Trial
- Identification of anoctamin 1 (ANO1) as a key driver of esophageal epithelial proliferation in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2020Trial
- Trial
- Multitrait analysis of genome-wide association studies expands eosinophilic esophagitis genetic susceptibility and polygenic risk scores.The Journal of allergy and clinical immunology · 2026Article
- Article
- Eosinophilic Esophagitis: Mechanisms of Disease and Approach to Treatment.Current allergy and asthma reports · 2026Review
- Compartment-based biomarker integration for clinical monitoring in eosinophilic esophagitis.Therapeutic advances in gastroenterology · 2026Review
- Emerging Insights into the Inflammatory Phenotypes of Eosinophilic Esophagitis.Journal of inflammation research · 2026Review
- Overlapping type 2, barrier, and remodeling endotypes shape clinical expression in eosinophilic esophagitis.Frontiers in immunology · 2026Review
- Epigenetic and transcriptional programming of murine eosinophils in the esophagus.Nature communications · 2025Article
- Unique epithelial proliferative transcriptomic signature in proton pump inhibitor-responsive pediatric eosinophilic esophagitis.JCI insight · 2025Article
- The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025Review
- Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- FOXM1 Modulation Alleviates Epithelial Remodeling and Inflammation in Eosinophilic Esophagitis.bioRxiv : the preprint server for biology · 2025Article
- Targeting IL-13 and IL-4 in Asthma: Therapeutic Implications on Airway Remodeling in Severe Asthma.Clinical reviews in allergy & immunology · 2025Review
- Eosinophilic Esophagitis Complicated by an Esophageal Stricture in a 15-Month-Old Child.Case reports in pediatrics · 2025Article
- Esophageal ILC2s mediate abnormal epithelial remodeling in eosinophilic esophagitis via Areg-EGFR signaling.Cellular & molecular immunology · 2025Article
- Eosinophil specialization is regulated by exposure to the esophageal epithelial microenvironment.Journal of leukocyte biology · 2024Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Eosinophilic esophagitis (EE) is an emerging disease associated with both food and respiratory allergy characterized by extensive esophageal tissue remodeling and abnormal esophageal gene expression, including increased IL-13. We investigated the ability of increased airway IL-13 to induce EE-like changes. Mice with pulmonary (but not esophageal) overexpression of IL-13 evidenced esophageal IL-13 accumulation and developed prominent esophageal remodeling with epithelial hyperplasia, angiogenesis, collagen deposition, and increased circumference. IL-13 induced notable changes in esophageal transcripts that overlapped with the human EE esophageal transcriptome. IL-13-induced esophageal eosinophilia was dependent on eotaxin-1 (but not eotaxin-2). However, remodeling occurred independent of eosinophils as demonstrated by eosinophil lineage-deficient, IL-13 transgenic mice. IL-13-induced remodeling was significantly enhanced by IL-13Ralpha2 deletion, indicating an inhibitory effect of IL-13Ralpha2. In the murine system, there was partial overlap between IL-13-induced genes in the lung and esophagus, yet the transcriptomes were divergent at the tissue level. In human esophagus, IL-13 levels correlated with the magnitude of the EE transcriptome. In conclusion, inducible airway expression of IL-13 results in a pattern of esophageal gene expression and extensive tissue remodeling that resembles human EE. Notably, we identified a pathway that induces EE-like changes and is IL-13-driven, eosinophil-independent, and suppressed by IL-13Ralpha2.
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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.