ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Coordinate interaction between IL-13 and epithelial differentiation cluster genes in eosinophilic esophagitis.
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. It is linked to trial NCT06665971 (Effect of Dupilumab on Esophageal Peristaltic Function in Participants with Eosinophilic Esophagitis), which is not on this map. Cited by 176 papers, 1 of them a synthesis that pooled it.
What it found
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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
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.
Effect of Dupilumab on Esophageal Peristaltic Function in Participants with Eosinophilic Esophagitis
Who cites it
176 citing papers in PubMed, 1 synthesis or guideline pooled it, 285 citations in OpenAlex.
- Causal relationship between eosinophilic esophagitis and inflammatory bowel disease: a bidirectional two-sample Mendelian randomization study.Frontiers in immunology · 2024Pooled it
- Identification of anoctamin 1 (ANO1) as a key driver of esophageal epithelial proliferation in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2020Trial
- Histological Response to Fluticasone Propionate in Patients With Eosinophilic Esophagitis Is Associated With Improved Functional Esophageal Mucosal Integrity.The American journal of gastroenterology · 2015Trial
- Trial
- The Food Allergy-Eosinophilic Esophagitis Continuum: Implications for Food Allergy Immunotherapy.The journal of allergy and clinical immunology. In practice · 2026Review
- Multitrait analysis of genome-wide association studies expands eosinophilic esophagitis genetic susceptibility and polygenic risk scores.The Journal of allergy and clinical immunology · 2026Article
- Review
- IL-13 and calpain-14 suppress the expression of SPINK7 by regulating OVOL1 in eosinophilic esophagitis.JCI insight · 2026Article
- Eosinophilic Esophagitis: Mechanisms of Disease and Approach to Treatment.Current allergy and asthma reports · 2026Review
- Eosinophilic esophagitis in children: Clinical perspectives and evolving therapeutic strategies.World journal of gastrointestinal endoscopy · 2026Review
- PSMB8 stratifies therapy response in eosinophilic esophagitis.Clinical and experimental immunology · 2026Article
- Emerging Insights into the Inflammatory Phenotypes of Eosinophilic Esophagitis.Journal of inflammation research · 2026Review
- Compartment-based biomarker integration for clinical monitoring in eosinophilic esophagitis.Therapeutic advances in gastroenterology · 2026Review
- Overlapping type 2, barrier, and remodeling endotypes shape clinical expression in eosinophilic esophagitis.Frontiers in immunology · 2026Review
- Distinct Roles for Thymic Stromal Lymphopoietin (TSLP) and IL-33 in Experimental Eosinophilic Esophagitis.Allergy · 2025Article
- Unique epithelial proliferative transcriptomic signature in proton pump inhibitor-responsive pediatric eosinophilic esophagitis.JCI insight · 2025Article
- Article
- The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025Review
- Genetic Background of Eosinophilic Esophagitis and Esophageal Atresia in Children.Digestive diseases and sciences · 2025Article
- Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
116 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
We have previously proposed that the pathogenesis of eosinophilic esophagitis (EE) is mediated by an IL-13-driven epithelial cell response associated with marked gene dysregulation including eotaxin-3 overproduction. In this study, we compared epithelial responses between healthy patients and those with EE, aiming to uncover molecular explanations for EE pathogenesis. Esophageal epithelial cells could be maintained for up to five passages, with 67% and 62% of cell lines reaching confluence in healthy controls and EE cases, respectively. Both sets of epithelial cells avidly responded to IL-13 at similar levels as assessed by eotaxin-3 production. Acidic pH increased cellular release of eotaxin-3 (4.6 +/- 1.98 ng/ml versus 12.46 +/- 2.90 ng/ml at pH 7.4 and 4, respectively; p < 0.05). Numerous epidermal differentiation complex (EDC) genes, such as filaggrin and SPRR3, were downregulated both in IL-13-stimulated esophageal epithelial cells and in EE biopsies specimens compared with healthy controls. Whereas the filaggrin loss of function mutation 2282del4 was overrepresented in EE compared with control individuals (6.1% versus 1.3% respectively; p = 0.0172), the decreased filaggrin expression was uniformly seen in all EE cases in vivo. Indeed, expression of the EDC genes filaggrin and involucrin was strongly decreased directly by IL-13. These results establish that the epithelial response in EE involves a cooperative interaction between IL-13 and expression of EDC genes.
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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.