ArticleThe Journal of allergy and clinical immunology2024
Tissue-specific inducible IL-33 expression elicits features of eosinophilic esophagitis.
Article in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- IL-13 and calpain-14 suppress the expression of SPINK7 by regulating OVOL1 in eosinophilic esophagitis.JCI insight · 2026Article
- Emerging Insights into the Inflammatory Phenotypes of Eosinophilic Esophagitis.Journal of inflammation research · 2026Review
- Distinct Roles for Thymic Stromal Lymphopoietin (TSLP) and IL-33 in Experimental Eosinophilic Esophagitis.Allergy · 2025Article
- Article
- Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 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
- Advances and ongoing challenges in eosinophilic gastrointestinal disorders presented at the CEGIR/TIGERs Symposium at the 2024 American Academy of Allergy, Asthma & Immunology meeting.The Journal of allergy and clinical immunology · 2024Review
- Animal models of eosinophilic esophagitis.Journal of leukocyte biology · 2024Review
- Mononuclear cell composition and activation in blood and mucosal tissue of eosinophilic esophagitis.Frontiers in immunology · 2024Article
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Authors and funding
17 authors.
Funding
Abstract
backgroundIL-33 is a type 2 inflammatory cytokine that is elevated in the esophageal epithelium of eosinophilic esophagitis (EoE) subjects. We previously developed a mouse model of EoE dependent on constitutive overexpression of IL-33 from the esophageal epithelium (EoE33).
objectiveOur objective was to develop an inducible, IL-33-dependent model of EoE and examine induction of EoE-associated pathology.
methodsWe utilized a tetracycline-inducible system to express IL-33 in the esophagus by generating 2 transgenic mice. The first (iSophagus) expresses a reverse tetracycline transactivator from the esophageal epithelium. The second (TRE33) features a tetracycline response element driving expression of IL-33. When crossed, these mice generate an inducible model of EoE (iEoE33). Mice were administered doxycycline-infused chow for up to 2 weeks. Cytokines were assessed by ELISA or bead-based multiplex analysis. T cells were assessed by flow cytometry. Pathology was assessed by histology and immunohistochemistry for IL-33, eosinophil peroxidase, CD4, and Ki-67. iEoE33 was treated with steroids and crossed with IL-13
resultsDoxycycline-treated iEoE33 mice demonstrated expression of IL-33 in the esophageal epithelium, and esophageal pathology including eosinophilia, CD4
conclusionInducible IL-33 expression in the esophageal epithelium elicited features pathognomonic of EoE. iEoE33 enables investigation of EoE disease mechanisms as well as initiation, progression, and resolution.
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