Insights into the pathogenesis of eosinophilic esophagitis using mouse models

Insights into the pathogenesis of eosinophilic esophagitis using mouse models

Anish Dsilva
1
,
Ariel Munitz
1,2,*
*Correspondence to: Ariel Munitz, Department of Clinical Microbiology and Immunology, Gray Faculty of Medical and Health Sciences, Tel Aviv University, Ramat Aviv 69978, Israel. E-mail: arielm@tauex.tau.ac.il
Myeloid Cells. 2026;1:202604. 10.70401/mc.2025.0003
Received: March 24, 2026Accepted: May 18, 2026Published: May 18, 2026
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This manuscript is made available in its unedited form to allow early access to the reported findings. Further editing will be completed before final publication. As such, the content may include errors, and standard legal disclaimers are applicable.

Abstract

Eosinophilic esophagitis (EoE) is a chronic, food antigen-driven, type 2 immune-mediated disease of the esophagus characterized by eosinophil-predominant mucosal inflammation, epithelial remodeling and subepithelial fibrosis. Although patient biopsies have established the EoE transcriptome and identified key cellular and molecular mediators, biopsy-based research is inherently correlative and cannot resolve causal disease mechanisms, temporal disease progression or the functional hierarchy of immune cell interactions. Thus, animal models are indispensable tools for addressing these limitations. In this Review, we examine the landscape of experimental EoE models. We assess the capacity of each model to recapitulate key disease features including lamina propria and intraepithelial eosinophilia, subepithelial fibrosis, basal cell hyperplasia, epithelial barrier dysfunction and angiogenesis. We further map these models to human EoE transcriptomic overlap and disease endotype relevance. Across this analysis, we highlight mechanistic insights that were obtained from these models including the eosinophil-independence of IL-13-driven esophageal remodeling, the respective roles of thymic stromal lymphopoietin and IL-33, the critical role of epithelial-expressed IL-13Rα1. We further highlight the profibrotic functions of amphiregulin-producing T helper 2 cells and CSF1-dependent macrophages. We discuss the anatomical, genetic and functional limitations of current models and outline directions for the next generation of EoE preclinical systems.

Keywords

EGIDs, eosinophilic esophagitis, allergy, IL-13, IL-13R1, TSLP, IL-33

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Dsilva A, Munitz A. Insights into the pathogenesis of eosinophilic esophagitis using mouse models. Myeloid Cells. 2026;1:202604. https://doi.org/10.70401/mc.2025.0003

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