Clinical and translational gastroenterology · 2026
Pathogenesis of Eosinophilic Esophagitis: A PRISMA-Based Systematic Review of Genetic, Immunological, and Molecular Drivers.
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Lachowicz Joanna, Di Petrillo Amalia, Floris Sonia, Favale Agnese, Lutzu Nicola, Onali Sara, Fantini Massimo Claudio
Аннотация
INTRODUCTION: Eosinophilic esophagitis (EoE) is a chronic, antigen-driven inflammatory disease characterized by esophageal dysfunction and tissue remodeling. Despite increasing prevalence, its pathogenesis remains incompletely understood. This review aims to systematically synthesize current evidence on the immunological, genetic, epithelial, and extracellular matrix mechanisms driving EoE. The goal is to identify upstream molecular targets and biomarkers to support precision medicine approaches.
METHODS: A PRISMA-based systematic literature search was conducted in PubMed, Web of Science, and Scopus for studies published between January 2014 and June 2025. Eligibility criteria were defined using the PECOS model, focusing on studies reporting quantitative biomolecular data. Risk of bias was assessed using validated tools for observational, in vivo , and in vitro studies. A total of 103 original research articles were included and categorized into 4 mechanistic domains.
RESULTS: The review identified epithelial barrier dysfunction, type 2 inflammation, and fibroblast activation as central features of EoE. Key cytokines (IL-4, IL-5, IL-13, TSLP) and transcriptional regulators (e.g., GATA-binding protein 3, Krüppel-like factor 5, resistin-like molecule alpha) were implicated in disease progression. Genetic and epigenetic analyses revealed susceptibility loci and persistent molecular alterations. Novel therapeutic targets and biomarkers were proposed, including TSLPR + pathogenic memory T-helper type 2A (Th2A) cells, lymphotoxin-like exhibits inducible expression competes with herpes simplex virus glycoprotein D for herpesvirus entry mediator a receptor expressed by T lymphocytes-herpesvirus entry mediator (LIGHT-HVEM) axis, and cluster of differentiation 73/ecto-5'-nucleotidase metabolic checkpoints.
DISCUSSION: EoE is a multifactorial disease involving complex immune-epithelial-stromal interactions. This review highlights emerging molecular pathways and supports a shift toward biomarker-guided, stratified treatment strategies. Integration of multiomics data and age-stratified analyses enhances understanding of disease heterogeneity. Future research should focus on longitudinal studies, pediatric cohorts, and validation of noninvasive biomarkers.
METHODS: A PRISMA-based systematic literature search was conducted in PubMed, Web of Science, and Scopus for studies published between January 2014 and June 2025. Eligibility criteria were defined using the PECOS model, focusing on studies reporting quantitative biomolecular data. Risk of bias was assessed using validated tools for observational, in vivo , and in vitro studies. A total of 103 original research articles were included and categorized into 4 mechanistic domains.
RESULTS: The review identified epithelial barrier dysfunction, type 2 inflammation, and fibroblast activation as central features of EoE. Key cytokines (IL-4, IL-5, IL-13, TSLP) and transcriptional regulators (e.g., GATA-binding protein 3, Krüppel-like factor 5, resistin-like molecule alpha) were implicated in disease progression. Genetic and epigenetic analyses revealed susceptibility loci and persistent molecular alterations. Novel therapeutic targets and biomarkers were proposed, including TSLPR + pathogenic memory T-helper type 2A (Th2A) cells, lymphotoxin-like exhibits inducible expression competes with herpes simplex virus glycoprotein D for herpesvirus entry mediator a receptor expressed by T lymphocytes-herpesvirus entry mediator (LIGHT-HVEM) axis, and cluster of differentiation 73/ecto-5'-nucleotidase metabolic checkpoints.
DISCUSSION: EoE is a multifactorial disease involving complex immune-epithelial-stromal interactions. This review highlights emerging molecular pathways and supports a shift toward biomarker-guided, stratified treatment strategies. Integration of multiomics data and age-stratified analyses enhances understanding of disease heterogeneity. Future research should focus on longitudinal studies, pediatric cohorts, and validation of noninvasive biomarkers.