P1.003. Causal Immune-Inflammation Mapping of the GERD-Barrett-Adenocarcinoma Cascade Identifies FGF19-HLA-DR+ T-Cell Axis Driving Esophagogastric Junction Metaplasia

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ID: 326229
2026
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Ranked #212 of 453 articles by views in diseases of the esophagus : official journal of the international society for diseases of the esophagus

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Abstract
Abstract Topic Benign Disease: Barrett’s Esophagus: Pathology and Pathophysiology; Non-invasive Neoplasia Background Gastroesophageal reflux disease (GERD), Barrett’s esophagus (BE), and esophageal adenocarcinoma (EAC) form a recognized pathological continuum, but the causal immune and inflammatory processes driving progression remain incompletely defined. Methods Summary-level GWAS data were analyzed for 91 circulating inflammatory proteins (n = 14,824), 731 immune cell phenotypes (n = 3,757), and three esophageal diseases (GERD, BE, and EAC). Bidirectional and two-step Mendelian randomization (MR) were used to infer causal effects and mediation, with Cochran’s Q, MR-Egger, and MR-PRESSO applied to assess heterogeneity and pleiotropy. Causal interaction networks were reconstructed to map immune- and inflammation-dominant regulatory patterns across disease stages, and MR-prioritized signals were experimentally validated in EGJ organoids and mouse models. Results MR supported a causal GERD-BE-EAC sequence, with BE mediating 31.95% of the total GERD-to-EAC effect. In total, 139 immune cell traits and 29 inflammatory proteins showed causal links to disease risk. Mediation analyses highlighted M-CSF1 and HLA-DR+CD4+ T cells as central hubs. Guided by the MR-prioritized FGF19-HLA-DR+ T-cell axis, experimental studies demonstrated that FGF19 promotes esophagogastric junction (EGJ) glandular conversion and increases infiltration of HLA-DR+ CD4+/CD8+ T cells, validated in EGJ organoids and mouse models. Conclusion This integrated genetic and experimental framework delineates a bidirectional immune-inflammation regulatory network underlying progression from GERD to BE and EAC. FGF19 emerges as a key cytokine driving EGJ glandular remodeling through HLA-DR+ CD4+/CD8+ T-cell associated immune activation, providing candidate molecular targets for early prevention and intervention.
Reference Key
openalex_W7203970359 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Yixin Liu, Jianfeng Zhou, Yushang Yang, Zhipeng Gong
Journal diseases of the esophagus : official journal of the international society for diseases of the esophagus
Year 2026
DOI
10.1093/dote/doag077.151
URL
https://doi.org/10.1093/dote/doag077.151
Keywords Keywords not found

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