ArticleCellular & molecular immunology2025
Esophageal ILC2s mediate abnormal epithelial remodeling in eosinophilic esophagitis via Areg-EGFR signaling.
Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Immune functions of the esophagus.The Journal of allergy and clinical immunology · 2026Review
- The Immune Architecture of Eosinophilic Esophagitis: Mechanisms, Therapeutic Targets, and Precision Management.ImmunoTargets and therapy · 2026Review
- The Potential Link Between Eosinophilic Esophagitis and Food Allergy: Inflammatory Pathogenesis and Management.Journal of inflammation research · 2026Review
- Overlapping type 2, barrier, and remodeling endotypes shape clinical expression in eosinophilic esophagitis.Frontiers in immunology · 2026Review
- Epigenetic and transcriptional programming of murine eosinophils in the esophagus.Nature communications · 2025Article
- Optimization and characterization of acute radiation-induced esophagitis in mice.Radiation oncology (London, England) · 2025Article
- Spatiotemporal multi-omics analysis uncovers NAD-dependent immunosuppressive niche triggering early gastric cancer.Signal transduction and targeted therapy · 2025Article
- The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025Review
- Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Bridging inflammation and proliferation: scRNA-seq analysis of chemotactic and growth factor signaling in mouse skin wound repair.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eosinophilic esophagitis (EoE) is a chronic allergic disorder characterized by eosinophilia and epithelial thickening, resulting in dysphagia. While emerging evidence implicates increased frequencies of group 2 innate lymphoid cells (ILC2s) and increased interleukin (IL)-33 expression in EoE pathogenesis, the precise mechanisms remain unclear. In this study, we investigated the role of ILC2s in EoE pathogenesis. We observed an abundance of KLRG1
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