Fig. 4

Areg expression by ILC2s in EoE development and its role in epithelial thickness and basal cell hyperplasia. A Representative flow cytometry plots of IL-5- and IL-13- producing esophageal ILCs. B Frequencies of IL-5- and IL-13-producing esophageal ILCs. C Flow cytometry analysis showing Areg production by esophageal ILCs. D Frequencies of Areg-producing esophageal ILCs (left) or CD4⁺ T cells (right). E Schematic illustration of the Areg-EGFR signaling cascade. F Immunofluorescence image analysis of the epithelium in the control, acute, and chronic EoE groups (red: p-EGFR; green: Ki67; blue: DAPI). (Epi: epithelium, LP: lamina propria, Mus: muscle). G Quantification of Ki67⁺ basal cells in the region of uncropped original images (magnification x200). H Comparison of the gene expression of EGFR ligands during EoE. I Schematic diagram of the intraperitoneal injection of recombinant murine Areg (rmAreg) in mice. J H&E-stained esophageal sections from control and rmAreg-treated mice. K Quantification of the esophageal epithelium (left) and basal cell layer (right) thickness in rmAreg-treated mice. L Immunofluorescence analysis of epithelial and basal cell hyperplasia in control and rmAreg-treated mice (red: p-EGFR; green: Ki67; blue: DAPI). M Quantification of Ki67⁺ basal cells in uncropped images of rmAreg-injected mice (magnification ×200). All scale bars = 50 µm. The data were compiled from at least 2‒3 independent experiments and are presented as the means ± SEMs. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001, ns, not significant