ST2 gene deficiency alleviates acute gastric injury in mice by modulating inflammation and epithelial cell death

Figure 4 The interplay between interleukin-33, ILC2s, and eosinophils exacerbates acute gastric injury. A-C: Total count of ILC2 (Lin^-GATA3⁺) in gastric tissue (A), interleukin (IL)-13-producing (B), and IL-4-producing (C) ILC2 subsets following ethanol administration; D-H: Total count of eosinophils (SiglecF⁺) (D); interferon-γ-producing (E) and IL-10-producing eosinophils (F); CD80+ (G), CXCR4+ and CXCR3+ (H) eosinophils in gastric tissue following ethanol administration. All parameters were analyzed by flow cytometry. Data are expressed as mean ± SEM; n = 10 mice per group. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. GATA3: GATA binding protein 3; WT: Wild type; ST2: Suppression of tumorigenicity 2; IL: Interleukin; IFN: Interferon; CXCR: C-X-C motif chemokine receptor.