ICAM-1−/− ILC2s fail to induce lung inflammation. (A) Equal number of lung ILC2s (1.5 × 104) sorted from IL-33-challenged WT or ICAM-1−/− mice were intravenously injected into NCG mice, followed by intranasal challenge with IL-33 (n = 6 per group) or PBS (n = 4 per group) for 3 d. Mice were sacrificed 24 h after the last challenge. (B and C) The number of ILC2s in lungs (B) and total numbers of CD45+ immune cells in BAL (C) were determined by flow cytometry. (D) The frequencies and absolute number of eosinophils in BAL. (E) The amount of IL-5 and IL-13 in BAL was measured by ELISA. (F) Representative H&E staining of lung sections (bars, 100 µm). (G–J) Equal number of lung ILC2s (1.5 × 104) sorted from IL-33–challenged WT or ICAM-1−/− mice were intravenously injected into NCG mice, followed by intranasal challenge with papain for 3 d (n = 5 per group). Mice were sacrificed 24 h after the last challenge. The number of Lung ILC2 (G), CD45+ BAL cells (H), and levels of eosinophils in BAL (I) were determined by flow cytometry. The amount of IL-5 and IL-13 in BAL was measured by ELISA (J). Data are representative of two independent experiments. Error bars show mean ± SEM; *, P < 0.05; **, P < 0.01. ns, not significant. Numbers within flow plots indicate the percentages of cells gated.