Blocking ICAM-1 and LFA-1 interaction attenuates IL-33–induced lung inflammation. Rag1^−/− and Rag^−/−ICAM-1^−/− mice were injected intraperitoneally with anti-mouse CD11a (100 µg/mouse) or IgG (100 µg/mouse) on day 0, followed by intranasally challenge with IL-33 (500 ng/mouse/d) for three consecutive days (n = 4 or 6 per group). Mice were sacrificed on day 4 after 24 h of the last challenge. (A) Representative flow plots of eosinophils, pregated on CD45⁺ cells and their numbers were shown. (B) The amount of IL-5 and IL-13 in BAL was determined by ELISA. (C) The proliferation of lung ILC2s was determined by Ki-67 staining (n = 3–4). (D) The frequencies and absolute number of ILC2s in lung. (E) Frequencies of IL-5⁺IL-13⁺ in ILC2s from lung were shown. Cells were pretreated with stimulation cocktail for 4 h before flow cytometric analysis. (F) Representative lung histology by H&E staining (bars, 100 µm). (G) Rag1^−/− mice (n = 4 per group) were injected intraperitoneally with anti-mouse CD11a (100 µg/mouse) or IgG (100 µg/mouse) antibodies on day 0. Mice were sacrificed on day 3. Representative flow plots of lung ILC2, pregated on CD45⁺Lin⁻ cells and the number of lung ILC2 was evaluated by flow cytometry. (H) Human ILC2s were treated with IgG, anti-human ICAM-1 or anti-human CD11a in the presence of IL-2 (20 ng/ml), IL-7 (20 ng/ml), and IL-33 (20 ng/ml) for 3 d. The amount of IL-5 and IL-13 in the supernatant was determined by ELISA. Data are representative of two (A–G) to three (H) independent experiments. Error bars show mean ± SEM; *, P < 0.05; **, P < 0.01; ***, P < 0.001 by unpaired Student's t test. ns, not significant. Numbers within flow plots indicate the percentages of cells gated.