Correction: ICAM-1 controls development and function of ILC2

ICAM-1 deficiency attenuates papain and A. alternata–induced lung inflammation. (A–E) WT and ICAM-1^−/− mice were intranasally administered with papain or PBS for 5 d (n = 6 for each group). Mice were sacrificed 24 h after the last treatment. (A) The frequencies and number of eosinophils in BAL were evaluated by flow cytometry. (B) The amount of IL-5 and IL-13 in BAL was measured by ELISA. (C) Representative lung histology by H&E staining (bars, 100 µm). (D) The frequencies and number of lung ILC2s were determined by flow cytometry. (E) Flow cytometric analysis of frequencies of IL-5⁺IL-13⁺ in lung ILC2s after cell stimulation cocktail treatment for 4 h. Papain treated groups were analyzed. (F–J) WT and ICAM-1^−/− mice were intranasally challenged with extract of A. alternata for 4 d (n = 7). Mice were sacrificed 24 h after the last challenge. (F) The number of eosinophils in BAL was evaluated by flow cytometry. (G) The amount of IL-5 and IL-13 in BAL was measured by ELISA. (H) Total number of ILC2 in lung after A. alternata treatment. (I) The frequencies of IL-5⁺IL-13⁺ in lung ILC2s after cell stimulation cocktail treatment for 4 h. (J) Representative H&E staining of lung sections in A. alternata–treated groups (bars, 100 µm). Data are representative of two independent experiments. Error bars show mean ± SEM; **, P < 0.01; ***, P < 0.001 by unpaired Student's t test. Numbers within flow plots indicate the percentages of cells gated.