Figure 1.

Deficiency in signaling via type Is interferon receptor results in increased ILC2 cells and type 2 immunopathology. (a,b) Pathology scores, as density of inflammatory infiltration (a), and hyperplasia of alveolar type 2 pneumocytes (left), bronchial and bronchiolar epithelial hyperplasia (middle), and alveolar wall thickening and fibrosis in affected parenchyma (right) (b), in lungs obtained from wild-type (WT) C57BL/6 and Ifnar1^−/− mice (age and sex matched; n = 3–7 per group) treated with PBS (Mock) or infected intranasally with 20 plaque-forming units of IAV, assessed by microcopy as in c. (c) Microscopy of sections of lungs from mice as in a,b, stained with hematoxylin and eosin (H&E) 5 d after infection, with periodic acid Schiff (PAS) 10 d after infection, or with Masson’s trichrome (MT) 15 d after infection. Scale bars, 200 μm. (d) Quantification of neutrophils and eosinophils from lungs as in a,b, assessed by flow cytometry. (e) Enzyme-linked immunosorbent assay (ELISA) of IgE in serum from mice as in a,b. (f,g) Quantitative RT-PCR analysis of the pulmonary expression of Il33 and Ifnb in mice as in a,b; results were calculated by the change-in-cycling-threshold (Ct) method and were normalized to those of the control gene Gapdh and are presented relative to those of mice treated with PBS (Mock). (h) Quantification of ILC2 cells in PBS-perfused lungs from mice as in a,b, assessed by flow cytometry. ND, not detectable. Each symbol (a,b,d,h) represents an individual mouse; small horizontal lines indicate the mean (± s.d. of triplicates). *P ≤ 0.05, **P ≤ 0.01 and ***P ≤ 0.001 (Mann-Whitney test). Data are representative of three independent experiments (mean and s.d. of triplicates in e–g).