Fig 1.

RoRγt -expressing cells drive protease-induced airway inflammation. A, Detection of pulmonary IL-13, IL-17A, IL-22, and IL-23 by ELISA following acute papain challenge. B, ILC3s (Lin^–CD45⁺CD127⁺ICOS^–RoRγt-GFP⁺), ILC2s (Lin^–CD45⁺CD127⁺ICOS⁺RoRγt-GFP^–), and T_H17 T cells (CD3⁺CD4⁺RoRγt-GFP⁺) were detected in the lung by flow cytometry by using RoRγt-GFP reporter mice following acute papain challenge. C, Phorbol myristate acetate restimulation of lung cells potentiated production of IL-13 but not IL-17 by CD4⁺ T cells in papain-treated mice, as measured by flow cytometry. But CD45⁺CD3^–Lin^– cells did show IL-17 production following phorbol myristate acetate restimulation. D, Representative hematoxylin and eosin staining of lung sections, pathology scoring, and quantification of airway epithelial integrity by using EB following papain challenge of RAG2^–/–– and IL-23–depleted RAG2^–/– mice. Airway cellular infiltration and detection of pulmonary IL-13 and IL-17A by ELISA is also shown. E, Representative hematoxylin and eosin staining of lung sections, pathology scoring, and quantification of airway epithelial integrity by using EB following papain challenge of C57BL/6 and Rorc^–/– mice. Airway resistance to methacholine challenge following papain challenge in Rorc^–/– mice. Airway cellular infiltration in Rorc^–/– mice. Detection of pulmonary IL-13 and IL-17A by ELISA in papain-challenged Rorc^–/– mice. Detection of ILC2s (Lin^–CD45⁺CD127⁺ICOS⁺) and NCR⁺ ILC3s (Lin^–CD45⁺CD127⁺ICOS^–NKp46⁺) in the lung by flow cytometry. Data are representative of 2 or 3 equivalent experiments; n = 3 to 9 mice/group. All data are a comparison of unchallenged and saline-treated or papain-challenged C57BL/6 background mice. Values represent means ± SDs; ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. BAL, Bronchoalveolar lavage fluid; Eos., eosinophil; Gra., granulocyte; Lymp, lymphocyte; Mono., monocyte.