Fig. 1

C3a signaling is required to develop allergen-driven type 2 immunity. a Wildtype C57BL/6 mice were given PBS or HDM intraperitoneally (i.p.) (days 0 and 7), followed by intratracheal (i.t.) PBS or HDM (100 µg) on days 14 and 21, on day 24 BAL C3a was determined by ELISA. b Normal human bronchial epithelial (NHBE) cells were exposed to media or HDM for 24 h and C3a was measured in the supernatant. Wildtype BALBc/J and C3ar1^−/− mice were exposed to PBS or HDM (100 µg) i.t. on days 0 and 14. On day 17, c airway hyperresponsiveness, d levels of lung eosinophils, e serum IgE were determined. Lung single cell suspensions were restimulated with 30 µg/ml HDM for 3 days and supernatant levels of f IL-5, g IL-13, and h IFNγ were determined by ELISA. Lung cells (from non-lavaged mice) were analyzed for i CD4⁺ T cells j IL-13⁺CD4⁺ T cells, k CD8⁺ T cells, l Lin⁻ (CD11b, CD11c, Gr1, B220, CD19, TCRb, TCRgd, CD49b, CD4, CD8, FcER1) ICOS⁺IL-33R⁺ ILC2, and m IL-13⁺ICOS⁺IL-33R⁺ ILC2 were enumerated by flow cytometry. Data represents means + SEM. Data are representative from two to three independent experiments *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001