Fig. 6: PD-1 expression on ILC2s ameliorates AHR and lung inflammation.

a–f WT and PD-1 KO mice were challenged intranasally for 3 consecutive days with 0.5 µg rm-IL-33. On day 4, AHR and lung inflammation were assessed. b Lung resistance and c dynamic compliance measured in restrained tracheostomized mechanically ventilated mice exposed to increasing concentrations of methacholine; n = 4. d Total number of eosinophils in BAL gated as CD45⁺ SiglecF⁺ CD11c⁻; n = 7. e Total number of pulmonary ILC2s gated as lineage⁻ CD45⁺ ST2⁺ CD127⁺; n = 7. f Total number of IL-5⁺ and IL-13⁺ ILC2s identified by intracellular staining; n = 4. g–kRag2^−/− mice received intraperitoneal injection (i.p.) of anti-PD-1 blocking antibody (500 μg) or isotype control at day 1. Then mice were challenged intranasally on day 2–4 with 0.5 µg rm-IL-33. On day 5, AHR and lung inflammation were assessed. h Lung resistance and i dynamic compliance in response to increasing concentrations of methacholine; n = 4. j Total number of eosinophils in BAL and k total number of pulmonary ILC2s assessed by flow cytometry; n = 7. Data are representative of at least two independent experiments and are presented as means ± SEM (two-tailed Student’s t test or one-way ANOVA). Mouse image provided with permission from Servier Medical Art.