Fig. 4
p38α signaling in lung cDC1s regulates Th2-cell differentiation by modulating IL-12 expression. a GSEA of cDC1s. b IL-12p40 and (c) IL-12p35 expression in HDM-treated WT and p38α-deficient lung DC subsets analyzed by flow cytometry (n = 4). d mRNA expression of Il4 and Il13 in CD4+ T cells activated with WT or p38α-deficient lung cDC1 or cDC2 subsets from HDM-treated mice with or without IL-12 for 3 days (n = 2–3, 1 DC subset sample pooled from at least three mice). e–h WT and p38αΔDC mice were sensitized with HDM on Days 0–2 and challenged with HDM on Days 14–16, and then IL-12p70 was i.n. administered during HDM treatment. Mice were sacrificed for analysis on Day 17 (n = 3–4). Airway resistance was measured (e). Eosinophil infiltration in the BALF and lung tissues was detected by flow cytometry and quantified (f and g). The concentrations of IL-4, IL-5 and IL-13 in the BALF were detected by ELISA (h). **P < 0.01; ns, not significant. Data are representative of three (b–d and f–h) or two (e) independent experiments. Student’s t test (b, c, g and h) or two-way ANOVA (d and e) was performed, and the data are presented as the mean ± SEM
