Fig. 7
Deletion of p38α in DCs promotes FITC-induced skin contact hypersensitivity and antiparasite immunity. a–d CHS was induced in WT and p38αΔDC mice with FITC. Change in ear thickness (a) (n = 4). Histological analysis of ear sections and quantification. Scale bars represent 100 μm (b) (n = 4). Percentage and cell number of eosinophils in the ear (c) (Vehicle, n = 2, 1 sample pooled from 2 mice; FITC, n = 4). IL-4+CD4+ T cells in the skin-draining lymph nodes analyzed by flow cytometry (d) (n = 5). e, f WT and p38αΔDC mice were immunized with Schistosoma japonicum eggs (n ≥ 11). dLN cells were stimulated with SEA for 48 or 72 h. The cells were harvested for mRNA analysis (e), and the supernatant was harvested for ELISA (f). g, h WT and p38αΔDC mice were immunized with Schistosoma japonicum eggs, and IL-12 was injected into the footpad at the time of S. japonicum egg injection (n = 5). dLN cells were stimulated with SEA for 48 or 72 h. The cells were harvested (48 h) for mRNA analysis (g), and the supernatant was harvested (72 h) for ELISA (h). *P < 0.05; **P < 0.01; ns, not significant. Data are representative of two independent experiments (a–d, g, h) or pooled from three independent experiments with consistent results (e, f). Student’s t test (b, d–h) or two-way ANOVA (a, c) was performed, and the data are presented as the mean ± SEM
