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. 2019 Apr 18;15(4):e1007657. doi: 10.1371/journal.ppat.1007657

Fig 2. Mice lacking the TGFβ-activating integrin αvβ8 on DCs have delayed expulsion of the small intestinal helminth T. spiralis.

Fig 2

Wild-type and Itgb8 (CD11c-cre) mice were infected with 300 T. spiralis larvae and examined at the indicated time-points post-infection. (A) Representative flow cytometry plots for p-Smad 2/3 staining in small intestinal lamina propria CD4+ T-cells. (B) IL-13, IL-4, IL-9, and IL-17 cytokine levels from T. spiralis antigen-stimulated mLN cells from wild-type and Itgb8 (CD11c-cre) mice, determined via ELISA. (C) Representative flow cytometry plots for intracellular IL-17 and IL-13 expression in small intestinal lamina propria CD4+ T-cells isolated from wild-type and Itgb8 (CD11c-cre) mice at day 13 post-infection. Number of (D) IL-17+ and (E) Foxp3+ CD4 T-cells in the small intestinal lamina propria of wild-type and Itgb8 (CD11c-cre) mice, assessed via flow cytometry. (F) Worm burdens from wild-type and Itgb8 (CD11c-cre) mice at days 7, 13 and 18 p.i. (G) Percentage change in basal start weight in wild-type and Itgb8 (CD11c-cre) mice over the course of infection. Data (n = 6–10 mice per group) are from two independent experiments performed. *, P<0.05; ***, P<0.005; N.S., not significant via Bonferonni’s multiple comparison following ANOVA (B), (D), and (E) or student’s t-test (F)and (G) for the indicated comparisons between groups.