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. 2006 Oct 30;203(11):2485–2494. doi: 10.1084/jem.20061082

Figure 1.

Figure 1.

H. hepaticus infection plus anti–IL-10R mAb treatment leads to severe typhlocolitis in WT and p35−/− mice but reduced inflammation in the ascending colon of IFN-γ−/− animals. B6 WT, p40−/−, p35−/−, IFN-γ−/−, and B10 IL-10−/− mice were infected with H. hepaticus and treated with control or anti–IL-10R mAb once a week for 4 wk. Uninfected mice were included as controls. 1 wk after the last mAb administration, pathology was analyzed in the cecum (A) and ascending colon (B). MLN cells were cultured with 5 μg/ml SHelAg, and IFN-γ (C) and IL-17 (D) were measured in 72-h supernatants. No IFN-γ or IL-17 was detected from cells cultured in medium alone. Data in A and B are pooled from two separate experiments and show histology scores from individual mice, with the horizontal line indicating the average for each group. Bars in C and D represent means ± SEM of culture duplicates of three to five mice/group from one representative experiment of the two shown in A and B. (E) Single cell analysis of IL-17 and IFN-γ–producing CD4+ T cells in anti–IL-10R–treated Hh+ WT and Hh+ IL-10−/− mice. MLN cells from uninfected (top) or 6-wk-infected anti–IL-10R–treated WT (bottom left) or 6-wk-infected IL-10−/− mice (bottom right) were cultured with SHelAg for 72 h. After an additional incubation for 18 h in medium, cells were stimulated with PMA and ionomycin in the presence of brefeldin A, and three-color staining for CD4, IL-17, and IFN-γ was performed. The FACS dot plots shown are gated on CD4+ cells and are representative of more than three experiments performed.