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. 2017 Sep 4;214(9):2629–2647. doi: 10.1084/jem.20161855

Figure 1.

Figure 1.

Hematopoietic Rptor ablation renders mice susceptible to L. monocytogenes infection. (A) Scheme of experimental design of tamoxifen (TAM) treatment and L. monocytogenes infection. (B) Total colony-forming units of L. monocytogenes per gram of tissue in WT, Rictor−/−, and Rptor−/− mice (n = 5 mice per group). (C) Immunohistochemistry for L. monocytogenes antigen in the spleen and liver tissues from WT and Rptor−/− mice (n = 4–5 mice per group). Bar, 0.1 mm. (D) Hematoxylin and eosin staining for general pathology and immunohistochemical detection of neutrophils (Neu7/4) and macrophages (MAC2, Iba1, and F4/80) in the liver of WT and Rptor−/− mice (n = 4–5 mice per group). Bars: (left) 1.0 mm; (right) 400 µm. (E) Flow cytometry analysis and numbers of CD11b+ myeloid cells in the spleen and liver of WT, Rictor−/−, and Rptor−/− mice (n = 5 mice per group). (F) Flow cytometry analysis of neutrophils (CD11b+Ly6G+) in spleen and liver of WT, Rictor−/−, and Rptor−/− mice (n = 5 mice per group). (G) Number of neutrophils in spleen and liver of WT, Rictor−/−, and Rptor−/− mice (n = 5 mice per group). (H) Flow cytometry analysis of inflammatory monocytes (CD11b+Ly6C+) in spleen and liver of WT, Rictor−/−, and Rptor−/− mice (n = 5 mice per group). (I) Number of inflammatory monocytes in spleen and liver of WT, Rictor−/−, and Rptor−/− mice (n = 5 mice per group). Numbers indicate percentages of cells in gates. Data are mean ± SEM and representative of four (E–I) or two (B–D) independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; NS, not significant; one-way ANOVA with Dunnet’s post hoc test.