Loss of mTOR intrinsically disrupts macrophage development in mice. WT and ER-mTOR KO mice were injected intraperitoneally with tamoxifen for 4 days and then rested for 2 to 5 days for analysis. (A) Cells of spleen, peritoneal cavity, and colon from tamoxifen-treated WT and ER-mTOR KO mice were stained with anti-CD11b mAb and anti-F4/80 mAb and analyzed by flow cytometry. The percentages (B) and cell numbers (C) of CD11b⁺F4/80⁺ cells in peritoneal cavity, spleen, and colon from tamoxifen-treated WT and ER-mTOR KO mice were summarized. (D) Mixed chimeric mice were generated by adoptive transfer either CD45.2⁺ WT or ER-mTOR KO BMCs mixed with CD45.1⁺ WT BMCs at the ratio of 1:1 into lethally irradiated CD45.1⁺ recipient mice. (E) The staining patterns of CD45.1⁺ and CD45.2⁺ CD11b⁺F4/80⁺ macrophages in mixed chimeras were shown. (F) The ratios of WT CD45.1⁺ and CD45.2⁺ WT or mTOR-deficient CD11b⁺F4/80⁺ macrophages in spleens, peritoneal cavity, and colon of mixed chimeric mice were calculated. Data are 1 representative of 3 independent experiments. *P < .05; **P < .01; ***P < .001 compared with WT control.