Responsiveness of MyD88^−/−, IL-1R^−/−, MyD88^−/− BM chimeric, tissue-targeted MyD88-deficient mice, and their respective controls to chemically induced skin carcinogenesis. (A–E) Left panels represent the mean number of skin tumors per mouse (mean ± SEM). Right panels represent the percentage of mice with skin tumors. Mice were treated with DMBA/0.2 ml acetone at time 0 then with 10 nmol TPA/0.2 ml acetone three times a week for up to 20 wk. Papilloma development was monitored during the course of the experiment. (A) WT (n = 10) and MyD88^−/− (n = 10). (B) WT (n = 12) and IL-1R^−/− (n = 10). (C) Mice were lethally irradiated and 2 h later injected i.v. with 20 × 10⁶ BM cells. 8 wk later, BM WT > WT (n = 9), BM MyD88^−/− > MyD88^−/− (n = 5), BM MyD88^−/− > WT (n = 9), and BM WT > MyD88^−/− (n = 9) groups were treated as in A, and papilloma development was followed during 25 wk. (D) MyD88^ΔKC (n = 13) and control littermates (n = 9). (E) MyD88^ΔBM (n = 4) and control littermates (n = 7). Data shown in A, B, and E are representative of three independent experiments, whereas data shown in C and D are representative of two independent experiments. Significant differences in the number of papillomas that develop at each time point were found by Student’s t test (*, P < 0.05). In C, comparisons of BM WT > WT and BM MyD88^−/− > WT (*, P < 0.05) and BM MyD88^−/− > MyD88^−/− and BM WT >MyD88^−/− (*, P < 0.05) were analyzed by Mann-Whitney U test.