Figure 2. IL-12–dependent sensitization of bone marrow–derived cells is critical for tumor regression.

(A) WT C57BL/6 mice were lethally irradiated (6-Gy + 6-Gy TBI) and reconstituted with either WT (WT→WT) or Il12rb2^–/– (Il12rb2^–/–→WT) bone marrow. Six weeks after the formation of chimeras, mice (n = 10/group) were implanted with subcutaneous B16 melanomas, sublethally irradiated (5-Gy TBI), and given 10⁵ IL-12 cells after tumors were established for 10 days. Data are expressed as mean ± SEM and are representative of 2 independent experiments. *P < 0.05, Wilcoxon’s rank-sum test compared with no treatment control; **P < 0.05, compared with IL-12 cells into Il12rb2^–/–→WT mice. (B) Il12rb2^–/– C57BL/6 mice were lethally irradiated (6-Gy + 6-Gy TBI) and reconstituted with either WT (WT→Il12rb2^–/–) or Il12rb2^–/– (Il12rb2^–/–→Il12rb2^–/– ) bone marrow. Six weeks after the formation of chimeras, mice (n = 10/group) were implanted with subcutaneous B16 melanomas, sublethally irradiated, and given 10⁵ IL-12 cells after tumors were established for 10 days. Data are expressed as mean ± SEM and are representative of 2 independent experiments. *P < 0.05, Wilcoxon’s rank-sum test compared with no treatment control; **P < 0.05, compared with IL-12 cells in Il12rb2^–/–→Il12rb2^–/– mice.