Figure 2
Figure 2. T-cell modulation improves intratumoral CpG vaccination efficacy. (A) Single mAb therapy can improve the therapeutic efficacy of CpG vaccination. Using the 2-tumor model, mice were either left untreated or treated with CpG intratumorally with or without one mAb for T-cell modulation, as described in Figure 1. A panel of 4 different antibodies was tested: anti-OX40 (400 μg/injection), anti-CTLA4 (100 μg/injection), anti-GITR (500 μg/injection), anti-FR4 (100 μg/injection). (B) Some double mAb therapy, but not all, can greatly enhance the therapeutic efficacy of CpG vaccination over single mAb therapy. Anti-OX40, anti-CTLA4, anti-GITR, and anti-FR4 were combined 2 by 2 in conjunction with CpG vaccination and tested for their ability to induce tumor regression. Similar to the previous experiment, mice bearing 2 tumors were either left untreated or treated with CpG intratumorally with or without injection of 2 different antibodies for T-cell modulation. Doses of antibodies were the same as previously described. To rule out a possible dose-effect, one additional group of mice received double dose (2x) of anti-OX40 mAb (800 μg/injection). All growth curves represent the size of the left (non-CpG–injected) tumor. Numbers indicate the ratio of tumor-free mice at day 100 (some groups experienced regression of the left [non-CpG–injected] tumor but eventually grew distant metastasic lymph nodes which are represented in the denominator shown).

T-cell modulation improves intratumoral CpG vaccination efficacy. (A) Single mAb therapy can improve the therapeutic efficacy of CpG vaccination. Using the 2-tumor model, mice were either left untreated or treated with CpG intratumorally with or without one mAb for T-cell modulation, as described in Figure 1. A panel of 4 different antibodies was tested: anti-OX40 (400 μg/injection), anti-CTLA4 (100 μg/injection), anti-GITR (500 μg/injection), anti-FR4 (100 μg/injection). (B) Some double mAb therapy, but not all, can greatly enhance the therapeutic efficacy of CpG vaccination over single mAb therapy. Anti-OX40, anti-CTLA4, anti-GITR, and anti-FR4 were combined 2 by 2 in conjunction with CpG vaccination and tested for their ability to induce tumor regression. Similar to the previous experiment, mice bearing 2 tumors were either left untreated or treated with CpG intratumorally with or without injection of 2 different antibodies for T-cell modulation. Doses of antibodies were the same as previously described. To rule out a possible dose-effect, one additional group of mice received double dose (2x) of anti-OX40 mAb (800 μg/injection). All growth curves represent the size of the left (non-CpG–injected) tumor. Numbers indicate the ratio of tumor-free mice at day 100 (some groups experienced regression of the left [non-CpG–injected] tumor but eventually grew distant metastasic lymph nodes which are represented in the denominator shown).

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