Fig. 3.

Anti-glucocorticoid induced TNF receptor (GITR) monoclonal antibody (mAb) enhances the antitumor immunity of intratumoral interferon (IFN)-α gene transfer. Data are representative of at least two separate experiments with similar results. (a) Growth suppression of subcutaneous tumors by anti-GITR mAb and a lower dose of Ad-mIFN. Pan02 cells were inoculated on both legs in C57BL/6 mice. The 100 μg of GITR mAb was intrapertioneally injected once at day 6, and then 1 × 10⁷ PFU of Ad-mIFN or Ad-AP was injected once into the tumors at day 11 (n = 8). (b) Antitumor effect by anti-GITR mAb and a higher dose of Ad-mIFN. Pan02 cells were inoculated on both legs in C57BL/6 mice. The 100 μg of GITR mAb was intrapertioneally injected once at day 6, and then 5 × 10⁷ PFU of Ad-mIFN or Ad-AP was injected once into the tumors at day 11 (n = 10). (c) Growth suppression of CT26 subcutaneous tumors by anti-GITR mAb and Ad-mIFN. CT26 cells were inoculated on right legs in BALB/c mice. The 30 μg of GITR mAb was intrepertioneally injected once at day 8, and then 3 × 10⁷ PFU of Ad-mIFN or Ad-AP were injected once into the tumors at day 11 (n = 9). (d) Growth of different tumors by a combination therapy. Pan02 cells were inoculated on right legs and CT26 cells were inoculated on left legs in (C57BL/6 × BALB/c) F1 mice. The 30 μg of anti-GITR mAb antibody was intraperitoneally injected into the mice at day 6, and 5 × 10⁷ PFU of Ad-mIFN was injected into the right Pan02 tumors at day 11.