Figure 7
Figure 7. The depletion of cyclophosphamide-resistant Tregs augments antitumor immunity. (A) Mice were injected intraperitoneally with cyclophosphamide (5 mg/mouse). Twelve days later, LNs were harvested for FACS analysis. The percentage of Tregs was higher after cyclophosphamide treatment. (B) Mice were treated with cyclophosphamide. One day later, mice were reconstituted with naive spleen cells and then injected with 1 × 105 MCA205 tumor cells. Anti–CD25 mAb were also administered to these mice to inhibit Tregs. Treg depletion in reconstituted cyclophosphamide-treated mice that received naive spleen cells significantly inhibited skin tumor progression.

The depletion of cyclophosphamide-resistant Tregs augments antitumor immunity. (A) Mice were injected intraperitoneally with cyclophosphamide (5 mg/mouse). Twelve days later, LNs were harvested for FACS analysis. The percentage of Tregs was higher after cyclophosphamide treatment. (B) Mice were treated with cyclophosphamide. One day later, mice were reconstituted with naive spleen cells and then injected with 1 × 105 MCA205 tumor cells. Anti–CD25 mAb were also administered to these mice to inhibit Tregs. Treg depletion in reconstituted cyclophosphamide-treated mice that received naive spleen cells significantly inhibited skin tumor progression.

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