Fig. 5.
Fig. 5. B7-CTLA4 interaction does not contribute to T-cell proliferation in vivo. / CD28+/+ or CD28−/− P1CTL were labeled with CFSE and injected into mice that had J558-Neo tumors. On days 0, 1, and 2, the tumor-bearing mice were injected with a mixture of either control rat/hamster immunoglobulin or anti–B7-1 and anti–B7-2 mAbs intraperitoneally (100 μg/antibody per mouse per injection). On day 3, spleen (A, C) or tumor (B) cells were harvested and analyzed. (A) Effect of anti-B7 mAb on the division of CD28−/− P1CTL accumulated in the spleen. (B) Effect of anti-B7 mAb on the division of tumor-infiltrating P1CTL. (C) Anti-B7 mAb blocks the division of CD28+/+ T cells. Data shown were CFSE intensity of gated Vα8+ T cells, as measured by flow cytometry, and were analyzed by Flowjo software, as detailed in legend to Figure 1. Five thousand gated P1CTL cells were analyzed. Data shown are representative of 3 independent experiments.

B7-CTLA4 interaction does not contribute to T-cell proliferation in vivo.

CD28+/+ or CD28−/− P1CTL were labeled with CFSE and injected into mice that had J558-Neo tumors. On days 0, 1, and 2, the tumor-bearing mice were injected with a mixture of either control rat/hamster immunoglobulin or anti–B7-1 and anti–B7-2 mAbs intraperitoneally (100 μg/antibody per mouse per injection). On day 3, spleen (A, C) or tumor (B) cells were harvested and analyzed. (A) Effect of anti-B7 mAb on the division of CD28−/− P1CTL accumulated in the spleen. (B) Effect of anti-B7 mAb on the division of tumor-infiltrating P1CTL. (C) Anti-B7 mAb blocks the division of CD28+/+ T cells. Data shown were CFSE intensity of gated Vα8+ T cells, as measured by flow cytometry, and were analyzed by Flowjo software, as detailed in legend to Figure 1. Five thousand gated P1CTL cells were analyzed. Data shown are representative of 3 independent experiments.

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