Fig. 5.
Fig. 5. Partial contribution of NK cells to inhibition of tumor growth and tumor-induced angiogenesis by α-GalCer. / Untreated, anti-AGM1 Ab–treated, or anti-NK1.1 mAb–treated wild-type B6 or BALB/c mice were intradermally inoculated with B16-BL6 (1 × 105) or colon 26-L5 (8 × 104) cells, and then intraperitoneally administered α-GalCer (2 μg/200 μL) or vehicle (200 μL) on days 0, 4, and 8. At 10 days after tumor inoculation, mice were killed and the tumor-inoculated skin was isolated. Tumor size was measured (panel A) and tumor-supplying vessels were counted (panel B). Serum IFN-γ level at 16 hours after the first administration of α-GalCer in B6 mice was also evaluated by ELISA (panel C). Data are represented as the mean ± SD of 5 mice in each group. Similar results were obtained in 2 independent experiments. *P < .05. **P < .01.

Partial contribution of NK cells to inhibition of tumor growth and tumor-induced angiogenesis by α-GalCer.

Untreated, anti-AGM1 Ab–treated, or anti-NK1.1 mAb–treated wild-type B6 or BALB/c mice were intradermally inoculated with B16-BL6 (1 × 105) or colon 26-L5 (8 × 104) cells, and then intraperitoneally administered α-GalCer (2 μg/200 μL) or vehicle (200 μL) on days 0, 4, and 8. At 10 days after tumor inoculation, mice were killed and the tumor-inoculated skin was isolated. Tumor size was measured (panel A) and tumor-supplying vessels were counted (panel B). Serum IFN-γ level at 16 hours after the first administration of α-GalCer in B6 mice was also evaluated by ELISA (panel C). Data are represented as the mean ± SD of 5 mice in each group. Similar results were obtained in 2 independent experiments. *P < .05. **P < .01.

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