Fig. 4.
Fig. 4. Critical contribution of IFN-γ and both NKT and NK cells to inhibition of HSE cell proliferation by splenic MNCs from α-GalCer–treated mice. / Untreated, anti-AGM1 Ab–treated, or anti-NK1.1 mAb–treated wild-type B6 mice were intraperitoneally administered α-GalCer (2 μg/200 μL) or vehicle (200 μL). Splenic MNCs were isolated 16 hours later and cocultured with HSE cells as in Figure 3 in the presence of 10 μg/mL anti–IFN-γ mAb (+) or control IgG (−). The number of HSE cells was determined by crystal violet staining (panel A) and the production of IFN-γ by splenic MNCs was determined by ELISA (panel B). Data are indicated as the mean ± SD of triplicate samples. Similar results were obtained in 3 independent experiments. *P < .05. **P < .01.

Critical contribution of IFN-γ and both NKT and NK cells to inhibition of HSE cell proliferation by splenic MNCs from α-GalCer–treated mice.

Untreated, anti-AGM1 Ab–treated, or anti-NK1.1 mAb–treated wild-type B6 mice were intraperitoneally administered α-GalCer (2 μg/200 μL) or vehicle (200 μL). Splenic MNCs were isolated 16 hours later and cocultured with HSE cells as in Figure 3 in the presence of 10 μg/mL anti–IFN-γ mAb (+) or control IgG (−). The number of HSE cells was determined by crystal violet staining (panel A) and the production of IFN-γ by splenic MNCs was determined by ELISA (panel B). Data are indicated as the mean ± SD of triplicate samples. Similar results were obtained in 3 independent experiments. *P < .05. **P < .01.

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