Figure 7
Figure 7. Residual NKT cells in Elf-1−/− mice are dysfunctional. (A) Splenocytes and liver leukocytes from WT and Elf-1−/− mice were stimulated with αGalCer. After 48 hours, cytokine levels in the supernatant were detected by ELISA. Error bars represent the SD of triplicate wells. Data shown are representative of 4 independent experiments (**P < .01). (B) WT and Elf-1−/− mice were injected with αGalCer. After 1 hour, liver leukocytes were harvested, stained with CD1d/αGalCer tetramer and anti–TCRβ, stained intracellularly with mAb against IFN-γ and IL-4, and then analyzed by flow cytometry. Filled histograms represent cytokine-producing iNKT cells based on tetramer+TCRβ+ gating. Control staining is represented as open histograms. Data shown are representative of 3 independent experiments.

Residual NKT cells in Elf-1−/−mice are dysfunctional. (A) Splenocytes and liver leukocytes from WT and Elf-1−/− mice were stimulated with αGalCer. After 48 hours, cytokine levels in the supernatant were detected by ELISA. Error bars represent the SD of triplicate wells. Data shown are representative of 4 independent experiments (**P < .01). (B) WT and Elf-1−/− mice were injected with αGalCer. After 1 hour, liver leukocytes were harvested, stained with CD1d/αGalCer tetramer and anti–TCRβ, stained intracellularly with mAb against IFN-γ and IL-4, and then analyzed by flow cytometry. Filled histograms represent cytokine-producing iNKT cells based on tetramer+TCRβ+ gating. Control staining is represented as open histograms. Data shown are representative of 3 independent experiments.

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