Figure 6
Complementation of the IL-12–dependent NK cell hyporesponsiveness. (A) PBMCs from one representative control individual, one representative IL-12Rβ1–deficient patient, and one IL-12p40–deficient patient were cultured for 24 hours in vitro with human recombinant IL-12 (1 ng/mL), and then assayed for IFN-γ production in response to 4-hour K562 stimulation. Results are expressed as the percentage of IFN-γ+ NK cells in patients normalized to the percentage of IFN-γ+ NK cells in the control individual (set to 100%). (B) NK cell cultures of indicated origin (healthy controls, IL-12Rβ– and IL-12p40–deficient patients) were generated by incubating NK cell–enriched PBMCs with recombinant human IL-2 (100 U/mL) for 3 weeks. Resting NK cells or IL-2–cultured NK cells of the same individuals were then compared in parallel in a 4-hour K562 stimulation.

Complementation of the IL-12–dependent NK cell hyporesponsiveness. (A) PBMCs from one representative control individual, one representative IL-12Rβ1–deficient patient, and one IL-12p40–deficient patient were cultured for 24 hours in vitro with human recombinant IL-12 (1 ng/mL), and then assayed for IFN-γ production in response to 4-hour K562 stimulation. Results are expressed as the percentage of IFN-γ+ NK cells in patients normalized to the percentage of IFN-γ+ NK cells in the control individual (set to 100%). (B) NK cell cultures of indicated origin (healthy controls, IL-12Rβ– and IL-12p40–deficient patients) were generated by incubating NK cell–enriched PBMCs with recombinant human IL-2 (100 U/mL) for 3 weeks. Resting NK cells or IL-2–cultured NK cells of the same individuals were then compared in parallel in a 4-hour K562 stimulation.

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