Figure 6.
Figure 6. Injection of influenza virus into NOD/SCID mice reconstituted with human DCs triggers IFN-α release into the blood. (A) NOD/SCID mice were engrafted (except for mouse no. 1, which served as control) with human CD34+ HPC and 10 weeks later injected intravenously with either PBS (vehicle control) or 3600 viral units (based on hemagglutinin titer) per mouse. Mice were killed 16 hours after injection. Human IFN-α concentration in the serum was measured using ELISA with human cytokine-specific antibodies that do not cross-react with mouse IFN-α. P = .02 in paired t test. (B) Human cells enriched from bone marrow were analyzed by real-time RT-PCR for the levels of MX1 message expression. Relative RNA expression (vertical axis, log scale) was compared to MX1 expression in PBMCs from healthy controls. As a positive control we have used human PBMCs cultured overnight with IFN-α.

Injection of influenza virus into NOD/SCID mice reconstituted with human DCs triggers IFN-α release into the blood. (A) NOD/SCID mice were engrafted (except for mouse no. 1, which served as control) with human CD34+ HPC and 10 weeks later injected intravenously with either PBS (vehicle control) or 3600 viral units (based on hemagglutinin titer) per mouse. Mice were killed 16 hours after injection. Human IFN-α concentration in the serum was measured using ELISA with human cytokine-specific antibodies that do not cross-react with mouse IFN-α. P = .02 in paired t test. (B) Human cells enriched from bone marrow were analyzed by real-time RT-PCR for the levels of MX1 message expression. Relative RNA expression (vertical axis, log scale) was compared to MX1 expression in PBMCs from healthy controls. As a positive control we have used human PBMCs cultured overnight with IFN-α.

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