Figure 6.
Figure 6. Correction of the patient's IL-12Rβ1 defect by retroviral-mediated gene tranfer. (A) PHA-T-cell blasts from the patient (P), a negative control (C-), MND-IL-12Rβ1-transduced PHA-T-cell blasts from the patient (Ptd), or the negative control (C-td) were stained with anti-IL-12Rβ1 mAb (24E6 or 2B10, plain line) or matched isotype control (dotted line). (B) IFN-γ production in response to IL-12. PHA-T-cell blasts from the patient (P), a negative control (C-), and MND-IL-12Rβ1-transduced PHA-T-cell blasts from the patient (Ptd) or the negative control (C-td) were plated in 24-well plates and were either left unstimulated (NS) or were stimulated with increasing concentrations of IL-12 for 48 hours. Supernatants were harvested, and IFN-γ was quantified by ELISA.

Correction of the patient's IL-12Rβ1 defect by retroviral-mediated gene tranfer. (A) PHA-T-cell blasts from the patient (P), a negative control (C-), MND-IL-12Rβ1-transduced PHA-T-cell blasts from the patient (Ptd), or the negative control (C-td) were stained with anti-IL-12Rβ1 mAb (24E6 or 2B10, plain line) or matched isotype control (dotted line). (B) IFN-γ production in response to IL-12. PHA-T-cell blasts from the patient (P), a negative control (C-), and MND-IL-12Rβ1-transduced PHA-T-cell blasts from the patient (Ptd) or the negative control (C-td) were plated in 24-well plates and were either left unstimulated (NS) or were stimulated with increasing concentrations of IL-12 for 48 hours. Supernatants were harvested, and IFN-γ was quantified by ELISA.

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