Figure 1.
iMC augments NK cell proliferation in vitro. (A) Schematic of the retroviral vector design for iRC9-ΔCD19-iMC encoding iRC9, signaling-defective truncated human CD19, and iMC with the transgenes separated by T2A and P2A ribosomal skipping sequences and the control vector iRC9-ΔCD19 encoding iRC9 and truncated human CD19. (B-C) Flow cytometric analysis to determine transduction efficiency using anti-CD19 and anti-CD56 antibodies 8 days after transduction. (D) At day 5 posttransduction, iMC.iRC9- or iRC9-modified NK cells were cultured in the presence or absence of 1 nM of rimiducid (Rim). At day 10 posttransduction, the live cells were counted using acridine orange and propidium iodide staining. Paired Student t test was used to compare indicated groups. *P < .05. NS, not significant.

iMC augments NK cell proliferation in vitro. (A) Schematic of the retroviral vector design for iRC9-ΔCD19-iMC encoding iRC9, signaling-defective truncated human CD19, and iMC with the transgenes separated by T2A and P2A ribosomal skipping sequences and the control vector iRC9-ΔCD19 encoding iRC9 and truncated human CD19. (B-C) Flow cytometric analysis to determine transduction efficiency using anti-CD19 and anti-CD56 antibodies 8 days after transduction. (D) At day 5 posttransduction, iMC.iRC9- or iRC9-modified NK cells were cultured in the presence or absence of 1 nM of rimiducid (Rim). At day 10 posttransduction, the live cells were counted using acridine orange and propidium iodide staining. Paired Student t test was used to compare indicated groups. *P < .05. NS, not significant.

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