Figure 4
Figure 4. Augmentation of NKG2D ligand mRNA expression in CEM.NKR T cells expressing HIV-1 Vpr. CEM.NKR T cells were transduced with lentiviral vectors expressing GFP alone (WPI) or coexpressing GFP and VprWT (WPI-VprWT). GFP+ cells were sorted for analysis 48 hours after transduction. Alternatively, transduced cells were treated (or not) with 4μM APC for 24 hours. DNase-treated RNA was analyzed for NKG2D ligand expression by real-time reverse-transcriptase polymerase chain reaction. Target gene expression in Vpr-transduced and APC-treated CEM.NKR T cells was normalized for glyceraldehyde 3-phosphate dehydrogenase and hypoxanthine-guanine phosphoribosyltransferase (HPRT) expression, and the data were subsequently expressed as a fold increase relative to WPI-transduced or untreated cells, respectively. Results shown represent a mean fold increase. Error bars represent SEM. Results are representative of the data obtained from 4 independent experiments.

Augmentation of NKG2D ligand mRNA expression in CEM.NKR T cells expressing HIV-1 Vpr. CEM.NKR T cells were transduced with lentiviral vectors expressing GFP alone (WPI) or coexpressing GFP and VprWT (WPI-VprWT). GFP+ cells were sorted for analysis 48 hours after transduction. Alternatively, transduced cells were treated (or not) with 4μM APC for 24 hours. DNase-treated RNA was analyzed for NKG2D ligand expression by real-time reverse-transcriptase polymerase chain reaction. Target gene expression in Vpr-transduced and APC-treated CEM.NKR T cells was normalized for glyceraldehyde 3-phosphate dehydrogenase and hypoxanthine-guanine phosphoribosyltransferase (HPRT) expression, and the data were subsequently expressed as a fold increase relative to WPI-transduced or untreated cells, respectively. Results shown represent a mean fold increase. Error bars represent SEM. Results are representative of the data obtained from 4 independent experiments.

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