Figure 6
Figure 6. NF-κB/p65 and STAT1 recruitment to IRF1 promoter after exogenous IFN-γ stimulation. Ex vivo PBMCs from HIV-S (n = 10, ▵) and HIV-R (n = 11, □) individuals were stimulated with exogenous IFN-γ (10 ng/mL). At the indicated time points after stimulation, chromatin was isolated and immunoprecipitated with antibodies specific for STAT1 and NF-κB/p65. Chromatin-immunoprecipitated DNA products were analyzed for the presence of IRF1 promoter using quantitative PCR. Quantitative PCR signals were normalized to input DNA. There was no difference in the levels of STAT1 or NF-κB/p65 between the unstimulated samples cultured in media alone for 0, 60, or 180 minutes. Unstimulated sample from time = 0 is used as reference for calculating relative fold increases.

NF-κB/p65 and STAT1 recruitment to IRF1 promoter after exogenous IFN-γ stimulation. Ex vivo PBMCs from HIV-S (n = 10, ▵) and HIV-R (n = 11, □) individuals were stimulated with exogenous IFN-γ (10 ng/mL). At the indicated time points after stimulation, chromatin was isolated and immunoprecipitated with antibodies specific for STAT1 and NF-κB/p65. Chromatin-immunoprecipitated DNA products were analyzed for the presence of IRF1 promoter using quantitative PCR. Quantitative PCR signals were normalized to input DNA. There was no difference in the levels of STAT1 or NF-κB/p65 between the unstimulated samples cultured in media alone for 0, 60, or 180 minutes. Unstimulated sample from time = 0 is used as reference for calculating relative fold increases.

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