Figure 6
Figure 6. Induction of CCR5 transcription by inflammatory stimuli. (A) mRNA expression levels of CCR5, HLA-DRA, and NF-κB p50 in human monocyte-derived DCs (DC) and human primary astrocytes (astro) after stimulation with LPS (100 ng/mL) or IFN-γ (500 U/mL) for 24 (DC) or 8 (astro) hours, as determined by RT-PCR. CCR5 expression is not enhanced in DCs nor induced in astrocytes by either LPS or IFN-γ treatment, whereas NF-κB p50 expression is enhanced in DCs by either treatment, and HLA-DR and NF-κB p50 expression is induced in astrocytes by IFN-γ and TNF-α, respectively. (B) mRNA expression levels of CCR5, CIITA-PIV, and NF-κB p50 in human primary microglia (μglia) after stimulation with TNF-α (10 ng/mL) or IFN-γ (500 U/mL) for 8 hours, as determined by RT-PCR. IFN-γ or TNF-α does not enhance CCR5 expression in microglia, whereas expression of CIITA-PIV and NF-κB p50 is enhanced by either treatment. (C) Quantification of the PCR products. Relative optical densities (ODs) corrected for GAPDH expression are shown.

Induction of CCR5 transcription by inflammatory stimuli. (A) mRNA expression levels of CCR5, HLA-DRA, and NF-κB p50 in human monocyte-derived DCs (DC) and human primary astrocytes (astro) after stimulation with LPS (100 ng/mL) or IFN-γ (500 U/mL) for 24 (DC) or 8 (astro) hours, as determined by RT-PCR. CCR5 expression is not enhanced in DCs nor induced in astrocytes by either LPS or IFN-γ treatment, whereas NF-κB p50 expression is enhanced in DCs by either treatment, and HLA-DR and NF-κB p50 expression is induced in astrocytes by IFN-γ and TNF-α, respectively. (B) mRNA expression levels of CCR5, CIITA-PIV, and NF-κB p50 in human primary microglia (μglia) after stimulation with TNF-α (10 ng/mL) or IFN-γ (500 U/mL) for 8 hours, as determined by RT-PCR. IFN-γ or TNF-α does not enhance CCR5 expression in microglia, whereas expression of CIITA-PIV and NF-κB p50 is enhanced by either treatment. (C) Quantification of the PCR products. Relative optical densities (ODs) corrected for GAPDH expression are shown.

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