Fig. 1.
Fig. 1. IL-10 inhibits IFN-γ–induced ICAM-1 cell surface expression and mRNA accumulation. Monocytes were untreated (control) or treated with IFN-γ (100 U/mL), IL-10 (100 U/mL) or the combination for the indicated times. (A) Cell surface expression was measured by flow cytometry. Monocytes were identified by staining with PE-labeled anti-CD14 monoclonal antibody (mAb), and ICAM-1 was identified on CD14+ cells by staining with FITC-labeled anti–ICAM-1 mAb. (B) RNA was isolated from cytokine-stimulated monocytes, and total RNA was analyzed by Northern blot with ICAM-1 and GAPDH probes. (C) Normalized absorption values were obtained by densitometry scanning of ICAM-1 and GAPDH mRNA bands. From the ratio of ICAM-1 to GAPDH, the fold increase over untreated control cells was calculated. Data are representative of 3 experiments.

IL-10 inhibits IFN-γ–induced ICAM-1 cell surface expression and mRNA accumulation. Monocytes were untreated (control) or treated with IFN-γ (100 U/mL), IL-10 (100 U/mL) or the combination for the indicated times. (A) Cell surface expression was measured by flow cytometry. Monocytes were identified by staining with PE-labeled anti-CD14 monoclonal antibody (mAb), and ICAM-1 was identified on CD14+ cells by staining with FITC-labeled anti–ICAM-1 mAb. (B) RNA was isolated from cytokine-stimulated monocytes, and total RNA was analyzed by Northern blot with ICAM-1 and GAPDH probes. (C) Normalized absorption values were obtained by densitometry scanning of ICAM-1 and GAPDH mRNA bands. From the ratio of ICAM-1 to GAPDH, the fold increase over untreated control cells was calculated. Data are representative of 3 experiments.

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