Figure 5
Figure 5. B7-H1 expression on patient blasts. (A) The percentages of B7-H1+ cells in blasts from freshly isolated bone marrow samples. (B) The induction of B7-H1 expression on blasts from 7 patients. The cells had been cultured for 2 days with IFNγ and/or TNFα. (C) Purified CD34+ blasts from a patient (no. 38) were incubated with no additive (Medium), PDTC (100μM), IFNγ, or IFNγ and PDTC. After incubation, the blasts were separated into cytoplasmic and nuclear fractions. The NF-κB p65 contents in each fraction were analyzed using Western blotting to show representative (top panel) and quantified (bottom panel) data (mean + SD) of 2 experiments. In each experiment, the band intensity of cell fractions from blasts that had been cultured with no additive was defined as 1. (E) The inhibitor of NF-κB, PDTC, blocked B7-H1 induction by IFNγ on patient blasts. Purified CD34+ blasts from patients were cultured as indicated, and their B7-H1 expression was analyzed.

B7-H1 expression on patient blasts. (A) The percentages of B7-H1+ cells in blasts from freshly isolated bone marrow samples. (B) The induction of B7-H1 expression on blasts from 7 patients. The cells had been cultured for 2 days with IFNγ and/or TNFα. (C) Purified CD34+ blasts from a patient (no. 38) were incubated with no additive (Medium), PDTC (100μM), IFNγ, or IFNγ and PDTC. After incubation, the blasts were separated into cytoplasmic and nuclear fractions. The NF-κB p65 contents in each fraction were analyzed using Western blotting to show representative (top panel) and quantified (bottom panel) data (mean + SD) of 2 experiments. In each experiment, the band intensity of cell fractions from blasts that had been cultured with no additive was defined as 1. (E) The inhibitor of NF-κB, PDTC, blocked B7-H1 induction by IFNγ on patient blasts. Purified CD34+ blasts from patients were cultured as indicated, and their B7-H1 expression was analyzed.

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