Figure 7.
Blocking AHR on AML cells increases susceptibility to NK cell IFN-y production and cytotoxicity. (A) EOL-1 cells were treated for 5 days with AHR agonist (FICZ) or AHR antagonist (CH223191) and then washed and cocultured with NK cells in the presence of IL-12 and IL-18 (10 ng/mL) for 48 hours and evaluated for the production of soluble IFN-γ by enzyme-linked immunosorbent assay. (B) Primary AML blasts were cultured for 5 days with AHR antagonist (red, CH223191) or vehicle control (blue, DMSO). Cells were then washed to remove antagonist. Normal donor NK cells were cocultured with the primary AML targets for 4 hours in a standard chromium release assay. Six representative primary AML donors depicted (n = 10 total evaluated). Student t test, *P < .05; **P < .01; ***P < .001. Error bars indicate SD.

Blocking AHR on AML cells increases susceptibility to NK cell IFN-y production and cytotoxicity. (A) EOL-1 cells were treated for 5 days with AHR agonist (FICZ) or AHR antagonist (CH223191) and then washed and cocultured with NK cells in the presence of IL-12 and IL-18 (10 ng/mL) for 48 hours and evaluated for the production of soluble IFN-γ by enzyme-linked immunosorbent assay. (B) Primary AML blasts were cultured for 5 days with AHR antagonist (red, CH223191) or vehicle control (blue, DMSO). Cells were then washed to remove antagonist. Normal donor NK cells were cocultured with the primary AML targets for 4 hours in a standard chromium release assay. Six representative primary AML donors depicted (n = 10 total evaluated). Student t test, *P < .05; **P < .01; ***P < .001. Error bars indicate SD.

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