Figure 6.
Figure 6. Up-regulation of ULBP and NCR ligands increases the susceptibility of AML blasts to NK cell–mediated cytotoxicity. (A) Up-regulation of ULBP and NCR ligands on AML blasts from 3 patients, as determined by FACS analysis of blasts cultured for 4 days in medium only (▪), with GFs (FL + SCF + GM-CSF; ▦) or GFs + IFN-γ (□). (B) Killing of blasts cultured for 4 days without (medium; circles) or with GFs + IFN-γ (triangles) was determined without (open symbols) or with (closed symbols) blocking of HLA class 1 molecules with mAb (10 μg/mL), as indicated. NK cells derived from healthy donors were used at the indicated effector-target ratios. The HLA status of donor and target cells revealed the KIR ligand incompatibility in patient A and at least 1 matching HLA allele in patients B and C (Cw1/Cw3 and Cw3/Cw7, respectively).

Up-regulation of ULBP and NCR ligands increases the susceptibility of AML blasts to NK cell–mediated cytotoxicity. (A) Up-regulation of ULBP and NCR ligands on AML blasts from 3 patients, as determined by FACS analysis of blasts cultured for 4 days in medium only (▪), with GFs (FL + SCF + GM-CSF; ▦) or GFs + IFN-γ (□). (B) Killing of blasts cultured for 4 days without (medium; circles) or with GFs + IFN-γ (triangles) was determined without (open symbols) or with (closed symbols) blocking of HLA class 1 molecules with mAb (10 μg/mL), as indicated. NK cells derived from healthy donors were used at the indicated effector-target ratios. The HLA status of donor and target cells revealed the KIR ligand incompatibility in patient A and at least 1 matching HLA allele in patients B and C (Cw1/Cw3 and Cw3/Cw7, respectively).

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