Functional depletion of Jak2^VF disease-initiating stem cells after IFNα treatment. (A) Normal HCT in recipients from IFNα-treated but not vehicle-treated donor Jak2^VF chimeric mice bone marrow 4 weeks after transplantation (vehicle: 60.5 ± 9.2% vs IFNα: 42.6 ± 0.8%: P < .01; n = 5). (B) Reduced Jak2^VF chimerism in recipients 4 weeks after transplantation from IFNα-treated mice but not from vehicle-treated donor mice (vehicle: 42.6 ± 18.8% vs IFNα: 8.2 ± 6.7%; P < .01; n = 5). (C) Absolute engraftment (total CD45.2+ cells in peripheral blood) 4 weeks after transplantation in secondary transplant recipient (WT vehicle: 3.5 ± 1.3% vs IFNα: 1.5 ± 0.3%; P < .05; n = 5; Jak2^VF vehicle: 2.9 ± 2.3% vs IFNα: 0.2 ± 0.2%; P < .05; n = 5; vehicle WT vs Jak2^VF: 3.5% vs 2.9%; P = .64; IFNα-treated WT vs Jak2^VF: 1.5% vs 0.2%; P < .01). (D) Sixteen weeks of chimerism demonstrating sustained reduction in Jak2^VF chimerism in recipients of bone marrow from IFNα-treated mice but not vehicle-treated donor mice (vehicle: 30.6 ± 20.2% vs IFNα: 6.1 ± 4.2%; P < .05; n = 5). (E) Engraftment in secondary transplant recipients 16 weeks after transplantation (WT vehicle: 1.5 ± 0.7% vs IFNα: 1.6 ± 2.4%; P = .90; n = 5; Jak2^VF vehicle: 0.6 ± 0.5% vs IFNα: 0.04 ± 0.02%; P < .05; n = 5). Each data point represents an individual mouse. Data shown are representative of at least 2 independent experiments. Similar results were found in each experiment. Results given are mean ± standard deviation.