Effect on HSPC populations of 4 weeks of daily IFNα on Jak2VF chimeric mice. (A) Representative flow cytometry plots showing reduction in lineagelowKithighSca1+CD150+CD48− LT-HSCs from the Jak2VF IFNα-treated cells (expressed as percentage of parent LKS+ gate). (B) Reduction in LT-HSCs expressed as absolute number per lower limb cellularity (vehicle-treated WT: 8896 ± 6612 vs Jak2VF 6930 ± 6128; P = .34; n = 14; IFNα-treated WT: 6503 ± 8885 vs Jak2VF 2020 ± 3007; P = .01; n = 15; vehicle vs IFNα: Jak2VF; P = .01; vehicle vs IFNα WT: P = .78). Experimental replicates are shown as circles, squares, and diamonds (experiments 1, 2, and 3, respectively). (C) Representative flow cytometry plots showing that IFNα treatment in WT cells causes a relative reduction in MEPs (lineagelowKithighSca1−CD34−FcGR−), with relative expansion of GMP (lineagelowKithighSca1−CD34+FcGR+). Conversely, IFNα treatment in Jak2VF cells causes further expansion in MEP and relative reduction in GMP. (Percentage of parent lineagelowKithigh, LK+ gate). (D) Two weeks of IFNα treatment in WT cells increases GMP differentiation (WT vehicle: 60.8 ± 2.7% vs IFNα: 80.5 ± 3.3%; P < .01; n = 4-5) and reduces GMP differentiation in Jak2VF cells (Jak2VF vehicle: 36.8 ± 8.1% vs IFNα: 19.6 ± 2.7%; P < .01; n = 4-5). (E) Two weeks of IFNα treatment in WT cells reduces MEP differentiation (WT vehicle: 19.8 ± 2.8% vs IFNα: 12.9 ± 3.2%; P < .01; n = 4-5) and increases MEP differentiation in Jak2VF cells (Jak2VF vehicle: 50.7 ± 9.6% vs IFNα: 76.3 ± 1.9%; P < .01; n = 4-5). 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.