Figure 2.
Ifnar1 deletion leads to reductions in phenotypic HSCs and MPPs during the neonatal, juvenile, and adult stages of life. (A-E) Numbers of indicated HSC and MPP subpopulations in livers of P0 Ifnar1+/− and Ifnar1–/– mice, n = 21-35. (F-J) Numbers of indicated HSC and MPP subpopulations in bone marrow (2 hindlimbs) of P14 Ifnar1+/− and Ifnar1–/–-mice, n = 12-27. (K-O) Numbers of indicated HSC and MPP subpopulations in bone marrow of 10-week-old control (Cre–) and Ubc-CreER; Ifnar1f/f mice after tamoxifen treatment at 6 weeks old, n = 5. For all panels, error bars reflect standard deviation. Surface marker phenotypes are specified in supplemental Table 2, and gating strategies are shown in supplemental Figure 2. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 using two-tailed t test.

Ifnar1 deletion leads to reductions in phenotypic HSCs and MPPs during the neonatal, juvenile, and adult stages of life. (A-E) Numbers of indicated HSC and MPP subpopulations in livers of P0 Ifnar1+/− and Ifnar1–/– mice, n = 21-35. (F-J) Numbers of indicated HSC and MPP subpopulations in bone marrow (2 hindlimbs) of P14 Ifnar1+/− and Ifnar1–/–-mice, n = 12-27. (K-O) Numbers of indicated HSC and MPP subpopulations in bone marrow of 10-week-old control (Cre–) and Ubc-CreER; Ifnar1f/f mice after tamoxifen treatment at 6 weeks old, n = 5. For all panels, error bars reflect standard deviation. Surface marker phenotypes are specified in supplemental Table 2, and gating strategies are shown in supplemental Figure 2. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 using two-tailed t test.

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