Figure 2
IRF2 deficiency permits efficient HSC replacement.Irf2+/− (○) or Irf2−/− (●) mice (CD45.1−CD45.2+) were untreated (Irf2+/−; n = 14, Irf2−/−; n = 6) or treated with either 5-FU (Irf2+/−; n = 15, Irf2−/−; n = 8) or 150 cGy TBI (Irf2+/−; n = 15, Irf2−/−; n = 7) alone, and were then given 5 × 106 whole BM cells from congenic mice (CD45.1+CD45.2+). Data shown is the percentage of donor-derived B cells (B220+, lower) and myeloid (Gr1+ plus CD11b+, upper) cells 4 months after BMT. Each symbol represents an individual mouse.

IRF2 deficiency permits efficient HSC replacement.Irf2+/− (○) or Irf2−/− (●) mice (CD45.1CD45.2+) were untreated (Irf2+/−; n = 14, Irf2−/−; n = 6) or treated with either 5-FU (Irf2+/; n = 15, Irf2−/−; n = 8) or 150 cGy TBI (Irf2+/−; n = 15, Irf2−/−; n = 7) alone, and were then given 5 × 106 whole BM cells from congenic mice (CD45.1+CD45.2+). Data shown is the percentage of donor-derived B cells (B220+, lower) and myeloid (Gr1+ plus CD11b+, upper) cells 4 months after BMT. Each symbol represents an individual mouse.

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