Figure 5
Immature, KIR- NK cells exert alloreactivity toward pediatric BCP-ALL in vivo. (A) Experimental setup for humanization of NSG mice. (B) huNSG mice exhibit alloreactivity toward pediatric BCP-ALL in vivo. P23T was injected into huNSG or nonhumanized control mice, and leukemic burden was quantified 20 hours later in the BM. Given is the number of vital blasts normalized to vital murine CD45+ cells. Figure represents pooled data of 2 independent experiments obtained on a total of 7 huNSG and 3 control mice. (C) Experimental setup for Figure 5D-E. (D) KIR expression (KIR2DL1/S1/S4, KIR2DL2/L3/S2, and KIR3DL1) on BM-derived CD56+ NK cells of huNSG mice. (E) HuNSG-derived NK cells from SSC21D exert significantly higher in vivo alloreactivity against P3B than toward P23T. Given is the number of BM-residing vital blasts normalized to vital murine CD45+. Data are representative of 2 independent experiments with a total of 4 huNSG mice.

Immature, KIR- NK cells exert alloreactivity toward pediatric BCP-ALL in vivo. (A) Experimental setup for humanization of NSG mice. (B) huNSG mice exhibit alloreactivity toward pediatric BCP-ALL in vivo. P23T was injected into huNSG or nonhumanized control mice, and leukemic burden was quantified 20 hours later in the BM. Given is the number of vital blasts normalized to vital murine CD45+ cells. Figure represents pooled data of 2 independent experiments obtained on a total of 7 huNSG and 3 control mice. (C) Experimental setup for Figure 5D-E. (D) KIR expression (KIR2DL1/S1/S4, KIR2DL2/L3/S2, and KIR3DL1) on BM-derived CD56+ NK cells of huNSG mice. (E) HuNSG-derived NK cells from SSC21D exert significantly higher in vivo alloreactivity against P3B than toward P23T. Given is the number of BM-residing vital blasts normalized to vital murine CD45+. Data are representative of 2 independent experiments with a total of 4 huNSG mice.

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