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. 2019 Jul 4;18(3):2394–2403. doi: 10.3892/ol.2019.10559

Figure 3.

Figure 3.

NK cell function is altered in both Notch1-T-ALL mice and patients with T-ALL. Splenic NK1.1+CD3− NK cells were isolated from Notch1-T-ALL mice and control WT C57BL/6 mice. Splenic Notch1-T-ALL blasts were isolated using fluorescence-activated cell sorting from the same Notch1-T-ALL mice. A standard chromium release cytotoxicity assay was performed with autologous (A) Notch1-T-ALL blasts and (B) EL4 murine lymphoma targets at the indicated ratios. (C) Relative IFNγ expression levels in splenic NK cells from Notch1-T-ALL mice and control WT C57BL/6 mice. (D) Relative IFNγ expression levels in NK cells from the peripheral blood of patients with T-ALL and the healthy control group. (E) Relative NKG2D expression levels of splenic NK cells from Notch1-T-ALL mice and control WT C57BL/6 mice. (F) Relative NKG2D expression levels in NK cells from patients with T-ALL and the healthy control group. A-C and E: n=10 mice per group; D and F: n=8 healthy control group, n=8 untreated patients with T-ALL. The data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01, as determined using one-way ANOVA or the unpaired Student's t-test. T-ALL, T-cell acute lymphoblastic leukemia; NK, natural killer; Notch1, neurogenic locus notch homolog protein 1; IFN, interferon; NKG2D, natural killer receptor group 2, member D; ns, not significant.