Fig. 6

hnCD16FR-iNK cells effectively mediate ADCC for anti-tumor responses in an in vivo Raji lymphoma model. A Schematic of the experimental design to test in vivo anti-tumor function of hnCD16FR-iNK cells using luciferase-expressing Raji cells in a mouse xenograft model treated with Obinutuzumab and iPSC-NK populations and cytokine administration. NPG mice were inoculated IV with 1 × 10⁵ Luc-expressing Raji cells. On day 1 after transplant, mice were left untreated (n = 5), received IV injection of Obinutuzumab alone (n = 5), or were treated with 1 × 10⁶ Control(eGFP) iNK cells alone (n = 6), hnCD16FR-iNK cells alone (n = 6), or 1 × 10.⁶ Control(eGFP) iNK cells in combination with 100 mg/kg of Obinutuzumab (n = 6), hnCD16FR-iNK cells in combination with 100 mg/kg of Obinutuzumab (n = 6). NK cells were supported by injection of IL-15 for the first week and by injection of IL-2 for 2 weeks; IVIS imaging was performed weekly to track tumor progression. i.v., intravenously; i.p., intraperitoneally; q.d., every day; q.o.d., every other day. B Tumor burden was determined by weekly bioluminescent imaging (BLI). C BLI data of the tumor burden of each group were monitored for 42 days after immune effector cell infusion. The BLI data are plotted, and mean ± SD are shown. Statistical significance was determined by two-tailed Student’s t-test; p > 0.05 (ns), p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***), p ≤ 0.0001 (****). D Kaplan–Meier curve representing the percent survival of the experimental groups: tumor only or treated with Control(eGFP)-iNK cells, hnCD16FR-iNK cells. Untreated versus Obinutuzumab, p = 0.0051; Obinutuzumab versus Control(eGFP) iNK+Obinutuzumab, p = 0.7989; Obinutuzumab versus hnCD16FR-iNK+Obinutuzumab, p = 0.0228; Control(eGFP) iNK+Obinutuzumab versus hnCD16FR-iNK+Obinutuzumab, p = 0.0096; hnCD16FR-iNK versus hnCD16FR-iNK+Obinutuzumab, p = 0.0006. Statistical significance was determined using a Log-rank (Mantel–Cox) test. p > 0.05 (ns), p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***)