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. 2021 Jan 21;9(1):e001933. doi: 10.1136/jitc-2020-001933

Figure 3.

Figure 3

exNK cells sensitize patients’ non-responding tumors to PD1-blockade therapy. (A) exNK cells were incubated with or without lung cancer patient tumors. Per cent PD1+ exNK cells and representative histogram of PD1 expression after 48-hour incubation. (B, C) A549s were left untreated or treated with rhIFNγ (20 ng/mL) for 48 hours to induce PDL1 expression, then washed three times and incubated with exNK cells with or without nivolumab (1 µg/mL) for 5 hours. Relative exNK cell killing of (B) IFNγ-treated (PDL1+) A549s or (C) untreated (PDL1−) A549s. (D–F) Schematic shows experimental design: patient tumors were seeded on apical and basolateral transwell surfaces. exNK cells and/or nivolumab (Nivo; 1 µg/mL) were added to the apical chamber for 48 hours. (D) Tumor killing in the apical chamber. (E) Tumor killing by endogenous TILs in the basolateral chamber. (F) Correlation between change in tumor PDL1 expression induced by exNK cells and apical tumor killing. (G) Graphical summary of the study’s main findings. Data show means±SEM of 4–36 replicates per condition. Results analyzed via unpaired t-test (A) two-way ANOVA (B, C, E), one-way ANOVA (D) or pearson correlation (F). *P<0.05, **p<0.01, ***p<0.001, ****p<0.0001. ANOVA, analysis of variance; exNK, expanded natural killer; pbNK, peripheral blood NK; PD1, programmed death receptor-1; PDL1, programmed death receptor ligand-1; rhIFNγ, recombinant human interferon-gamma; taNK, tumor-associated NK; TILs, tumor-infiltrating lymphocytes.