Fig. 7: CD8+ T cells, NK cells and IFN-γ mediate the antitumor effect of M1-mutIL-18. | Nature Communications

Fig. 7: CD8+ T cells, NK cells and IFN-γ mediate the antitumor effect of M1-mutIL-18.

From: Suppression of multiple mouse models of refractory malignancies by reprogramming IL-18 ligand-receptor interaction

Fig. 7: CD8+ T cells, NK cells and IFN-γ mediate the antitumor effect of M1-mutIL-18.

a−d Female C57BL/6 J mice (a, d), female rag1−/− mice (b) and male rag1−/− mice (c) aged 4−6 weeks were implanted with B16F10 cells and treated with M1 (a, 4 × 106 PFU; b–d, 1.5 × 107 PFU) or M1-mutIL-18 (a, 4 × 106 PFU; b–d, 1.5 × 107 PFU) via tail vein injection for 5 consecutive days. For depletion study, CD8 antibody, CD4 antibody, NK1.1 antibody and IFN-γ antibody were intraperitoneally injected every 3 days for a total of 5 times. Antibodies were administered 2 days before oncolytic virus therapy. a n = 8 mice per group; b, c n = 5 mice per group; (d) n = 6 mice per group. In all figures, data with error bars represent mean ± SD. P-values were calculated using unpaired, two-tailed Student’s t-test (a−d, tumor growth curves) and log rank test (a−d, Kaplan–Meier survival curves).

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