Extended Data Fig. 5: (related to Fig. 2). VDAC2 deficiency-associated improvement of anti-tumour immunity depends on CD8+ T cell-derived IFNγ.
From: VDAC2 loss elicits tumour destruction and inflammation for cancer therapy
a, b, C57BL/6 mice inoculated with control or VDAC2-deficient B16-OVA tumours were treated with anti-IFNγ (or isotype) on days –1, 3, 7 after tumour challenge (a, n = 6 for isotype-treated groups; 6 for sgNTC + anti-IFNγ; 5 for sgVdac2 + anti-IFNγ), or on days 7, 11, 15 after tumour challenge (b, n = 6 for isotype-treated groups; 6 for sgVdac2 + anti-IFNγ; 5 for sgNTC + anti-IFNγ). Tumour growth was monitored. c, Relative expression of Ifng in indicated cell populations from control or VDAC2-deficient B16-OVA tumours from scRNA-seq profiling described in Fig. 2a. d, Frequency of CD8+ T cells in peripheral blood of mice receiving anti-CD8α depleting antibody (or isotype control) on days –1, 2, 5, 8 and 11 after tumour inoculation (n = 5 per group). e, C57BL/6 mice were inoculated with control or VDAC2-deficient B16-OVA tumours, followed by treatment with anti-CD8α (or isotype control) as described in d. Tumour growth (left) and mouse survival (right) were monitored (n = 10 per group). f, Frequencies of IFNγ+ CD8+ T cells in the peripheral blood of B16-OVA tumour-bearing control Ifngfl/fl or Cd8CreIfngfl/fl chimeras (n = 13 per group). g, Control and VDAC2-deficient B16-OVA tumour growth in Ifngfl/fl (n = 10 per group) and Cd8CreIfngfl/fl (n = 5 for sgNTC; 7 for sgVdac2) chimeras. Data are representative of two (f, g) or one (a, b, d, e) independent experiments and are mean ± s.e.m. Two-tailed unpaired Student’s t-test (f). Two-way ANOVA (a, b, d; tumour size of e; g). Mantel−Cox test (survival of e).
