Fig. 6: Ablation of Notch signaling abolishes antitumor effect of Rubcn deficiency and PLD inhibition.
From: Exclusion of Notch from the contact site during efferocytosis restricts anticancer immunity
a, Growth of subcutaneously engrafted B16BL6 melanoma in WT mice treated with vehicle control or a combination of 15 mg kg−1 (body weight) PLD1 inhibitor VU0359595 and 5 mg kg−1 (body weight) PLD2 inhibitor VU0364739 every other day through i.p. injection starting on day 7 after tumor cell injection (n = 10 mice per group). b, Absolute cell number of NK cells, CD4+ T cells and CD8+ T cells in tumors shown in a. Statistical analysis was conducted using a Student’s t-test. Data are the mean ± s.d. c, Absolute cell number of cytotoxic CD8+ T cells that are granzyme B+, IL-2+ or IFNγ+TNF+ in tumors shown in a. Statistical analysis was conducted using a Student’s t-test. Data are the mean ± s.d. d, Tumor growth in WT, LysM-cre− and LysM-cre+;Rbpjf/f mice treated with vehicle or a combination of PLD1 and PLD2 inhibitors as in a. Vehicle group, n = 8 mice; WT inhibitor group, n = 6 mice; RbpjΔM inhibitor group, n = 4 mice. e, Growth of subcutaneously engrafted B16BL6 melanoma in control (WT or Rubcn−/+, n = 6), Rubcn−/− (LysM-cre−;Rbpjf/f;Rubcn−/−, n = 12), RbpjΔM (LysM-cre+;Rbpjf/f, n = 9) and RbpjΔM Rubcn−/− (LysM-cre+;Rbpjf/f;Rubcn−/−, n = 8) mice. Statistical analysis for tumor growth was conducted using a two-way ANOVA. Data are the mean ± s.e.m.
