Skip to main content
Fig. 6 | BMC Medicine

Fig. 6

From: Optimized dose selective HDAC inhibitor tucidinostat overcomes anti-PD-L1 antibody resistance in experimental solid tumors

Fig. 6

CD8+ T cells are required for antitumor immunity induced by tucidinostat and aPD-L1 blockade. a Schema of the experiment. Mouse CT26 cells (5 × 105 cells) were engrafted into the flank of BALB/c mice. When established tumors were palpable 7 days after tumor cell inoculation, mice were treated with tucidinostat (25 mg/kg, gavage, daily, n=7) ± aPD-L1 (200 μg, i.p. injection, once every 3 days, n=7) regimen as indicated, in the presence or absence of aCD8 (CD8+ T depletion; 200 μg, i.p. injection, once every 3 days, n=7) or clodronate liposomes (macrophage depletion; 1.4 mg/20 g body weight, i.p. injection, once every 3 days, n=7). The following groups were included: vehicle, tucidinostat, tucidinostat+aCD8, tucidinostat+clodronate liposomes, tucidinostat+aPD-L1; tucidinostat+aPD-L1+aCD8, and tucidinostat+aPD-L1+clodronate liposomes. Tumor volume was measured with calipers every 3 days. b Tumor growth curves of these mice are shown in the CT26 mouse tumor model. c Survival differences between the tucidinostat group and the tucidinostat+aCD8/clodronate liposome group were evaluated. d Survival differences between the tucidinostat+aPD-L1 group and the tucidinostat+aPD-L1+aCD8/clodronate liposome group were evaluated. The error bars indicate mean ± SEM. *P<0.05, **P<0.01, ***P<0.001 by one-way ANOVA or log-rank test. ns not significant, CON control group, Tuc tucidinostat, aPD-L1 anti-programmed cell death ligand 1 antibody, aCD8 anti-CD8 antibody, Clo Lipo clodronate liposomes

Back to article page