Fig. 3
From: Tumor extracellular vesicles mediate anti-PD-L1 therapy resistance by decoying anti-PD-L1
TEV-mediated αPD-L1 consumption blunts the antitumor effect of αPD-L1. a–c Mice with MC38 tumors were intravenously injected with 10 μg of αPD-L1 with or without the indicated doses (a) or with 20 μg (b, c) of MC38-EVs or MC38 Pdl1−/−-EVs every 2 days starting when the tumor size reached 100–200 mm3. PD-L1-free αPD-L1 levels in sera were measured by ELISAs 2 h after the first treatment (a), the interaction of αPD-L1 and tumor PD-L1 was detected by PLA on Day 21 (b), and the tumor sizes were monitored every other day (c). d, e Mice with MC38 tumors were intravenously injected with the indicated doses of αPD-L1 with or without 20 μg of MC38-EVs every 2 days starting when the tumor size reached 100–200 mm3. Tumor sizes were monitored every other day (d), and the interaction of αPD-L1 and tumor PD-L1 was detected by PLA on Day 21 (e). f PD-L1-free αPD-L1 levels in the sera of the mice with MC38 or MC38 Rab27a−/− tumors were measured by ELISAs on Day 7. g–k Mice with MC38, MC38 Rab27a−/− (g, h, j) or MC38 Coro1a−/− (i, k) tumors were intravenously injected with 3 μg of αPD-L1 (g–i) or αPD-L1Exe (j, k) every 2 days starting when the tumor size reached 100–200 mm3. The interaction of αPD-L1 and tumor PD-L1 was detected by PLA on Day 21 (g), and the tumor sizes were monitored every other day (h–k). Scale bar, 10 μm. Representative results from two independent experiments are shown (n = 3 in a, b, e–g; n = 5 in c, d, h–k). *P < 0.05; **P < 0.01; ***P < 0.001; ns not significant (one-way ANOVA followed by Tukey’s test except for unpaired two-tailed Student’s t test in f, g; mean and s.d.)
