Figure 8. Suppressing macrophage-elicited NF-κB activation augments immunotherapeutic efficacy of a PD-L1 Ab.

(A and B) Mice bearing Hepa1-6 hepatoma in dorsal tissues for 15 days were left untreated or were treated with isotype, αCSF1R Ab, αPD-L1 Ab, or αCSF1R Ab plus αPD-L1 Ab as described (A). Tumor sizes over the indicated time were analyzed (B, n = 8). (C and D) WT (untreated or shNC) or P65 knockdown (shRELA) Hepa1-6 cells were inoculated in dorsal tissues of C57BL/6 mice. Thereafter, mice bearing P65 knockdown (shRELA) Hepa1-6 hepatoma were untreated or treated with isotype or αPD-L1 Ab (C). Tumor sizes over the indicated time were analyzed (D, n = 8). (E) Correlation between CD68 expression and the scoring of the NF-κB pathway were calculated in HCC, STAD, COAD, and LUAD patients from the TCGA data set. (F) Statistical analysis was conducted based on the scoring of the NF-κB pathway and recurrence rate in HCC, STAD, COAD, and LUAD patients from the TCGA data set. P values and R values were calculated based on the analysis of Pearson’s correlation. Data represent mean ± SEM. Results are representative of 3 separate experiments. ***P < 0.001, 1-way ANOVA with Bonferroni’s post test (B and D) or χ² test (F).