Interleukin-17A facilitates tumor progression via upregulating programmed death ligand-1 expression in hepatocellular carcinoma

Figure 6 An interleukin-17A inhibitor suppressed tumor growth and enhanced the therapeutic efficacy of an anti-programmed cell death ligand-1 antibody. A: Flow diagram of the construction of the mouse model and treatment scheme for programmed cell death ligand-1 (PD-L1) inhibitors and/or interleukin-17A (IL-17A) inhibitors in mice. Images of the tumors in different treatment groups (the control group, PD-L1 inhibitor group, IL-17A inhibitor group, and combined group) are shown. Each group contained nine mice; B: Tumor growth curves of the mice after PD-L1 inhibitor and/or IL-17A inhibitor treatment. A PD-L1 inhibitor combined with an IL-17A inhibitor demonstrated a much greater antitumor effect on the hepatocellular carcinoma mouse model; C: Tumor weights of mice in the four groups after treatment. The tumor weights of mice in the combined group were significantly lower than those of mice in the control group; D: Flow cytometry analysis of the differences in the infiltration of cluster of differentiation 8+ T cells and cluster of differentiation 4+ T cells in tumor tissues among the four groups; E: The levels of serum soluble (s)PD-L1 and IL-17A were compared among the four groups. The sPD-L1 and IL-17A levels were lower in the combined group than in the control group. The sPD-L1 level was positively correlated with the serum IL-17A level in the control group; F: Immunohistochemical staining revealed the expression of PD-L1, IL-17A, and Ki67 in tumor tissues. Scale bars, 100 μm (× 200) and 50 μm (× 400). The number of positive cells was determined using ImageJ2x software. Boxplots displaying the expression of PD-L1, IL-17A, and Ki67 in the four groups. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. APC-CD4: Allophycocyanin-cluster of differentiation 4; FACS: Fluorescence-activated cell sorting; PE-CD8: Phycoerythrin-cluster of differentiation 8.