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. 2019 Apr 4;10:671. doi: 10.3389/fimmu.2019.00671

Figure 1.

Figure 1

EGT augments tumor-growth retardation induced by cancer vaccine using TLR2/6 ligand. (A) Protocol for this study. (B) WT B6 mice were challenged with LLC-OVA cells (Day 0). Daily i.p. administration of 500 μg EGT was started on day 9 and vaccination (s.c. injection of 15 nmol Pam2CSK4 and 100 μg OVA protein) was performed on day 10 and 14. At day 18, tumors were harvested, and the weight was measured in addition to tumor volume. Data were pooled from two independent experiments with similar results. n = 9–10 mice per group. (C) Tumor growth in sole treatment of EGT. Schedule of EGT administration is shown in (A) Mice were challenged with LLC-OVA cells and i.p. treated with EGT alone or PBS control. At timed intervals, tumor growth was measured. n = 4 mice per group. (D) Mice were challenged with LLC-OVA cells and s.c. treated with OVA, EGT + OVA, Pam2CSK4 or EGT + Pam2CSK4. PBS was used as a control. Tumor growth was chased every other day. n = 4 mice per group. (E) Mice were challenged with EG7 tumor cells and treated with PBS, EGT, Pam2CSK4 + OVA, EGT + Pam2CSK4 + OVA as in (A). Tumor growth were measured. n = 4–5 mice per group. (F) LLC-OVA cells were cultured with 1 or 10 mM EGT for 24 h, and then treated with 50 nM Pam2CSK4. Cell viability was assessed by WST-1 reagent 48 h after Pam2CSK4 treatment. n = 3–4. (G) Anti-CD8β antibody was i.p. injected into LLC-OVA-bearing mice on day 9 and 13 and the treatment described in (A) was performed. n = 4–5 mice per group. *P < 0.05, **P < 0.01. n.s., not significant.