Figure 9. Val-boroPro-mediated acceleration of DC trafficking depends, in part, on the CCR7-CCL19/21 chemokine axis.

(A) No change in CCR7 expression on DCs from Val-bor-Pro treated mice. Representative dot plots of gated CD11c⁺CD11b⁺ cells from MB49-bearing mice that were treated with Val-boroPro or saline during week one (days 3–7) and the first day of week two. Mice were sacrificed on day 10 and TDLN were harvested and stained for flow cytometry. (B) CCR7^−/− chimeric mice were generated by transplanting T cell depleted bone marrow (5×10⁶) from CCR7^−/− mice into lethally irradiated C57BL/6 recipients on day −30. C57BL/6 T cells (CCR7⁺, 1×10⁷) were administered to both groups on day −16, and mice were challenged with 10⁶ MB49 on day 0. CCR7^−/− chimeras (open triangles) and C57BL/6 transplanted controls (closed squares) were treated with 20 µg Val-boroPro 5×/week for two weeks (n = 5/group). Tumor volumes were significantly larger in CCR7−/− chimerics receiving Val-boroPro compared to treated recipients of C57BL/6 wildtype bone marrow. p<0.001 at all timepoints beyond day 10. (C) Female C57BL/6 mice and plt/plt mice were inoculated with MB49 (10⁶) on day 0 and treated with Val-boroPro or saline 5×/week for 2 weeks (n = 5/group). Val-boroPro-treated plt/plt mice (closed diamonds) had significantly larger tumors than treated C57BL/6 wildtype mice. P<0.01 at all timepoints beyond day 15. Figures 6A–C are each representative of 3 or more experiments. Experiments in Figures A–C were conducted 2 times.