Induction of potent antitumor immunity by in situ targeting of intratumoral DCs
J. Clin. Invest. Katsuyoshi Furumoto, et al. 113:774 doi:10.1172/JCI19762 [Go to this article.]

Figure 7
CCL20 alone or in combination with CpG induces a systemic T cell–dependent antitumor response. Mice were inoculated subcutaneously with 2 × 10⁶ CT26 parent, CT26 mock, or CT26-CCL20–transduced tumor cells (A and B), or 5 × 10⁴ B16 parent, B16 mock, or B16-CCL20 tumor cells in addition to intratumoral injections of CpG or ODN-CTR (C and D). Thirty days later graded numbers of spleen and LN cells were cultured in the presence of irradiated parental tumors for 5 days, and tumor-specific cytotoxic T cell activity against nontransduced parental tumor cell targets was measured using a standard 4-hour ⁵¹Cr release assay as described in Methods (A and C). Results shown are representative of two separate experiments. (B) Mice were injected intraperitoneally with depleting anti-CD8, anti-CD4, or control rat Ab’s to deplete circulating T cells, or anti–asialo-GM1 serum, or control rabbit serum for NK cell depletion. *P < 0.05 between CCL20/control IgG and CCL20/CD4 Ab– and CCL20/CD8 Ab–treated groups. (D) CD4^–/–, CD8^–/–, or WT mice were inoculated with B16-CCL20 tumor cells followed by intratumoral CpG injections. NK cell depletion was done as in B. *P < 0.05 between WT mice and CD8^–/– mice treated with CCL20 + CpG. There was no significant difference in tumor growth between WT mice and CD4^–/– mice treated with CCL20 + CpG.