Figure 6.
Figure 6. Enhancement of tumor regression in mice immunized with Ii AS ODN-treated DCs. (A) B16/F10.9-OVA tumor cells were implanted subcutaneously in C57BL/6 mice followed 3 days later by treatment with OVA or influenza matrix (M1) mRNA-transfected DCs exposed to Ii AS (AE40) or control (SE40) ODNs as indicated (5 mice per group). Mice were monitored for the appearance of palpable tumors. Using the log-rank test, the P values were .006 for the Ii AS ODN group relative to the control ODN group, and .0015 for the control ODN group relative to the Flu M1 group. There was no statistical difference between the OVA mRNA relative to the OVA mRNA + control ODN groups, or the Flu M1 mRNA group relative to the Flu M1 mRNA + Ii AS ODN group (P = .9). The median time to tumor onset was 8 days for the Flu M1 with or without control ODN groups, 16 days for the OVA mRNA group, 16 days for the OVA mRNA + control ODN group, and 35 days for the OVA mRNA + Ii AS ODN group. (B) Experiment is the same as in panel A, except that B16/F10.9 tumor cells were used and mice were immunized with either TRP-2 mRNA or B16/F10.9 tumor RNA-transfected DCs. P values by the log-rank test were .0535 for the TRP-2 mRNA + Ii AS ODN group relative to the TRP-2 mRNA + control ODN group, .03 for the B16 RNA + Ii AS ODN group relative to the B16 RNA + control ODN group, .0563 for the TRP-2 mRNA + control ODN group relative to the Flu M1 + control ODN group, and .0079 for the B16 RNA + control ODN relative to the Flu M1 group. The median time of tumor onset was 8 days for the Flu M1 group, 18 days for the B16 RNA + control ODN group, 15 days for the TRP-2 mRNA + control ODN group, 21 days for the B16 RNA + Ii AS ODN group, and 25 days for the TRP-2 mRNA + Ii AS ODN group. Data are representative of 2 experiments.

Enhancement of tumor regression in mice immunized with Ii AS ODN-treated DCs. (A) B16/F10.9-OVA tumor cells were implanted subcutaneously in C57BL/6 mice followed 3 days later by treatment with OVA or influenza matrix (M1) mRNA-transfected DCs exposed to Ii AS (AE40) or control (SE40) ODNs as indicated (5 mice per group). Mice were monitored for the appearance of palpable tumors. Using the log-rank test, the P values were .006 for the Ii AS ODN group relative to the control ODN group, and .0015 for the control ODN group relative to the Flu M1 group. There was no statistical difference between the OVA mRNA relative to the OVA mRNA + control ODN groups, or the Flu M1 mRNA group relative to the Flu M1 mRNA + Ii AS ODN group (P = .9). The median time to tumor onset was 8 days for the Flu M1 with or without control ODN groups, 16 days for the OVA mRNA group, 16 days for the OVA mRNA + control ODN group, and 35 days for the OVA mRNA + Ii AS ODN group. (B) Experiment is the same as in panel A, except that B16/F10.9 tumor cells were used and mice were immunized with either TRP-2 mRNA or B16/F10.9 tumor RNA-transfected DCs. P values by the log-rank test were .0535 for the TRP-2 mRNA + Ii AS ODN group relative to the TRP-2 mRNA + control ODN group, .03 for the B16 RNA + Ii AS ODN group relative to the B16 RNA + control ODN group, .0563 for the TRP-2 mRNA + control ODN group relative to the Flu M1 + control ODN group, and .0079 for the B16 RNA + control ODN relative to the Flu M1 group. The median time of tumor onset was 8 days for the Flu M1 group, 18 days for the B16 RNA + control ODN group, 15 days for the TRP-2 mRNA + control ODN group, 21 days for the B16 RNA + Ii AS ODN group, and 25 days for the TRP-2 mRNA + Ii AS ODN group. Data are representative of 2 experiments.

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