Figure 3
Ad.DCs stimulate in vivo significant NK-cell antitumor activity via cell-to-cell contact. NS.IL2Rγ−/− mice (4 or 5 mice per group) were injected subcutaneously with 4 × 106 K562 leukemia cells. On day 1 after tumor cell injection, mice were randomized into 6 groups. They were injected with: (1) PBS into tumor (Vehicle), (2) NK cells alone into tumor (NK), (3) Ad.DCs alone into tumor, (4) mixture of iDCs and NK (iDC/NK) into tumor, (5) Ad.DCs into contralateral, tumor-free flank, and NK cells into tumor (Ad.DCcl-NKt), and (6) mixture of Ad.DCs and NK (Ad.DC/NK) into tumor. Tumor growth was followed by caliper measurements every second day. Data are means of tumor volumes (mm3). Individual mouse tumor volumes are presented in supplemental Figure 4. Percentage inhibition of tumor growth of Ad.DC/NK-treated versus control mice is presented in supplemental Figure 5. *Statistical significance of differences of tumor volumes for Ad.DC/NK-treated versus control mice (also detailed in supplemental Figure 6).

Ad.DCs stimulate in vivo significant NK-cell antitumor activity via cell-to-cell contact. NS.IL2Rγ−/− mice (4 or 5 mice per group) were injected subcutaneously with 4 × 106 K562 leukemia cells. On day 1 after tumor cell injection, mice were randomized into 6 groups. They were injected with: (1) PBS into tumor (Vehicle), (2) NK cells alone into tumor (NK), (3) Ad.DCs alone into tumor, (4) mixture of iDCs and NK (iDC/NK) into tumor, (5) Ad.DCs into contralateral, tumor-free flank, and NK cells into tumor (Ad.DCcl-NKt), and (6) mixture of Ad.DCs and NK (Ad.DC/NK) into tumor. Tumor growth was followed by caliper measurements every second day. Data are means of tumor volumes (mm3). Individual mouse tumor volumes are presented in supplemental Figure 4. Percentage inhibition of tumor growth of Ad.DC/NK-treated versus control mice is presented in supplemental Figure 5. *Statistical significance of differences of tumor volumes for Ad.DC/NK-treated versus control mice (also detailed in supplemental Figure 6).

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