Figures & data
Figure 1. The morphology of mature DCs After stimulated with TNF-α, HPVm16E7-pulsed DCs in irregular shape showed mature characteristics of larger soma with plenty of dendritic long and small bulges on their surfaces (400 × magnification). White arrow indicates long bulge and black arrow indicates small bulge.
![Figure 1. The morphology of mature DCs After stimulated with TNF-α, HPVm16E7-pulsed DCs in irregular shape showed mature characteristics of larger soma with plenty of dendritic long and small bulges on their surfaces (400 × magnification). White arrow indicates long bulge and black arrow indicates small bulge.](/cms/asset/0f1b7370-430b-48b1-88e9-4cc15eee5460/kbie_a_1230573_f0001_b.gif)
Table 1. Percentage of DCs expressing CD1 a, CD80, CD83, CD86, HLA-DR.
Figure 2. Cytotoxicity assay (A) Detected by flow cytometry, 23.6% CaSki cells expressed PDL1. (B)The cytotoxicity of effector cells at 10:1, 30:1 and 90:1 E/T ratios against CaSki cells was analyzed using CCK 8 assay. When lymphocytes incubated with MPDL3280A, DCCIKs increased the cytotoxic activity against CaSki cells with 37.9% at the E:T of 30 in relative to DCCIKs in the absence of MPDL3280A (p < 0 .01).
![Figure 2. Cytotoxicity assay (A) Detected by flow cytometry, 23.6% CaSki cells expressed PDL1. (B)The cytotoxicity of effector cells at 10:1, 30:1 and 90:1 E/T ratios against CaSki cells was analyzed using CCK 8 assay. When lymphocytes incubated with MPDL3280A, DCCIKs increased the cytotoxic activity against CaSki cells with 37.9% at the E:T of 30 in relative to DCCIKs in the absence of MPDL3280A (p < 0 .01).](/cms/asset/4d588129-1fb0-416c-83e2-cf09c346a441/kbie_a_1230573_f0002_b.gif)
Figure 3. In vivo antitumor activity analysis. (A) The therapeutic effect of DCCIKs in combination with MPDL3280A against mice bearing tumors was investigated in the groups of 10 BALB/C mice received 1×106 CaSki cells. The therapy was initiated with normal human IgG, DCCIKs, MPDL3280A and DCCIKs in combination with MPDL3280A on day 7. Tumor volume and time experiment was analyzed using student's t-test. *p < 0.01(DCCIKs/MPDL3280A vs DCCIKs or MPDL3280A or IgG control); <0.05 (DCCIKs vs MPDL3280A or IgG control) (B) Survival rates were analyzed using the Kaplan-Meier method (log-rank test). The experiments were repeated, producing a significant statistical difference. *p < 0.01(DCCIKs/MPDL3280A vs DCCIKs or MPDL3280A or IgG control); <0.05 (DCCIKs vs MPDL3280A or IgG control).
![Figure 3. In vivo antitumor activity analysis. (A) The therapeutic effect of DCCIKs in combination with MPDL3280A against mice bearing tumors was investigated in the groups of 10 BALB/C mice received 1×106 CaSki cells. The therapy was initiated with normal human IgG, DCCIKs, MPDL3280A and DCCIKs in combination with MPDL3280A on day 7. Tumor volume and time experiment was analyzed using student's t-test. *p < 0.01(DCCIKs/MPDL3280A vs DCCIKs or MPDL3280A or IgG control); <0.05 (DCCIKs vs MPDL3280A or IgG control) (B) Survival rates were analyzed using the Kaplan-Meier method (log-rank test). The experiments were repeated, producing a significant statistical difference. *p < 0.01(DCCIKs/MPDL3280A vs DCCIKs or MPDL3280A or IgG control); <0.05 (DCCIKs vs MPDL3280A or IgG control).](/cms/asset/2f201523-2b77-4ebf-a402-3944e73a2ce8/kbie_a_1230573_f0003_b.gif)