Figure 6.

PeptiENV Targeting OVA Elicits Potent Anti-tumor Efficacy and Induces Robust Infiltration of Tumor-Specific CD8⁺ Effector T Cells into the Tumor in a Syngeneic Mouse Model of B16.OVA Melanoma

(A–F) Tumor growth curves for each mouse/group are shown. C57BL/6 mice were inoculated subcutaneously in right flank with 3.5 × 10⁵ B16.OVA melanoma cells and treated on days 11,13, and 19 with (C) OVA-PeptiENV VACV (n = 7), (B) VACV (n = 7), or (A) injection media alone as mock (n = 7), and in experiments using HSV-1 within the platform, mice were treated on days 10,12, and 18 with (F) OVA-PeptiENV HSV-1 (n = 7), (E) HSV-1 (n = 8), or (D) injection media alone as mock (n = 6). A threshold of 250 mm³ was set to define the percentage of mice responding to the different therapies (dotted line). The percentage of responders in each treatment group is shown on the right side of the dotted line. (G) The number of CD19⁻CD3⁺CD8⁺ tumor-infiltrating lymphocytes were evaluated for tumor antigen specificity (SIINFEKL-pentamer) for each group and plotted as fold increase over the mock group. (H) The number of CD19⁻CD3⁺CD8⁺ tumor-infiltrating lymphocytes were evaluated for virus antigen specificity (vaccinia-pentamer) for the OVA-PeptiENV VACV and VACV groups. (I) Kaplan-Meier survival curve for the OVA-PeptiENV VACV experiment. The median survival for each group is shown in the parentheses. Data shown as mean ± SEM. **p < 0.01; ns., not significant (one-way ANOVA or unpaired t test for H). Flow cytometry was performed with three biological replicates and two technical replicates from each sample.