Fig. 7: Ace-Resi efficacy requires T cells and IFN-I.

A Survival of Nu/Nu mice bearing CT2A tumors after resection and treatment with Ace-Blank (n = 4 mice), and Ace-Resi (n = 10 mice), one independent experiment. P-value, log-rank test. B Survival of Ifnar^−/− mice bearing CT2A tumors after resection and treatment with Ace-Blank (n = 5 mice), and Ace-Resi (n = 9 mice), one independent experiment. P-value, log-rank test. C Frequency of bone marrow T cells that are S1P1+ from wildtype C57BL6 (WT) and Ifnar^−/− mice comparing healthy (no tumor) controls to mice 7 days after tumor resection and treatment with Ace-Resi. WT: n = 5 healthy, n = 4 Ace-Resi mice. Ifnar^−/−: n = 3 healthy, n = 4 Ace-Resi mice. One independent experiment. P-value, two-tailed unpaired t-test. D Normalized T cell counts in the bone marrow from wildtype C57BL6 (WT) and Ifnar^−/− mice comparing healthy (no tumor) controls to mice 7 days after tumor resection and treatment with Ace-Resi. WT: n = 9 healthy, n = 10 Ace-Resi mice, two independent experiments. Ifnar^−/−: n = 3 healthy, n = 4 Ace-Resi mice, one independent experiment. P-value, two-tailed unpaired t-test. E Perioperative administration of Ace-Resi scaffold resets the immunosuppressive tumor microenvironment: depleting suppressive regulatory T cells (T-reg), decreasing tumor-associated macrophages (TAM), and activating microglia, natural killer (NK) cells, and dendritic cells (DC). An increase in S1P1 allows T cells to traffic out of the bone marrow and to the cervical lymph node where they can be primed by activated DCs and other activated antigen-presenting cells. A wave of CD8⁺ T cells traffics to the brain. These events help mount a robust immune response to clear residual tumor and ultimately lead to protection from tumor challenge.