Fig. 5.
ttIL-12 led to tumor conversion to the CD8HiIFNyHiCD33LowFOXP3Low immune profile through enriching CXCL9 and decreasing CXCL2 and CCL22 in tumors. 4 T1 tumor–bearing mice were treated with control pDNA (pCtrl), wild-type IL-12 pDNA (pwtIL-12), tumor-targeted IL-12 pDNA (pttIL-12), or ttIL-12 plus CXCL2 pDNA (pttIL-12 + pCSCL2) or CCL22 pDNA (pttIL-12 + pCCL22). Seven days after the second injection of CXCL2 or CCL22 plasmid DNA, primary tumors and lungs were surgically removed. a Levels of CCL5, CXCL2, CXCL9, CXCL10, and CCL22 proteins were determined by ELISA in the primary tumors (upper panels) and lung metastatic nodules (lower panels). b Samples of tumors were subjected to flow cytometry to determine percentages of CD8+ T cells, NKG2D+CD8+ T cells (non-exhausted), and myeloid-derived suppressor cells (MDSCs). Proportions of CD8+ T cells, NKG2D+CD8+ T cells, and MDSCs in primary tumors were calculated from flow cytometry data. c Primary tumor sections were stained with FOXP3 and numbers of FOXP3+ (T regulatory) cells determined by microscopy. Means ± standard error of the mean are shown. NS, not significant; *P < 0.05, **P < 0.01