Fig. 8

CCL2/CCR2 blockade inhibits tumor progression and overcomes resistance to anti-PD-1 therapy. a–f iRFA treatment was performed in CT26 and MC38 colon cancer models as shown in Fig. 2a. Anti-PD-1 mAb (200 μg, clone: J43) was administered through intraperitoneal injection to mice every 3 days for a total of four times. The CCR2 antagonist (CCR2a) (RS504393, Tocris) was given subcutaneously at a dose of 5 mg/kg twice per day for 9 days. a Growth curve of the CT26 and MC38 residual tumor (one-sided ANOVA test, n = 8). b The weight of the residual CT26 and MC38 tumor examined on day 14 after iRFA by dissection of the mice (n = 6). c The number of metastases examined on day 14 after iRFA by dissection the mice (n = 6). d Kaplan–Meier survival curves are shown, and the log-rank test was performed (n = 8). e Flow cytometric analysis and quantification of CD3⁺ and CD8⁺ infiltration (gate on single live cells) in residual CT26 tumors. f Granzyme B and IFNγ expression on CD8⁺ cells in residual CT26 tumors. (gate on CD8⁺ cells) (n = 5). g, h iRFA treatment was performed in mice bearing wild type and CCL2^−/− CT26 or MC38 tumor. g Growth curve of the CT26 and MC38 residual tumor (one-sided ANOVA test, n = 5). h Kaplan–Meier survival curves are shown, and the log-rank test was performed (n = 8). Data represent results from 1/2 independent experiments. The data are represented as mean ± SEM. Statistical differences between pairs of groups were determined by a two-tailed Student’s t-test (ns present not significant, *P < 0.05, **P < 0.01, ***P < 0.001). Source data are provided as a Source Data file.