Fig. 8

MET expression in the tumor affects the abundance of tumor-infiltrating lymphocytes. A. GL-261 cells, pretreated for 24 h as indicated, were used as target cells in a 20-h cytotoxicity assay. Syngeneic splenocytes were used as effector cells at various effector to target (E:T) ratios. Data are presented as mean ± SD (**, P < 0.01). B-C. GL-261 wildtype or Met knockout cells were intracranially implanted into C57/BL6 wildtype mice. Mice were treated with 100 mg/kg tepotinib or solvent from day 6 to 8, or with a single dose of 10 Gy on day 7, or a combination thereof, and tumor-infiltrating lymphocytes were isolated on day 9 from the tumor-bearing hemisphere and analysed by flow cytometry. The gating strategy is shown in B and abundance of each immune cell population in the wildtype versus Met KO-deficient tumor-bearing hemisphere for each treatment group is shown in C (^* p < 0.05, ^** p < 0.01, versus WT control; ^# p < 0.05, versus WT tepotinib; ⁺ p < 0.05, versus WT 10 Gy; ^φ p < 0.05, ^{φ φ} p < 0.01, versus WT 10 GyTepotinib + RT)