Fig 2: Representative flow cytometry images. The populations of PD-1 and LAG-3 double-positive cells among the CD8-positive cells were comparable between the control and the HAE groups.CD8: cluster of differentiation 8; HAE: hepatic artery embolization; LAG-3: lymphocyte activation gene 3; PD-1: programmed cell death 1

Fig 3: Changes in TIMC counts, CD8-positive cell counts, and the exhausted CD8-positive cell population after HAE were evaluated using a cell counter and flow cytometer.(a) TIMC counts per unit tumor weight decreased significantly after HAE (control group vs. HAE group, 7.08 ± 3.75 × 106/g and 2.16 ± 0.53 × 106/g; p < 0.01).(b) CD8-positive cell counts per unit tumor weight decreased significantly after HAE (control group vs. HAE group, 0.46 ± 0.27 × 106/g and 0.13 ± 0.09 × 106/g; p < 0.01).(c) Population of PD-1 and LAG-3 double-positive exhausted cells among all CD8-positive cells remained unchanged after HAE (control group vs. HAE group, 8.88 ± 2.60% and 8.24 ± 3.66%; p = 0.72).CD8: cluster of differentiation 8; HAE: hepatic artery embolization; LAG-3: lymphocyte activation gene 3; PD-1: programmed cell death 1; TIMC: tumor-infiltrating mononuclear cell

Fig 4: Changes in CD8-positive, PD-1-positive, and LAG-3-positive cells after HAE on immunohistochemistry.(a) The CD8-positive cell counts decreased significantly after HAE (control group vs. HAE group, 31.56 ± 20.98 cells/FOV and 14.67 ± 15.17 cells/FOV; p < 0.05).(b) The population of PD-1-positive cells among all CD8-positive cells remained unchanged after HAE (control group vs. HAE group, 15.62 ± 11.84% and 14.25 ± 13.58%; p = 0.82).(c) Population of LAG-3 positive cells among all CD8 positive cells remained unchanged after HAE (control group vs. HAE group, 6.89 ± 2.86% and 10.60 ± 15.78%; p = 0.50).CD8: cluster of differentiation 8; HAE: hepatic artery embolization; LAG-3: lymphocyte activation gene 3; PD-1: programmed cell death 1