Fig 2: Quadrant Analysis of CD8+ T Cells via Flow Cytometry. (A) CD4/CD8 two-parameter flow cytometry quadrant analysis of CD8+T cell subsets. Among them, Comp-FL2-A, a CD4 fluorescent signal channel, was used to define CD8+T cell population. Q1 to Q4 represent four quadrants corresponding to cell subsets with different CD4/CD8 expression profiles, and the percentage of cells in each quadrant has been annotated in figure. (B) The results of pairwise comparison showed that: Compared with the model group, the proportion of CD8+T cells in the chemotherapy group (p = 0.010), the moxibustion combined with chemotherapy group (p = 0.037) and the moxibustion group (p < 0.001) were significantly different. Compared with the chemotherapy group, the proportion of CD8+T cells in the moxibustion group was significantly different (p = 0.008), while there was no significant difference between the chemotherapy group and the moxibustion combined with chemotherapy group (p = 0.329). There was no significant difference in the proportion of CD8+T cells between the moxibustion combined with chemotherapy group and the moxibustion group (p = 0.111). *P < 0.05, **P < 0.01, ***P < 0.001 (α = 0.05).

Fig 3: Immunohistochemistry of CD8 and LAG-3 in rat hepatocellular carcinoma. In the HAE group, the number of CD8-positive cells decreased.CD8: cluster of differentiation 8; HAE: hepatic artery embolization; LAG-3: lymphocyte activation gene 3

Fig 4: RAB10 from tumor-derived exosomes interacts with IFNAR1 on macrophages, inhibiting the JAK1-STAT1 pathway and subsequent M1 polarization. This impairs CD8⁺ T cell activation, fostering an immunosuppressive microenvironment

Fig 5: Immunohistochemistry of CD8 and PD-1 in rat hepatocellular carcinoma. In the HAE group, the number of CD8-positive cells decreased.CD8: cluster of differentiation 8; DAPI: 4’,6-diamidino-2-phenylindole; PD-1: programmed cell death 1