Fig. 5: Higher TIM-1 expression in HCA-1 murine HCC after STING agonist treatment than control. | Nature Communications

Fig. 5: Higher TIM-1 expression in HCA-1 murine HCC after STING agonist treatment than control.

From: Inhibiting B cells enhances the efficacy of STING agonism or immune checkpoint blockade in hepatocellular carcinoma

Fig. 5: Higher TIM-1 expression in HCA-1 murine HCC after STING agonist treatment than control.The alternative text for this image may have been generated using AI.

a Heatmap showing the expression levels of Breg markers in both tumor and liver tissues from the control and STING agonist-treated groups. The color indicates the Z-score of gene expression levels, n = 3/group. b Breg score comparison among tumor and liver tissues from the control and STING agonist-treated groups. n = 3/group. P-value from two-sided Student’s t test. c The expression level of the Havcr1 gene was higher in the STING agonist-treated group. TPM, transcripts per million. n = 3/group. Box plots in (b) and (c) show the median (center line), interquartile range (box bounds), and whiskers extending to the minimum and maximum values within 1.5× the interquartile range. d The concentration of IL-10 measured by ELISA was higher in the plasma collected from the STING agonist-treated group than in the control. P-value from two-sided Student’s t test, n = 5 for the control group, and n = 6 for the STING agonist group. Data of (d) are presented as mean ± SD. e A schematic for the in vitro treatment of B cells. f PCA plot showing the B cells clustered differently among groups (n = 3/group). g The heatmap of the z-scores of different B-cell-related pathways demonstrates that STING agonism with anti-TIM-1 treatment induces B-cell differentiation and proliferation. Source data are provided as a Source Data file.

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