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. 2023 Jan 17;9:7. doi: 10.1038/s41421-022-00504-0

Fig. 2. MLKL deficiency activates anti-tumor immunity in HCC tumors.

Fig. 2

a Endpoint tumor weight of MLKL-KO and control murine HCC cells in nude mice. MLKL-KO Hepa 1–6-luc (sgMLKL) or control (sgNC) cells were orthotopically implanted in the liver of nude mice (n = 8 for sgNC; n = 9 for sgMLKL #1 and sgMLKL #2). b, c Percentage of CD8+ T cells and TNFα+ CD8+ T cells in orthotopic tumors. MLKL-KO and control cells as described in a were orthotopically implanted in the liver of C57BL/6 mice and tumor-infiltrating immune cells were analyzed. d, e Relative expression of Granzyme B and TNFα in tumor-infiltrating immune cells as described in b. f, g Percentage of CD8+ T cells and TNFα+ CD8+ T cells in subcutaneous tumors. MLKL-KO and control cells as described in a were subcutaneously implanted in the right flank of C57BL/6 mice and tumor-infiltrating immune cells were analyzed. h Endpoint tumor weight upon treatment of anti-PD-1. Mice carrying MLKL-KO or control tumors as described in b were treated with anti-PD-1 antibody or isotype control antibodies every 3 days for 21 days (n = 7). i Correlation between checkpoint expression and MLKL expression in HCC patients. Data were from TCGA public database. Data are represented as means ± SEM. Two-tailed Student’s t-test was used for statistical analysis. ns, not significant; *P < 0.05, **P < 0.01, ***P < 0.001.