Fig. 8: Inhibition of RNASEH2C in macrophages enhanced the effectiveness of immune checkpoint inhibitors. | Cell Death & Disease

Fig. 8: Inhibition of RNASEH2C in macrophages enhanced the effectiveness of immune checkpoint inhibitors.

From: RNASEH2C enhances TRAF3IP1 to degrade RAI14 in lysosomes thus hindering macrophage antigen presentation and advancing liver cancer

Fig. 8

A Operation flow chart. B Immunoblotting showing the expression of RNASEH2C protein in human macrophages (n = 3, n = 6). To knock out RNASEH2C in human macrophages, Ad5f35 adeno-associated virus was employed, and these modified cells were then introduced into huHSC-C-NKG-ProF mice with humanized immune systems. C, D Effect of knockout of RNASEH2C on human macrophages and anti-PD1 or anti-CTLA4 antibodies on the progression of orthotopic carcinoma (n = 6). HCC tissues from patients were processed into single-cell suspensions and implanted into the livers of huHSC-C-NKG-ProF mice. Subsequently, either human macrophages or neutralizing antibodies were administered to the tumor-bearing mice. The health status of the mice was monitored, and their survival times were documented. Upon the death of the mice, HCC tissues were collected for further analysis. C Representative. D Survival curve. E Left: TIDE examining the mRNA expression of RNASEH2C in patients who demonstrated either responsiveness or non-responsiveness to immunotherapy (n = 371). Right: TIDE evaluating the sensitivity to immunotherapy in HCC patients exhibiting varying levels of RNASEH2C expression (n = 371). F Mechanism diagram. B Represented mean ± SD analyzed by unpaired t test, D was analyzed by log-rank test, E represented mean ± SD analyzed by Wilcoxon test. *P < 0.05, **P < 0.01. HCC hepatocellular carcinoma, TIDE tumor immune dysfunction and exclusion.

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