Fig. 2: High expression of CTSE inhibits the infiltration of Jurkat T cells and induces their apoptosis through up-regulation of ROS. | Cell Death & Disease

Fig. 2: High expression of CTSE inhibits the infiltration of Jurkat T cells and induces their apoptosis through up-regulation of ROS.

From: CTSE inhibits anti-tumor T cell response by promoting des-γ-carboxy prothrombin releasing in hepatocellular carcinoma

Fig. 2

A Representative image of HCC tissue microarray staining. CD3+ (red), CD68+ (yellow), CTSE (green), DAPI (blue), (scale bar = 50 μm). Statistical analysis of the proportion of CD3+ T cells (B) and CD68+ macrophages (C). D Using GeoMx DSP technology analysis the regions of interest (ROIs) in the tissue sections. PanCK+ (green), CD45+ (yellow), and CD68+ (red) segments (scale bar = 100 μm). E Heatmap of differential gene expression between CTSE high and low expression groups in the CD45+ ROIs. F Representative Kyoto Encyclopedia of Genes and Genomes (KEGG). G Workflow of Jurkat T cell and cancer cell co-culture experiment. H Flow cytometry analysis of ROS expression in HepG2 cells after CTSE knockdown. I, J Effect of CTSE knockdown and overexpression of HepG2 cells on ROS levels of Jurkat T cells. K, L Effect of CTSE knockdown and overexpression of Huh7 cells on ROS levels of Jurkat T cells. M, N Effect of CTSE knockdown and overexpression of HepG2 cells on apoptosis levels of Jurkat T cells. O, P Effect of CTSE knockdown and overexpression of Huh7 cells on apoptosis levels of Jurkat T cells. Date are resented are mean ± SEM. The p-values are calculated by student’s t-test or one-way ANOVA. *p < 0.05; **p < 0.01; ***p < 0.001; ns not significant.

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