Fig. 6
From: EGFR-TKI resistance promotes immune escape in lung cancer via increased PD-L1 expression
Downregulation of PD-L1 expression in EGFR-TKI resistant lung cancer restores the cytotoxic effect of human T lymphocytes in vivo. a Establishment of PD-L1 gene knockout cell lines. CRISPR-Cas9 knockout lentiviruses were used to delete the PD-L1 gene on a genome-wide scale. Control cells were named PC-9PD-L1+ and PC-9R PD-L1+, and PD-L1 gene deletion knockout cells were designated as PC-9PD-L1- or PC-9RPD-L1-. The sequencing results of the above cells are shown to evaluate the knockdown effect. b H&E staining, IHC staining and TUNEL assay results of PC-9 PD-L1+, PC-9R PD-L1+, PC-9 PD-L1-, PC-9R PD-L1- xenografts (× 400) with/without treatment of immunocyte mixtures or PBS (bars = 200 μm). c The cytotoxic effect of the immunocyte mixtures was evaluated by calculating xenografts volumes in PC-9 PD-L1+, PC-9R PD-L1+, PC-9 PD-L1-, PC-9R PD-L1- tumour xenografts, and the treatment effects are shown in the bar chart. Bars indicate standard error (SD). * P < 0.05. d-e Histograms showing the percentage of Ki-67+ or TUNEL+ cells in xenografts. Bars indicate SD. * P < 0.05; ** P < 0.01. f Different regulator models of PD-L1 in different subgroups of EGFR-TKI resistant NSCLC