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. 2023 Jan 31;11(1):e003837. doi: 10.1136/jitc-2021-003837

Figure 6.

Figure 6

tmTNF-α increases PD-L1 expression via reverse signaling. MDA-MB-468 cells were transfected with TNF-α or tmTNF-α-NTF for 48 hours. The expression of tmTNF-α, tmTNF-α-NTF and PD-L1 on the cell surface was detected by flow cytometry (A), and representative images of western blot for PD-L1 production, degradation of IκΒα and phosphorylation of p65 and AKT in the transfectants (B) and quantitative data. (C, D) The transfectants were treated with or without a nuclear factor-kappa B (NF-κΒ) inhibitor, 100 µM of PDTC, or an AKT inhibitor, 50 µM of LY294402 for another 24 hours, respectively, following 24 hours of the transfection. Representative images of western blot for PD-L1 expression, IκΒα degradation and phosphorylation of p65 and AKT, and quantitative data. All quantitative data represent means±SEM of three independent experiments. **P<0.01, ***P<0.001 versus parental. (E) Schematic illustration of mechanisms for tmTNF-α-induced PD-L1 expression in breast cancer cells. tmTNF-α, as a ligand, promotes PD-L1 expression through p38 pathway via TNFR, and as a receptor, enhances PD-L1 expression through NF-κΒ and AKT pathways. NTF, N-terminal fragment; tmTNF-α, transmembrane tumor necrosis factor alpha.