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• W2967202427 abstract "Programmed cell death protein-1/programmed cell death ligand-1 (PD-1/PD-L1) pathway blockade is a promising new cancer therapy. Although PD-1/PD-L1 treatment has yielded clinical benefits in several types of cancer, further studies are required to clarify predictive biomarkers for drug efficacy and to understand the fundamental mechanism of PD-1/PD-L1 interaction between host and tumor cells. Here, we show that exosomes derived from lung cancer cells express PD-L1 and play a role in immune escape by reducing T-cell activity and promoting tumor growth. The abundance of PD-L1 on exosomes represented the quantity of PD-L1 expression on cell surfaces. Exosomes containing PD-L1 inhibited interferon-gamma (IFN-γ) secretion by Jurkat T cells. IFN-γ secretion was restored by PD-L1 knockout or masking on the exosomes. Both forced expression of PD-L1 on cells without PD-L1 and treatment with exosomes containing PD-L1 enhanced tumor growth in vivo. PD-L1 was present on exosomes isolated from the plasma of patients with non-small cell lung cancer, and its abundance in exosomes was correlated with PD-L1 positivity in tumor tissues. Exosomes can impair immune functions by reducing cytokine production and inducing apoptosis in CD8+ T cells. Our findings indicate that tumor-derived exosomes expressing PD-L1 may be an important mediator of tumor immune escape." @default.
• W2967202427 created "2019-08-22" @default.
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• W2967202427 date "2019-08-01" @default.
• W2967202427 modified "2023-10-14" @default.
• W2967202427 title "Exosomal PD-L1 promotes tumor growth through immune escape in non-small cell lung cancer" @default.
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• W2967202427 doi "https://doi.org/10.1038/s12276-019-0295-2" @default.
• W2967202427 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6802663" @default.
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• W2967202427 hasPublicationYear "2019" @default.
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