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- W4283727493 abstract "Radiotherapy combined with immune checkpoint blockade has gradually revealed the superiority in the antitumor therapy; however, the contribution of host PD-L1 remains elusive. In this study, we found that the activation of CD8+ T cells was strikingly increased in both irradiated PD-L1-expressing primary tumor and distant non-irradiated syngeneic tumor in PD-L1-deficient mouse host, and thus enhanced radiation-induced antitumor abscopal effect (ATAE) by activating cGAS-STING pathway. Notably, the autophagy inhibitors distinctively promoted dsDNA aggregation in the cytoplasm and increased the release of cGAS-STING-regulated IFN-β from irradiated cells, which further activated bystander CD8+ T cells to release IFN-γ and contributed to ATAE. These findings revealed a signaling cascade loop that the cytokines released from irradiated tumor recruit CD8+ T cells that in turn act on the tumor cells with amplified immune responses in PD-L1-deficient host, indicating a potential sandwich therapy strategy of RT combined with PD-L1 blockage and autophagy inhibition." @default.
- W4283727493 created "2022-07-01" @default.
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- W4283727493 date "2022-08-01" @default.
- W4283727493 modified "2023-09-26" @default.
- W4283727493 title "Irradiation combined with PD-L1−/− and autophagy inhibition enhances the antitumor effect of lung cancer via cGAS-STING-mediated T cell activation" @default.
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- W4283727493 doi "https://doi.org/10.1016/j.isci.2022.104690" @default.
- W4283727493 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35847556" @default.
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