AI Article Synopsis
- PD-L1/PD-1 blocking antibodies have shown effectiveness in treating various cancers, but there is a need for more research to maximize their benefits for patients.
- The study highlights that dendritic cells (DCs) are significant targets of PD-L1 blocking antibodies, not just T cells, as PD-L1 binding affects their ability to activate T cells.
- In patients with specific cancers, those treated with PD-L1 blockers like atezolizumab showed a gene signature in DCs linked to better survival rates, indicating that this treatment enhances the immune response against cancer.
Article Abstract
PD-L1/PD-1 blocking antibodies have demonstrated therapeutic efficacy across a range of human cancers. Extending this benefit to a greater number of patients, however, will require a better understanding of how these therapies instigate anticancer immunity. Although the PD-L1/PD-1 axis is typically associated with T cell function, we demonstrate here that dendritic cells (DCs) are an important target of PD-L1 blocking antibody. PD-L1 binds two receptors, PD-1 and B7.1 (CD80). PD-L1 is expressed much more abundantly than B7.1 on peripheral and tumor-associated DCs in patients with cancer. Blocking PD-L1 on DCs relieves B7.1 sequestration in cis by PD-L1, which allows the B7.1/CD28 interaction to enhance T cell priming. In line with this, in patients with renal cell carcinoma or non-small cell lung cancer treated with atezolizumab (PD-L1 blockade), a DC gene signature is strongly associated with improved overall survival. These data suggest that PD-L1 blockade reinvigorates DC function to generate potent anticancer T cell immunity.
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| http://dx.doi.org/10.1126/scitranslmed.aav7431 | DOI Listing |
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