Activation of the PD-1 pathway contributes to immune escape in EGFR-driven lung tumors
作者： Esra A. Akbay , Shohei Koyama , Julian Carretero , Abigail Altabef , Jeremy H. Tchaicha
DOI: 10.1158/2159-8290.CD-13-0310
关键词:
摘要: The success in lung cancer therapy with Programmed Death (PD)-1 blockade suggests that immune escape mechanisms contribute to tumor pathogenesis. We identified a correlation between Epidermal Growth Factor Receptor (EGFR) pathway activation and signature of immunosuppression manifested by upregulation PD-1, PD-L1, cytotoxic T lymphocyte antigen-4 (CTLA-4), multiple tumor-promoting inflammatory cytokines. observed decreased cells increased markers cell exhaustion mouse models EGFR-driven cancer. PD-1 antibody improved the survival mice adenocarcinomas enhancing effector function lowering levels Expression mutant EGFR bronchial epithelial induced PD-L1 expression was reduced inhibitors non-small lines activated EGFR. These data suggest oncogenic signaling remodels microenvironment trigger escape, mechanistically link treatment response inhibition.
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