B7-H1 maintains the polyclonal T cell response by protecting dendritic cells from cytotoxic T lymphocyte destruction
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- Ling Chen
- Institute of Immunotherapy, Fujian Medical University, Fuzhou 350122, Peoples’ Republic of China;
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- Takeshi Azuma
- Department of Oncology, Johns Hopkins University, Baltimore, MD 21218;
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- Weiwei Yu
- Laboratory of Immunotherapy, Sun Yat-Sen University, Guangzhou 510080, Peoples’ Republic of China;
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- Xu Zheng
- Laboratory of Immunotherapy, Sun Yat-Sen University, Guangzhou 510080, Peoples’ Republic of China;
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- Liqun Luo
- Institute of Immunotherapy, Fujian Medical University, Fuzhou 350122, Peoples’ Republic of China;
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- Lieping Chen
- Institute of Immunotherapy, Fujian Medical University, Fuzhou 350122, Peoples’ Republic of China;
説明
<jats:title>Significance</jats:title><jats:p>Antibody blockade of the B7-H1/PD-1 interaction induces regression of advanced human cancers in some patients, while recurrence occurs in others due to tumor escape from T cell attack. Here, we describe a possible mechanism of tumor escape from therapy caused by biased stimulation of T cells to dominant antigen. Based on this finding, we tested a split immunization approach to prevent cancer recurrence in mouse tumor models. These findings may help design approaches for combination cancer immunotherapies.</jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 115 (12), 3126-3131, 2018-03-05
Proceedings of the National Academy of Sciences