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- W2033899272 endingPage "e22837" @default.
- W2033899272 startingPage "e22837" @default.
- W2033899272 abstract "The ability of T cells to recognize a vast array of antigens enables them to destroy tumor cells while inflicting minimal collateral damage. Nevertheless, tumor antigens often are a form of self-antigen, and thus tumor immunity can be dampened by tolerance mechanisms that evolved to prevent autoimmunity. Since tolerance can be induced by steady-state antigen-presenting cells that provide insufficient co-stimulation, the exogenous administration of co-stimulatory agonists can favor the expansion and tumoricidal functions of tumor-specific T cells. Agonists of the co-stimulatory tumor necrosis factor receptor (TNFR) family members CD134 and CD137 exert antitumor activity in mice, and as monotherapies have exhibited encouraging results in clinical trials. This review focuses on how the dual administration of CD134 and CD137 agonists synergistically boosts T-cell priming and elaborates a multi-pronged antitumor immune response, as well as how such dual co-stimulation might be translated into effective anticancer therapies." @default.
- W2033899272 created "2016-06-24" @default.
- W2033899272 creator A5013574133 @default.
- W2033899272 creator A5027034727 @default.
- W2033899272 date "2013-01-01" @default.
- W2033899272 modified "2023-10-16" @default.
- W2033899272 title "Betting on improved cancer immunotherapy by doubling down on CD134 and CD137 co-stimulation" @default.
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