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The programmed death-1 protein (PD-1) pathway is an inhibitory mechanism exploited by tumors to evade destruction by the host immune system. Immunogenic cancers such as lymphoma and melanoma overexpress the PD-1 receptor ligand (PD-L1), which selectively inhibits the host T-cell–mediated antitumor response. Nivolumab, a humanized IgG4 anti–PD-1 antibody, stimulates the native T-cell response by inhibiting PD-1 receptor ligand binding to T cells,1 leading to impressive tumor control. This action is nonspecific, and immune-related adverse events (irAEs) are well described after checkpoint inhibition.
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Griffin et al. (2018) studied this question.
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