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Highlights • Mechanisms of inflammatory adverse events induced by checkpoint blockade • Colitis-associated differentiation of CD8 Trm cells to cytotoxic effector cells • Persistence and expansion of CTLA-4+ Treg cells • Inflammatory pathways provide opportunities for therapeutic intervention Summary Checkpoint blockade with antibodies specific for the PD-1 and CTLA-4 inhibitory receptors can induce durable responses in a wide range of human cancers.
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