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Tumor cell phagocytosis is a key innate immune process where macrophages and other phagocytes recognize and engulf tumor cells, bridging innate and adaptive immunity through antigen presentation. Tumor cells evade this via "don't eat me" signals like CD47 (interacting with SIRPα on phagocytes), PD-L1, MHC-I, and CD24, which inhibit cytoskeletal rearrangement and engulfment. Pro-phagocytic "eat me" signals include calreticulin and SLAMF7. Efferocytosis of apoptotic tumor cells by macrophages resolves inflammation but promotes immune escape and tumor progression. Therapeutic strategies target these checkpoints to enhance phagocytosis, reprogramming macrophage metabolism toward oxidative phosphorylation and immunosuppressive phenotypes in tumor-associated macrophages.
Blockade of "don't eat me" signals (e.g., CD47-SIRPα interaction inhibition to promote engulfment), Enhancement of pro-phagocytic signals (e.g., calreticulin-LRP1 activation), Checkpoint inhibition to increase macrophage phagocytosis activity
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