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Although the specific mechanism of hemolysis induced by bacterial and viral infection is largely unclear, it has been postulated that phagocytic leukocytes may play a role, through generation of hydrogen peroxide during the phagocytic process (61)
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Collectively, glucose restriction and lactate accumulation function as early metabolic checkpoints that converge to severely compromise DC maturation, antigen presentation and downstream T cell priming, ultimately driving tumour immune escape and attenuating responsiveness to immune-checkpoint inhibitors 4,7,77