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Immune cells and antioxidant enzymes represent a complex physiological system rather than a single molecular target. Immune cells, such as neutrophils and macrophages, utilize reactive oxygen species (ROS) as a primary defense mechanism to destroy pathogens during the oxidative burst (PMID: 30234151). To prevent self-inflicted damage and maintain cellular homeostasis, these cells rely on a network of antioxidant enzymes, including superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) (PMID: 29723951). This balance is critical; excessive ROS can lead to chronic inflammation and tissue damage, while insufficient ROS can impair host defense. In diseases like cancer, the antioxidant capacity of immune cells can be hijacked to promote tumor survival or suppress T-cell activity (PMID: 31515479). Therapeutic strategies often aim to modulate this axis by either enhancing antioxidant capacity to reduce inflammation or inhibiting specific enzymes to sensitize cancer cells to oxidative damage. Because this entry describes a broad biological interaction rather than a specific protein or receptor, it is classified as a system-level description.
Modulation of oxidative stress levels and immune cell signaling pathways through enzymatic scavenging of reactive oxygen species or regulation of leukocyte activity.
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