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Immune checkpoint receptors are a class of cell membrane receptors, such as programmed cell death protein 1 (PD-1), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), lymphocyte activation gene 3 (LAG-3), TIGIT, and many others, which act to either inhibit or stimulate immune cell activation by transmitting signals upon engaging their specific ligands. These molecules play central roles in maintaining immune tolerance and homeostasis under normal conditions. However, in the context of cancer and chronic infection, they can be exploited by malignant or infected cells to suppress the immune response. Therapeutic drugs ("checkpoint inhibitors") targeting these receptors have revolutionized cancer therapy by enhancing the body's own immune system to recognize and destroy tumor cells[1][4][5][6][7][8]. The term "immune checkpoint receptors" refers to a **family** of related but distinct proteins, not a single molecular entity, so for structured database use, refer to specific protein entries (e.g., PD-1, CTLA-4) for accurate mapping. Key points to note: - The term is a **broad category**, not a unique target; precise entries should focus on specific known checkpoint molecules for downstream data structuring. - Members of this class include receptors with both inhibitory and stimulatory functions, and drug development efforts predominantly target the inhibitory subset for cancer immunotherapy[1][4][6][7].
Blockade of inhibitory signals (releasing "brakes" on T cells and NK cells), leading to enhanced anti-tumor immunity; Activation or agonism (for a minority of stimulatory checkpoint receptors); Modulation of T cell or NK cell exhaustion, tolerance, or functional activity.
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