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Programmed cell death protein 1 (PD-1) is a type I transmembrane protein receptor of the immunoglobulin superfamily, expressed on activated T cells, B cells, and other immune cells. Its principal ligands are Programmed death-ligand 1 (PD-L1) and Programmed death-ligand 2 (PD-L2). PD-L1 is a type I transmembrane glycoprotein, belonging to the B7 family, and is widely expressed on immune cells and many tissue types, including a variety of tumor cells[3][4][8]. The PD-1/PD-L1 pathway acts as an essential immune checkpoint that dampens T cell activity upon ligand engagement, preventing overactive immune responses and preserving peripheral tolerance[7][8]. Tumors frequently exploit this axis by upregulating PD-L1 to evade immune detection[4][7]. Therapeutic antibodies that inhibit either PD-1 or PD-L1 have transformed cancer treatment by reactivating T-cell mediated immunity, particularly in advanced cancers with high PD-L1 expression. Safety concerns primarily relate to the risk of unleashing immune-related adverse events, but checkpoint inhibition remains a cornerstone of modern immuno-oncology[6].
Blocking the PD-1/PD-L1 interaction to reverse T cell exhaustion and re-activate anti-tumor immune response[6][7][4]; Immune checkpoint inhibition via monoclonal antibodies targeting PD-1 or PD-L1[6][2]; Restoration of cytotoxic T lymphocyte activity
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