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Programmed cell death 1 ligand 1 (PD-L1), also known as CD274, is a 40 kDa type I transmembrane protein and a critical immune checkpoint ligand belonging to the B7 family [3, 4, 15]. Its primary biological function is to provide inhibitory signals to T cells by binding to the Programmed death 1 (PD-1) receptor, which results in the suppression of T-cell activation, proliferation, and cytokine production to maintain self-tolerance and prevent autoimmunity [3, 10, 16]. In the context of cancer, tumor cells frequently overexpress PD-L1 to exploit this pathway, effectively 'cloaking' themselves from the immune system and inducing T-cell exhaustion [1, 2, 10, 19]. Therapeutic antibodies, such as atezolizumab and durvalumab, have been developed to target and block PD-L1, reinvigorating the host's anti-tumor immune response [2, 8, 13]. Clinical assessment of PD-L1 expression levels on tumor and immune cells serves as a cornerstone biomarker for selecting patients most likely to benefit from immune checkpoint inhibitor therapies across various solid tumors [5, 14, 15].
Drugs targeting this molecule act as immune checkpoint inhibitors by directly binding to the PD-L1 ligand expressed on tumor cells and antigen-presenting cells. This binding blocks the ligand's interaction with the PD-1 receptor and CD80 (B7-1) on T cells, effectively neutralizing the inhibitory signals that lead to T-cell exhaustion and restoring the host's anti-tumor immune response [2, 8, 13, 16, 19].
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