Programmed death ligand 1 (PD-L1), also known as B7 homolog 1 (B7-H1), is a transmembrane glycoprotein, which belongs to the B7 family of immune molecules and plays a pivotal role in regulating adaptive immune responses. Various stimuli, including inflammatory signals and interferon-gamma (IFN-ɣ), induce the expression of PD-L1 on antigen-presenting cells (APCs), such as dendritic cells, macrophages and B cells in peripheral tissues, as well as on epithelial and vascular endothelial cells. Its receptor, programmed cell death protein 1 (PD-1), which is expressed on activated T cells, recognizes PD-L1. This interaction serves as negative feedback mechanism to modulate T cell activation and to prevent excessive immune responses, contributing to immune homeostasis. Apparently, dysregulation of PD-L1 expression or function leads to the development of autoimmune diseases, such as rheumatoid arthritis. Tumor cells evade immune surveillance due to overexpression of PD-L1 on various cancer cell types. This enables inhibition of anti-tumor immune responses and promotes tumor growth and progression. PD-L1 expression in the tumor microenvironment has become a critical biomarker for predicting responses to immunotherapy. Immune checkpoint inhibition using monoclonal antibodies blocking the PD-1/PD-L1 interaction has emerged as excellent therapeutic strategy in cancer therapy. Further insights into PD-L1 biology will likely lead to improved treatment modalities and expanded applications in the field of immune-mediated diseases.
