Chunyan YUE and Zhiyuan HU
The PD-1/PD-L1 (programmed death-1, programmed death-1 ligand-1) checkpoint is involved in dampening autoimmunity of peripheral tissues to help control local inflammatory responses. It is reported that this pathway activation results in peripheral immunologic tolerance in T cells [1]. As an identified ligand of PD-1, PD-L1 expressed in tumor cells facilitates tumor escape by inducing a net immunosuppressive effect after binding to PD-1 present on the surface of activated T cells and B cells [2]. The enhanced understanding of the complex interplay between the tumor and the immune system has promoted the development of anti-PD therapy for the treatment of human cancers. Antibodies blocking PD-1/PD-L1 have demonstrated durable responses in a number of different advanced malignancies [3,4]. However, while increasing a baseline T-cell-specific immune response, immune checkpoint inhibitors might result in autoimmune-like/ inflammatory side-effects, which cause collateral damage to normal organ systems and tissues, such as skin, lung and liver [5]. Therefore, detection of potential biomarkers that may predict benefit is pivotal in order to optimize clinical efficacy and safety of checkpoint blockade immunotherapy.
இந்தக் கட்டுரையைப் பகிரவும்
English 
Spanish 
Chinese 
Russian 
German 
French 
Japanese 
Portuguese 
Hindi 