Abstract
PD-L1, also known as B7-H1, is a type I transmembrane protein, which is expressed in different kinds of tumor cells. It is correlated with poor clinical outcome of patients with various types of tumors. PD-L1 can regulate tumor microenvironment or tumor related immune response through suppressing T cell or NK cell mediated immune response. PD-L1 expression is regulated by various cytokines, such as LPS, GM-CSF, IL-4, TGF-β, TNF-α. PD-1 and PD-L1 are the members of B7 and CD28 superfamily, respectively. The B7/CD28 interaction plays a central role in immune tolerance. PD-L1 can bind to PD-1, which leads to the suppression of lymphocyte activation and apoptosis of lymphocytes. Anti-PD-L1 therapy is one of the immunotherapies to treat cancer (especially solid tumor). PD-L1 expression may be associated with efficacy of anti PD-1/PD-L1 therapy. In this review, we will focus on the regulation mechanism of PD-L1 expression, and describe the role of PD-1/PD-L1 binding on the anti-PD-1/PD-L1 therapy.
Highlights
Cancer is the first leading cause of death in China and second leading cause of death in United States in recent years [1, 2]
Dai et al showed that blockade of interaction of PD-1/programmed death ligand 1 (PD-L1) by anti-PD-L1 restored immune response generated by CD8+ T cell after being infected by human immunodeficiency virus (HIV) [52]
This study revealed that blockade of mitogen-activated protein kinase (MAPK)/ERK pathway and inhibition of signal transducer and activator of transcription 1(STAT1)suppressed the enhanced expression of PD-L1 induced by IFN-γ [20]
Summary
Cancer is the first leading cause of death in China and second leading cause of death in United States in recent years [1, 2]. Many studies showed that PD-L1 expression is present in various kinds of tumors, which suggested that PD-L1 may be closely related with cancer. The promoting effect of PD-L1 on cancer was shown by suppression of anti-PD-L1 antibody on the growth of myeloma cells [37]. Blockade of PD-1/PD-L1 interaction didn’t induce diabetes in NOR mice, showing the specific islet cell toxicity by mAbs treatment [39].
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