Abstract
The fruitful results of tumor immunotherapy establish its indispensable status in the regulation of the tumorous immune context. It seems that the treatment of programmed cell death receptor 1 (PD-1) blockade is one of the most promising approaches for cancer control. The significant efficacy of PD-1 inhibitor therapy has been made in several cancer types, such as breast cancer, lung cancer, and multiple myeloma. Even so, the mechanisms of how anti-PD-1 therapy takes effect by impacting the immune microenvironment and how partial patients acquire the resistance to PD-1 blockade have yet to be studied. In this review, we discuss the cross talk between immune cells and how they promote PD-1 blockade efficacy. In addition, we also depict factors that may underlie tumor resistance to PD-1 blockade and feasible solutions in combination with it.
Highlights
Immune surveillance functions of innate and adaptive immune cells can be suppressed by multiple mechanisms in the tumor microenvironment (TME); the most noted one is the programmed cell death receptor 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway
This study showed that tumor-draining lymph nodes (TDLNs) are enriched for tumor-specific PD-1+T cells which are closely associated with PD-L1+dendritic cells (DCs) [83]
We primarily describe a complex story of the relationship between anti-PD-1 and TME
Summary
Immune surveillance functions of innate and adaptive immune cells can be suppressed by multiple mechanisms in the tumor microenvironment (TME); the most noted one is the programmed cell death receptor 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway. Anti-PD-1 therapy is one of the most successful immune checkpoint blockade therapies that have been approved to treat a wide variety of cancer types (Table 1). Nivolumab and pembrolizumab are the primary clinically approved PD-1 inhibitors They are humanized IgG4 antibodies targeting PD-1 with high affinity [55]. To ensure that they elicit their inhibitory effects of PD-1/PD-L1 interactions primarily by direct occupancy and steric blockade of the PD-L1-binding site of PD-1 [56], they minimize the function of effector cells engaging other antibodies. In addition to nivolumab and pembrolizumab, cemiplimab is approved by FDA for the treatment of advanced cutaneous squamous cell carcinoma [70] and first-line NSCLC [53].
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