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PD-1/PD-L1 Checkpoint Pathway in Cancer Immunotherapy


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PD-1/PD-L1 Checkpoint Pathway in Cancer Immunotherapy

Tumor cells can escape the immune surveillance and disrupt immune checkpoint of host in several methods, therefore, to avoid the elimination from the host immune system. Numerous pathways are utilized by cancers to up-regulate the negative signals through cell surface molecules, thus inhibit T-cell activation or induce apoptosis and promote the progression and metastasis of cancers [1]. Immunotherapeutic approaches utilizing antagonistic antibodies to block checkpoint pathways, can release cancer inhibition and facilitate antitumor activity, so as to achieve the purpose of treating cancer.

The present research of immune checkpoint molecules is mainly focus on cytotoxic T lymphocyte-associated antigen 4 (CLTA-4), Programmed death-1 (PD-1) and its ligands PD-L1 (B7H1) and PD-L2 (B7-DC). PD-1 and its ligands have been rapidly established as the currently most important breakthrough targets in the development of effective immunotherapy.

PD-1/PD-L1 Checkpoint Pathway in Cancer Immunotherapy

What is the PD-1/PD-L1 pathway?

The PD-1 (programmed cell death-1) receptor is expressed on the surface of activated T cells. Its ligands, PD-L1 and PD-L2, are commonly expressed on the surface of dendritic cells or macrophages. PD-1 and PD-L1/PD-L2 belong to the family of immune checkpoint proteins that act as co-inhibitory factors, which is known to drive T cell dysfunction. In response to immune attack, cancer cells overexpress PD-L1 and PD-L2. They bind to PD-1 receptor on T cells, inhibiting the activation of T-cells, thus suppressing T-cell attack and inducing tumor immune escape. High-affinity anti-PD-1 or anti-PD-L1 monoclonal antibodies (mAbs), which block PD-1–PD-L1 interaction, can reverse the immune checkpoint.

The role of PD-1/PD-L1 in cancer

Under normal conditions, the immune system performs a series of steps which lead to an anticancer immune response and cancer cell death, known as the cancer immunity cycle1:

  1. Tumor cells produce mutated antigens that are captured by dendritic cells.
  2. The dendritic cells prime T cell with tumor antigen and stimulate the activation of cytotoxic T cells.
  3. Activated T cells then travel to the tumor and infiltrate the tumor environment.
  4. The activated T cells recognize and bind to the cancer cells.
  5. The bound effector T cells release cytotoxins, which induce apoptosis in their target cancer cells.

PD-1/PD-L1 pathway regulates immune suppression by multiple mechanisms

  1. Apoptosis of activated T cells [2,3].
  2. Facilitate T cell anergy and exhaustion [4].
  3. Enhance the function of regulatory T cells [5].
  4. Inhibit the proliferation of T cells [6].
  5. Restrain impaired T cell activation and IL-2 production [7].

Immune checkpoints are proteins which can turn up or turn down signals in the immune system. Inhibitors of immune-checkpoint proteins have been considered as new targets for cancer immunotherapies. To accelerate research progress of PD-1/PD-L1 pathway, we have developed a variety of PD-1/PD-L1 pathway-product panels including stable cell lines, viral particles and clones.


  1. Zou, W. Immunosuppressive networks in the tumour environment and their therapeutic relevance. J. Nat Rev Cancer. 5, 263–274 (2005).
  2. Curiel, T. J. et al. Blockade of B7-H1 improves myeloid dendritic cell–mediated antitumor immunity. J. Nature Medicine. 9, 562–567 (2003).
  3. Dong, H. et al. Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion. J. Nature Medicine. 8, 793–800 (2002).
  4. Barber, D. L. et al. Restoring function in exhausted CD8 T cells during chronic viral infectionv. J. Nature. 439, 682–687 (2005).
  5. Francisco, L. M. et al. PD-L1 regulates the development, maintenance, and function of induced regulatory T cells. J. J Exp Med. 206, 3015–3029 (2009).
  6. Patsoukis, N., Sari, D. & Boussiotis, V. A. PD-1 inhibits T cell proliferation by upregulating p27 and p15 and suppressing Cdc25A. J. Cell Cycle. 11, 4305–4309 (2012).
  7. Paterson, A. M. et al. The programmed death-1 ligand 1: B7-1 pathway restrains diabetogenic effector T cells in vivo. J. J Immunol. 187, 1097–1105 (2011).

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