PD‐1/PD‐L1 immune checkpoint: Potential target for cancer therapy

Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of immune inhibitory signaling proteins. One of the most critical checkpoint pathways in this system is a tumor‐induced immune suppression (immune c...

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Published inJournal of cellular physiology Vol. 234; no. 2; pp. 1313 - 1325
Main Authors Dermani, Fatemeh K., Samadi, Pouria, Rahmani, Golebagh, Kohlan, Alisa K., Najafi, Rezvan
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.02.2019
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Abstract Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of immune inhibitory signaling proteins. One of the most critical checkpoint pathways in this system is a tumor‐induced immune suppression (immune checkpoint) mediated by the programmed cell death protein 1 (PD‐1) and its ligand, programmed death ligand 1 (PD‐L1). PD‐1 is highly expressed by activated T cells, B cells, dendritic cells, and natural killer cells, whereas PD‐L1 is expressed on several types of tumor cells. Many studies have shown that blocking the interaction between PD‐1 and PD‐L1 enhances the T‐cell response and mediates antitumor activity. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD‐1 and PD‐L1 interaction in various cancers. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD‐1 and PD‐L1 interaction in various cancers.
AbstractList Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of immune inhibitory signaling proteins. One of the most critical checkpoint pathways in this system is a tumor-induced immune suppression (immune checkpoint) mediated by the programmed cell death protein 1 (PD-1) and its ligand, programmed death ligand 1 (PD-L1). PD-1 is highly expressed by activated T cells, B cells, dendritic cells, and natural killer cells, whereas PD-L1 is expressed on several types of tumor cells. Many studies have shown that blocking the interaction between PD-1 and PD-L1 enhances the T-cell response and mediates antitumor activity. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD-1 and PD-L1 interaction in various cancers.
Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of immune inhibitory signaling proteins. One of the most critical checkpoint pathways in this system is a tumor‐induced immune suppression (immune checkpoint) mediated by the programmed cell death protein 1 (PD‐1) and its ligand, programmed death ligand 1 (PD‐L1). PD‐1 is highly expressed by activated T cells, B cells, dendritic cells, and natural killer cells, whereas PD‐L1 is expressed on several types of tumor cells. Many studies have shown that blocking the interaction between PD‐1 and PD‐L1 enhances the T‐cell response and mediates antitumor activity. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD‐1 and PD‐L1 interaction in various cancers. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD‐1 and PD‐L1 interaction in various cancers.
Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of immune inhibitory signaling proteins. One of the most critical checkpoint pathways in this system is a tumor-induced immune suppression (immune checkpoint) mediated by the programmed cell death protein 1 (PD-1) and its ligand, programmed death ligand 1 (PD-L1). PD-1 is highly expressed by activated T cells, B cells, dendritic cells, and natural killer cells, whereas PD-L1 is expressed on several types of tumor cells. Many studies have shown that blocking the interaction between PD-1 and PD-L1 enhances the T-cell response and mediates antitumor activity. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD-1 and PD-L1 interaction in various cancers.Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of immune inhibitory signaling proteins. One of the most critical checkpoint pathways in this system is a tumor-induced immune suppression (immune checkpoint) mediated by the programmed cell death protein 1 (PD-1) and its ligand, programmed death ligand 1 (PD-L1). PD-1 is highly expressed by activated T cells, B cells, dendritic cells, and natural killer cells, whereas PD-L1 is expressed on several types of tumor cells. Many studies have shown that blocking the interaction between PD-1 and PD-L1 enhances the T-cell response and mediates antitumor activity. In this review, we highlight a brief overview of the molecular and biochemical events that are regulated by the PD-1 and PD-L1 interaction in various cancers.
Author Rahmani, Golebagh
Najafi, Rezvan
Samadi, Pouria
Kohlan, Alisa K.
Dermani, Fatemeh K.
Author_xml – sequence: 1
  givenname: Fatemeh K.
  surname: Dermani
  fullname: Dermani, Fatemeh K.
  organization: Research Center for Molecular Medicine, Hamadan University of Medical Sciences
– sequence: 2
  givenname: Pouria
  surname: Samadi
  fullname: Samadi, Pouria
  organization: Research Center for Molecular Medicine, Hamadan University of Medical Sciences
– sequence: 3
  givenname: Golebagh
  surname: Rahmani
  fullname: Rahmani, Golebagh
  organization: Research Center for Molecular Medicine, Hamadan University of Medical Sciences
– sequence: 4
  givenname: Alisa K.
  surname: Kohlan
  fullname: Kohlan, Alisa K.
  organization: Research Center for Molecular Medicine, Hamadan University of Medical Sciences
– sequence: 5
  givenname: Rezvan
  orcidid: 0000-0003-1326-1288
  surname: Najafi
  fullname: Najafi, Rezvan
  email: re.najafi@umsha.ac.ir, najafi2535@gmail.com
  organization: Research Center for Molecular Medicine, Hamadan University of Medical Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30191996$$D View this record in MEDLINE/PubMed
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programmed death ligand 1 (PD-L1)
programmed cell death protein 1 (PD-1)
immune checkpoints
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Snippet Recent studies show that cancer cells are sometimes able to evade the host immunity in the tumor microenvironment. Cancer cells can express high levels of...
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SubjectTerms Animals
Anticancer properties
Antineoplastic Agents, Immunological - adverse effects
Antineoplastic Agents, Immunological - therapeutic use
Antitumor activity
Apoptosis
B7-H1 Antigen - antagonists & inhibitors
B7-H1 Antigen - immunology
B7-H1 Antigen - metabolism
Cancer
Cancer therapies
Cell death
Dendritic cells
Humans
Immune checkpoint
immune checkpoints
Immunity
Immunotherapy - adverse effects
Immunotherapy - methods
Ligands
Lymphocytes
Lymphocytes B
Lymphocytes T
Molecular Targeted Therapy
Natural killer cells
Neoplasms - drug therapy
Neoplasms - immunology
Neoplasms - metabolism
Neoplasms - pathology
PD-L1 protein
Programmed Cell Death 1 Receptor - antagonists & inhibitors
Programmed Cell Death 1 Receptor - immunology
Programmed Cell Death 1 Receptor - metabolism
programmed cell death protein 1 (PD‐1)
programmed death ligand 1 (PD‐L1)
Proteins
Signal Transduction
Treatment Outcome
Tumor cells
Tumor Escape
Tumor Microenvironment
Tumors
Title PD‐1/PD‐L1 immune checkpoint: Potential target for cancer therapy
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcp.27172
https://www.ncbi.nlm.nih.gov/pubmed/30191996
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Volume 234
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