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PMID: 24780173 Published · ppublish English Journal Article Review

Programmed death-1 pathway in cancer and autoimmunity.

Clinical immunology (Orlando, Fla.) ·Vol. 153 ·No. 1 ·2014-07-00 ·Pages 145-52

Pedoeem A, Azoulay-Alfaguter I, Strazza M, Silverman GJ, Mor A

Abstract

Programmed death-1 (PD-1) is a co-receptor that is expressed predominantly by T cells. The binding of PD-1 to its ligands, PD-L1 or PD-L2, is vital for the physiologic regulation of the immune system. A major functional role of the PD-1 signaling pathway is the inhibition of self-reactive T cells, which serve to protect against autoimmune diseases. Elimination of the PD-1 pathway can therefore result in the breakdown of immune tolerance that can ultimately lead to the development of pathogenic autoimmunity. Conversely, tumor cells can at times co-opt the PD-1 pathway to escape from immunosurveillance mechanisms. Therefore, blockade of the PD-1 pathway has become an attractive target in cancer therapy. Recent clinical trials have shown that anti-PD-1 agents have profound effects on solid tumor regression. Current approaches include six agents that are either PD-1 and PD-L1 targeted neutralizing antibodies or fusion proteins. More than forty clinical trials are underway to better define the role of PD-1 blockade in variety of tumor types. In this review we will highlight the basic biology of the PD-1 system and discuss its potential roles in both autoimmunity and cancer. We propose that future research on PD-1 may lead to the translation of fundamental regulatory pathways into the development of practical new approaches for the treatment of autoimmune diseases and cancer.

Keywords
Adhesion Autoimmunity Programmed death-1 T cells
MeSH Terms
Animals Autoimmune Diseases/drug therapy,genetics,immunology,metabolism Autoimmunity B-Lymphocytes/immunology,metabolism Communicable Diseases/drug therapy,genetics,immunology,metabolism Humans Ligands Neoplasms/genetics,immunology,metabolism Programmed Cell Death 1 Receptor/antagonists & inhibitors,genetics,metabolism Signal Transduction T-Lymphocyte Subsets/immunology,metabolism
Chemicals
Ligands Programmed Cell Death 1 Receptor
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Pedoeem Ariel
Department of Medicine, New York University School of Medicine, NY, USA.
Azoulay-Alfaguter Inbar
Department of Medicine, New York University School of Medicine, NY, USA.
Strazza Marianne
Department of Medicine, New York University School of Medicine, NY, USA.
Silverman Gregg J
Department of Medicine, New York University School of Medicine, NY, USA; Department of Pathology, New York University School of Medicine, NY, USA.
Mor Adam
Department of Medicine, New York University School of Medicine, NY, USA; Department of Pathology, New York University School of Medicine, NY, USA. Electronic address: Adam.Mor@NYUMC.org.
Article Info
Journal
Clinical immunology (Orlando, Fla.)
Abbr.
Clin Immunol
ISSN
1521-7035
Published
2014-07-00
Epub
2014-00-26
Pages
145-52
Language
English
Region
United States
NLM ID
100883537
Subset
IM
Grants
NIAID NIH HHS · R01 AI068063 · United States
NIAID NIH HHS · R01 AI090118 · United States
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