Basics of PD-1 in self-tolerance, infection, and cancer immunity

Research output: Research - peer-reviewArticle

  • 12 Citations

Abstract

Successful cancer treatment requires understanding host immune response against tumor cells. PD-1 belongs to the CD28 superfamily of receptors that work as “checkpoints” of immune activation. PD-1 maintains immune self-tolerance to prevent autoimmunity and controls T-cell reaction during infection to prevent excessive tissue damage. Tumor cells that arise from normal tissue acquire mutations that can be targeted by lymphocytes. Accumulating lines of evidence suggest that tumor cells evade host immune attack by expressing physiological PD-1 ligands and stimulating PD-1 on the lymphocytes. Based on this idea, researchers have successfully demonstrated that systemic administration of monoclonal antibodies that inhibit the binding of PD-1 to the ligands reactivated T cells and augmented the anti-cancer immune response. In this review, I summarize the basics of T-cell biology and its regulation by PD-1 and discuss the current understanding and questions about this multifaceted molecule.

LanguageEnglish
Pages1-8
Number of pages8
JournalInternational Journal of Clinical Oncology
DOIs
StateAccepted/In press - 2016 Feb 10

Fingerprint

Self Tolerance
Immunity
Infection
Neoplasms
T-Lymphocytes
Lymphocytes
Ligands
Immune Tolerance
Autoimmunity
Cell Biology
Monoclonal Antibodies
Research Personnel
Mutation
Therapeutics

Keywords

  • Costimulation
  • CTLA-4
  • Immune checkpoint blockade
  • Immune tolerance
  • PD-1
  • T lymphocytes

ASJC Scopus subject areas

  • Oncology
  • Surgery
  • Hematology

Cite this

@article{90e7251381cf4d52852586044638f154,
title = "Basics of PD-1 in self-tolerance, infection, and cancer immunity",
abstract = "Successful cancer treatment requires understanding host immune response against tumor cells. PD-1 belongs to the CD28 superfamily of receptors that work as “checkpoints” of immune activation. PD-1 maintains immune self-tolerance to prevent autoimmunity and controls T-cell reaction during infection to prevent excessive tissue damage. Tumor cells that arise from normal tissue acquire mutations that can be targeted by lymphocytes. Accumulating lines of evidence suggest that tumor cells evade host immune attack by expressing physiological PD-1 ligands and stimulating PD-1 on the lymphocytes. Based on this idea, researchers have successfully demonstrated that systemic administration of monoclonal antibodies that inhibit the binding of PD-1 to the ligands reactivated T cells and augmented the anti-cancer immune response. In this review, I summarize the basics of T-cell biology and its regulation by PD-1 and discuss the current understanding and questions about this multifaceted molecule.",
keywords = "Costimulation, CTLA-4, Immune checkpoint blockade, Immune tolerance, PD-1, T lymphocytes",
author = "Shunsuke Chikuma",
year = "2016",
month = "2",
doi = "10.1007/s10147-016-0958-0",
pages = "1--8",
journal = "International Journal of Clinical Oncology",
issn = "1341-9625",
publisher = "Springer Japan",

}

TY - JOUR

T1 - Basics of PD-1 in self-tolerance, infection, and cancer immunity

AU - Chikuma,Shunsuke

PY - 2016/2/10

Y1 - 2016/2/10

N2 - Successful cancer treatment requires understanding host immune response against tumor cells. PD-1 belongs to the CD28 superfamily of receptors that work as “checkpoints” of immune activation. PD-1 maintains immune self-tolerance to prevent autoimmunity and controls T-cell reaction during infection to prevent excessive tissue damage. Tumor cells that arise from normal tissue acquire mutations that can be targeted by lymphocytes. Accumulating lines of evidence suggest that tumor cells evade host immune attack by expressing physiological PD-1 ligands and stimulating PD-1 on the lymphocytes. Based on this idea, researchers have successfully demonstrated that systemic administration of monoclonal antibodies that inhibit the binding of PD-1 to the ligands reactivated T cells and augmented the anti-cancer immune response. In this review, I summarize the basics of T-cell biology and its regulation by PD-1 and discuss the current understanding and questions about this multifaceted molecule.

AB - Successful cancer treatment requires understanding host immune response against tumor cells. PD-1 belongs to the CD28 superfamily of receptors that work as “checkpoints” of immune activation. PD-1 maintains immune self-tolerance to prevent autoimmunity and controls T-cell reaction during infection to prevent excessive tissue damage. Tumor cells that arise from normal tissue acquire mutations that can be targeted by lymphocytes. Accumulating lines of evidence suggest that tumor cells evade host immune attack by expressing physiological PD-1 ligands and stimulating PD-1 on the lymphocytes. Based on this idea, researchers have successfully demonstrated that systemic administration of monoclonal antibodies that inhibit the binding of PD-1 to the ligands reactivated T cells and augmented the anti-cancer immune response. In this review, I summarize the basics of T-cell biology and its regulation by PD-1 and discuss the current understanding and questions about this multifaceted molecule.

KW - Costimulation

KW - CTLA-4

KW - Immune checkpoint blockade

KW - Immune tolerance

KW - PD-1

KW - T lymphocytes

UR - http://www.scopus.com/inward/record.url?scp=84957691019&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84957691019&partnerID=8YFLogxK

U2 - 10.1007/s10147-016-0958-0

DO - 10.1007/s10147-016-0958-0

M3 - Article

SP - 1

EP - 8

JO - International Journal of Clinical Oncology

T2 - International Journal of Clinical Oncology

JF - International Journal of Clinical Oncology

SN - 1341-9625

ER -