NDLI: The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.

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The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.

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The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Horn, Lucas A. Haile, Samuel T. Ostrand-Rosenberg, Suzanne
Description	Author Affiliation: Ostrand-Rosenberg S ( Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, MD 21250 srosenbe@umbc.edu.); Horn LA ( Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, MD 21250.); Haile ST ( Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, MD 21250.)
Abstract	Programmed death ligand 1 (PD-L1, also known as B7 homolog 1 or CD274) is a major obstacle to antitumor immunity because it tolerizes/anergizes tumor-reactive T cells by binding to its receptor programmed death-1 (CD279), renders tumor cells resistant to CD8(+) T cell- and FasL-mediated lysis, and tolerizes T cells by reverse signaling through T cell-expressed CD80. PD-L1 is abundant in the tumor microenvironment, where it is expressed by many malignant cells, as well as by immune cells and vascular endothelial cells. The critical role of PD-L1 in obstructing antitumor immunity has been demonstrated in multiple animal models and in recent clinical trials. This article reviews the mechanisms by which PD-L1 impairs antitumor immunity and discusses established and experimental strategies for maintaining T cell activation in the presence of PD-L1-expressing cells in the tumor microenvironment.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401572
Journal	The Journal of Immunology
Issue Number	8
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd274 Immunology Antigens, Cd80 Cd8-positive T-lymphocytes Immune Tolerance Neoplasms Programmed Cell Death 1 Receptor Animals Apoptosis Fas Ligand Protein Lymphocyte Activation Lymphocytes, Tumor-infiltrating Mice Signal Transduction Tumor Microenvironment Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8+ T lymphocytes in human non-small cell lung cancer.

Programmed cell death 1 ligand 1 and tumor-infiltrating CD8+ T lymphocytes are prognostic factors of human ovarian cancer.

Progressive upregulation of PD-1 in primary and metastatic melanomas associated with blunted TCR signaling in infiltrating T lymphocytes.

Programmed death receptor-1/programmed death receptor ligand-1 blockade after transient lymphodepletion to treat myeloma.

Forced expression of programmed death-1 gene on T cell decreased the incidence of type 1 diabetes.

Control of Toxoplasma reactivation by rescue of dysfunctional CD8+ T-cell response via PD-1-PDL-1 blockade.

Soluble CD80 restores T cell activation and overcomes tumor cell programmed death ligand 1-mediated immune suppression.

Programmed death (PD)-1 molecule and its ligand PD-L1 distribution among memory CD4 and CD8 T cell subsets in human immunodeficiency virus-1-infected individuals.

PD-1, gender, and autoimmunity.

The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.

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Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8+ T lymphocytes in human non-small cell lung cancer.

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PD-1, gender, and autoimmunity.

The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.