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

Autor:	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.
Jazyk:	angličtina
Zdroj:	Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2014 Oct 15; Vol. 193 (8), pp. 3835-41.
DOI:	10.4049/jimmunol.1401572
Abstrakt:	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. (Copyright © 2014 by The American Association of Immunologists, Inc.)
Databáze:	MEDLINE
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