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Am J Physiol Cell Physiol. 2015 Nov 1;309(9):C569-79. doi: 10.1152/ajpcell.00207.2015. Epub 2015 Aug 26.

Hypoxia: a key player in antitumor immune response. A Review in the Theme: Cellular Responses to Hypoxia.

Author information

1
Institut National de la Santé et de la Recherche Médicale U1186, Equipe Labellisée Par La Ligue Contre Le Cancer, Gustave Roussy Campus, Villejuif, France;
2
Centre for Molecular Biophysics, Cell Recognition, and Glycobiology, UPR 4301 Centre National de la Recherche Scientifique, Orléans, France; and.
3
Laboratory of Experimental Cancer Research, Luxembourg Institute of Health, Strassen, Luxembourg.
4
Institut National de la Santé et de la Recherche Médicale U1186, Equipe Labellisée Par La Ligue Contre Le Cancer, Gustave Roussy Campus, Villejuif, France; salem.chouaib@gustaveroussy.fr.

Abstract

The tumor microenvironment is a complex system, playing an important role in tumor development and progression. Besides cellular stromal components, extracellular matrix fibers, cytokines, and other metabolic mediators are also involved. In this review we outline the potential role of hypoxia, a major feature of most solid tumors, within the tumor microenvironment and how it contributes to immune resistance and immune suppression/tolerance and can be detrimental to antitumor effector cell functions. We also outline how hypoxic stress influences immunosuppressive pathways involving macrophages, myeloid-derived suppressor cells, T regulatory cells, and immune checkpoints and how it may confer tumor resistance. Finally, we discuss how microenvironmental hypoxia poses both obstacles and opportunities for new therapeutic immune interventions.

KEYWORDS:

autophagy and antitumor immune response; cancer stem cells; circulating tumor cells; epithelial-mesenchymal transition; hypoxia; hypoxia-inducible factor; immune suppression; lymphoid cells; myeloid cells; programmed death-ligand 1; tumor microenvironment

PMID:
26310815
PMCID:
PMC4628936
DOI:
10.1152/ajpcell.00207.2015
[Indexed for MEDLINE]
Free PMC Article

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