Targeting hypoxia at the forefront of anticancer immune responses

MZ Noman, S Chouaib - Oncoimmunology, 2014 - Taylor & Francis
MZ Noman, S Chouaib
Oncoimmunology, 2014Taylor & Francis
Hypoxia influences immune checkpoint receptors and their respective ligands. In support,
we recently demonstrated that hypoxia selectively upregulates programmed cell death
ligand 1 (PD-L1) on myeloid-derived suppressor cells (MDSCs) via hypoxia inducible factor
1 α (HIF-1α) binding to a hypoxia-response element (HRE) in the PD-L1 proximal promoter.
Furthermore, blockade of PD-L1 under hypoxic conditions enhanced MDSC-mediated T-cell
activation by attenuating MDSC secretion of IL-6 and IL-10.
Hypoxia influences immune checkpoint receptors and their respective ligands. In support, we recently demonstrated that hypoxia selectively upregulates programmed cell death ligand 1 (PD-L1) on myeloid-derived suppressor cells (MDSCs) via hypoxia inducible factor 1 α (HIF-1α) binding to a hypoxia-response element (HRE) in the PD-L1 proximal promoter. Furthermore, blockade of PD-L1 under hypoxic conditions enhanced MDSC-mediated T-cell activation by attenuating MDSC secretion of IL-6 and IL-10.
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