The Unfolded Protein Response Mediator PERK Governs Myeloid Cell-Driven Immunosuppression in Tumors through Inhibition of STING Signaling
The primary mechanisms supporting immunoregulatory polarization of myeloid cells upon infiltration into tumors remain largely unexplored. Elucidation of these signals could enable better strategies to restore protective anti-tumor immunity. Here, we investigated the role of the intrinsic activation of the PKR-like endoplasmic reticulum (ER) kinase (PERK) in the immunoinhibitory actions of tumor-associated myeloid-derived suppressor cells (tumor-MDSCs). PERK signaling increased in tumor-MDSCs, and its deletion transformed MDSCs into myeloid cells that activated CD8
Journal
ImmunityAuthors
Funding
Functional reprogramming of tumor-MDSC through antibody-based therapies targeting Notch ligandsPTEN, Tregs and MDSCs in the tumor microenvironmentImmunobiology of Normal and Neoplastic LymphocytesReprogramming the TME for immunogenic antigen-presentationDevelopmental FundsInitiation and Evolution of the Ovarian Cancer MicroenvironmentEffects of Common Polymorphisms in Immune Sensors in Tumor ImmunosurveillanceCrosstalk between butyrophilins and gamma delta T cells in human cancerStress Pathways in Tumors Drive Global MDSC Activity and Survival through ChopNational Institutes of Health FundingOvarian Cancer Academy Funding