ER Stress in Dendritic Cells Promotes Cancer

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ER Stress in Dendritic Cells Promotes Cancer Christopher S. Garris, Mikael J. Pittet Cell Volume 161, Issue 7, Pages 1492-1493 (June 2015) DOI: 10.1016/j.cell.2015.06.006 Copyright © 2015 Elsevier Inc. Terms and Conditions

Figure 1 Model of XBP1-Driven ER Stress in Dendritic Cells (Left) XBP1WT DC. (Right) XBP1KO DC. Tumor-derived factors activate lipid peroxidation within DCs in a ROS-dependent mechanism. Lipid peroxidation byproducts trigger ER stress responses that activate XBP1. XBP1 activation is connected to lipid synthesis pathways that ultimately increase lipid load within the DCs and inhibit DC-mediated T cell priming. Loss of XBP1 eliminates ER stress responses and lipid synthesis/accumulation and enhances DC ability to prime anti-tumor T cell responses. Cell 2015 161, 1492-1493DOI: (10.1016/j.cell.2015.06.006) Copyright © 2015 Elsevier Inc. Terms and Conditions