Reactive Oxygen Species Regulate T Cell Immune Response in the Tumor Microenvironment

Figure 1

ROS produced in the tumor microenvironment. FasL ligation and TCR signaling in T cells could induce the production of ROS via NOX-2, DUOX-1, and mitochondria. Activated phagocytes (neutrophils, eosinophils, and mononuclear phagocytes) can produce large amounts of ROS by the NOX-2 during respiratory burst. Activated T cells can also induce respiratory burst by direct contacts with phagocytes or cytokines. TGF-β activates NOXs of Tregs, which trigger the production of ROS. Moreover, macrophage-derived ROS can induce Tregs accumulation in the tumor microenvironment. Mutations of mitochondrial DNA (mtDNA) in tumor cells result in a deficiency in respiratory complex I activity and contribute to the overproduction of ROS. MDSCs also produce amounts of ROS in the tumor microenvironment.