![tcel bonafide tcel bonafide](https://i0.wp.com/eatsinbaguio.files.wordpress.com/2017/04/img_3898.jpg)
Trained monocytes and macrophages produce reactive oxygen species (ROS), which trigger antioxidative glutathione (GSH) response to buffer the rising ROS. The antioxidative GSH pathway thus plays an unexpected role in metabolic integration and reprogramming during inflammatory T cell responses.
![tcel bonafide tcel bonafide](https://mir-s3-cdn-cf.behance.net/projects/202/5784539.546916f08e155.jpg)
In vivo, T-cell-specific ablation of murine Gclc prevented autoimmune disease but blocked antiviral defense. GSH deficiency compromised the activation of mammalian target of rapamycin-1 (mTOR) and expression of NFAT and Myc transcription factors, abrogating the energy utilization and Myc-dependent metabolic reprogramming that allows activated T cells to switch to glycolysis and glutaminolysis. Gclc-deficient T cells initially underwent normal activation but could not meet their increased energy and biosynthetic requirements. Conditional gene targeting of the catalytic subunit of glutamate cysteine ligase (Gclc) blocked GSH production specifically in murine T cells. We report that GSH is essential for T cell effector functions through its regulation of metabolic activity.
![tcel bonafide tcel bonafide](https://www.trustedreviews.com/wp-content/uploads/sites/54/2021/08/TCL-Roku-55RP620K-connections-320x213.jpg)
Activated T cells produce reactive oxygen species (ROS), which trigger the antioxidative glutathione (GSH) response necessary to buffer rising ROS and prevent cellular damage.