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. 2023 Jul 8;14(7):407. doi: 10.1038/s41419-023-05937-3

Fig. 3. Effect of altered glycolysis levels on CD8+ T cell effector and memory cell functions.

Fig. 3

For short-lived CD8+ T cells, deletion of Atg5 would promote glycolytic activity and OXPHOS, which in turn would lead to energy production. Meanwhile, TLR2 and TLR7 stimulate upregulation of glucose uptake and glycolysis in CD8+ T cells through regulation of the AKT-mTOR pathway and the downstream transcription factor IRF4, thereby promoting effector functions including IL-4, IFN-γ, and TNF-α secretion in CD8+ T cells in vitro. For tissue-resident memory CD8+ T cells, during metabolism, mTORC2 promotes respiration by activating PKB or AKT to inhibit GSK3β at the mitochondrial-endoplasmic reticulum (ER) junction, leading to recruitment of HK-I to the voltage-dependent anion channel (VDAC) of mitochondria, thereby promoting metabolite influx into mitochondria to facilitate respiration and thus the rapid production of IFN-γ. Meanwhile, miR-143 targets GLUT1 to promote glucose flux and glycolytic activity, further promoting memory-type functions.