mTOR participates in the formation, maintenance, and function of memory CD8T cells regulated by glycometabolism.

Memory CD8T cells participate in the fight against infection and tumorigenesis as well as in autoimmune disease progression because of their efficient and rapid immune response, long-term survival, and continuous differentiation. At each stage of their formation, maintenance, and function, the cell metabolism must be adjusted to match the functional requirements of the specific stage. Notably, enhanced glycolytic metabolism can generate sufficient levels of adenosine triphosphate (ATP) to form memory CD8T cells, countering the view that glycolysis prevents the formation of memory CD8T cells. This review focuses on how glycometabolism regulates memory CD8T cells and highlights the key mechanisms through which the mammalian target of rapamycin (mTOR) signaling pathway affects memory CD8T cell formation, maintenance, and function by regulating glycometabolism. In addition, different subpopulations of memory CD8T cells exhibit different metabolic flexibility during their formation, survival, and functional stages, during which the energy metabolism may be critical. These findings which may explain why enhanced glycolytic metabolism can give rise to memory CD8T cells. Modulating the metabolism of memory CD8T cells to influence specific cell fates may be useful for disease treatment.