mTOR participates in the formation, maintenance, and function of memory CD8+T cells regulated by glycometabolism

Xuepei Cai, Haokun Li, Manyi Wang, Edward Chu, Ning Wei, Jiayu Lin, Yun Hu, Jingtao Dai, Aijie Chen, Hua Zheng, Qianbing Zhang, Yuxia Zhong, Ruoshui Chang, Sha Wu, Yaomu Xiao, Chufeng Liu

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations


Memory CD8+T 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 CD8+T cells, countering the view that glycolysis prevents the formation of memory CD8+T cells. This review focuses on how glycometabolism regulates memory CD8+T cells and highlights the key mechanisms through which the mammalian target of rapamycin (mTOR) signaling pathway affects memory CD8+T cell formation, maintenance, and function by regulating glycometabolism. In addition, different subpopulations of memory CD8+T 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 CD8+T cells. Modulating the metabolism of memory CD8+T cells to influence specific cell fates may be useful for disease treatment.

Original languageEnglish (US)
Article number115197
JournalBiochemical Pharmacology
StatePublished - Oct 2022


  • Glycolysis
  • Glycometabolism
  • Memory CD8T cell
  • mTOR

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology


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