Abstract
Memory T cells persist for long term to mediate robust recall response upon rechallenging with previous encountered pathogens. The memory T cell pool is highly heterogeneous based on distinct phenotypic, functional, and locational properties, and contains discrete subsets, which contribute to diverse immune responses. In this mini-review, we will briefly discuss the distinct subsets of memory T cells and then focus on mitochondria-related metabolic and epigenetic regulations of CD8+ T cell memory formation. In particular, we discuss many aspects of mitochondrial quality control systems (biogenesis, dynamics, etc.) in regulating CD8+ T cell fate decision and antitumor immunity. Importantly, targeting mitochondrial metabolism to boost T cell memory formation and metabolic fitness might represent an attractive strategy to improve cancer immunotherapy including CAR-T therapy.
Highlights
Memory T cells persist for long term to mediate robust recall response upon rechallenging with previous encountered pathogens
Human memory T cells were primarily categorized into central memory (Tcm) and effector memory (Tem) subsets, characterized by CD62hiCCR7hi and CD62lowCCR7low phenotype, respectively, and with distinct functional/localization properties [5]
central memory T cell (Tcm) cells have vast proliferative potential and reside in secondary lymphoid organs to invoke robust recall responses, which further differentiate toward effector memory or terminally differentiated effector progenies to protect against infections or undergo self-renew
Summary
The memory T cell pool is highly heterogeneous based on distinct phenotypic, functional, and locational properties, and contains discrete subsets, which contribute to diverse immune responses. In this mini-review, we will briefly discuss the distinct subsets of memory T cells and focus on mitochondria-related metabolic and epigenetic regulations of CD8+ T cell memory formation. We discuss many aspects of mitochondrial quality control systems (biogenesis, dynamics, etc.) in regulating CD8+ T cell fate decision and antitumor immunity. Targeting mitochondrial metabolism to boost T cell memory formation and metabolic fitness might represent an attractive strategy to improve cancer immunotherapy including CAR-T therapy
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