Abstract
T cells are an important adaptive immune response arm that mediates cell-mediated immunity. T cell metabolism plays a central role in T cell activation, proliferation, differentiation, and effector function. Specific metabolic programs are tightly controlled to mediate T cell immune responses, and alterations in T cell metabolism may result in many immunological disorders. In this review, we will summarize the main T cell metabolic pathways and the important factors participating in T cell metabolic programming during T cell homeostasis, differentiation, and function.
Highlights
We provide a general overview of the metabolic regulation of T cell immunity
These findings indicate that c-Myc plays a multifaceted role in T cell activation and T cell metabolism
Many studies have shown that metabolism and T cell immunity are closely related
Summary
Different types of immune cells play specialized roles in host defense against tumor cells or pathogens [1,2]. During T cell activation, proliferation, and differentiation, energy metabolism mainly depends on aerobic glycolysis and OXPHOS. The inhibition of the key metabolic regulator, mTOR, during CD4+ T cell activation enhances FAO and reduces aerobic glycolysis favor Treg production [28]. The activation of mTOR signaling promotes fatty acid synthesis (FAS) and aerobic glycolysis, thereby further inhibiting Treg differentiation. Specific deletion of c-Myc in T cells reduces the expression of LAT1 and ASCT2 [45,78] and inhibits T cell uptake of amino acids. Instability of c-Myc expression leads to the downregulation of Glut, which reduces glutamine and arginine uptake of T cells and inhibits glutamine glutaminolysis and T cell glycolysis [79] These findings indicate that c-Myc plays a multifaceted role in T cell activation and T cell metabolism. Treg function is enhanced to impair effector T cell functions in the tumor microenvironment, which in turn facilitates tumor development
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