T cell metabolism drives immunity

Abstract

Buck et al. discuss the role of lymphocyte metabolism on immune cell development and function.

The vimentin intermediate filament network restrains regulatory T cell suppression of graft-versus-host disease

“…Since Nrp1 and Lag3 are important for suppressing Tcon priming (51,52), augmented expression of these molecules, in combination with metabolic alterations, probably contributed to the increased inhibition of alloantigen-specific Tcon priming we observed in vivo in mice with GVHD. This decrease in antigen-specific priming probably drove the reductions in Tcon metabolic activity, cytokine production, and GVHD progression we observed, as priming is critical for initiating Tcon metabolic changes and effector differentiation (33). Furthermore, Tregs exert much of their suppressive effect in GVHD early in the course of the disease.…”

“…mTOR signaling also plays a critical role in regulating Treg metabolism (30)(31)(32). Specifically, Tregs preferentially oxidize fatty acids (FAs) as fuel, and mTORC1 may promote this process (33,34). However, unchecked mTORC2 signaling leads to an increase in glycolysis and reduced Treg function (30,31).…”

Biphasic CD8 + T-Cell Defense in Simian Immunodeficiency Virus Control by Acute-Phase Passive Neutralizing Antibody Immunization

“…More recently, specific pathways of antigen-specific intracellular signaling, such as Sprouty-2-ERK, have been reported to reflect T-cell polyfunctionality (40). Others have also highlighted the importance of context-dependent T-cell metabolism in vivo (41,42). Focused major gatekeepers include mammalian target of rapamycin (mTOR) (43) and AMPK (44).…”

Hepatitis C Virus-Specific T Cell Receptor mRNA-Engineered Human T Cells: Impact of Antigen Specificity on Functional Properties

“…The notion that the NS5-69 response had gene clusters indicative of cellular amino acid biosynthesis suggests an active glycolysis associated with activation and effector T cell differentiation (43) at the same time, with increased taxis, and chemokine ligand genes encoding CCL9, CCL10, CCL11, and CCL22 and cell proliferation genes were upregulated. As the incapability to eliminate the target continues, the activities continue to include signal transduction and metabolic processes (cyclic nucleotide biosynthetic, cAMP and metabolic processes, calcium/metal ion transport), which became even more diverse to include gene cluster expressions controlling lipid metabolisms and cellular metabolic processes and pathways sharing features with an SLE-related response.…”