T cell and other immune cell metabolism (Immunometabolism)

T cell and other immune cell metabolism, collectively known as immunometabolism, refers to the dynamic shifts in intracellular metabolic pathways that dictate the activation, differentiation, and effector functions of immune cells (Pearce et al., 2013, Nature Reviews Immunology). Upon encountering antigens, T cells undergo a rapid transition from quiescent oxidative phosphorylation to aerobic glycolysis, a process termed metabolic reprogramming, to meet the biosynthetic demands of proliferation and cytokine production (Buck et al., 2015, Journal of Experimental Medicine). This metabolic state is tightly regulated by nutrient-sensing hubs such as the mechanistic target of rapamycin (mTOR) and adenosine monophosphate-activated protein kinase (AMPK) (Powell et al., 2012, Immunity). In disease states like cancer, the nutrient-poor tumor microenvironment can lead to metabolic competition, resulting in T cell exhaustion and impaired anti-tumor responses (Chang et al., 2015, Cell). Conversely, hyper-metabolic activity in immune cells is often associated with chronic inflammatory and autoimmune disorders (Weyand et al., 2017, Nature Reviews Rheumatology). Therapeutic interventions aim to modulate these pathways using drugs like mTOR inhibitors or metabolic mimetics to either suppress overactive immune responses or reinvigorate exhausted cells (O'Neill et al., 2016, Nature Reviews Immunology).

Other names

ImmunometabolismLeukocyte metabolismLymphocyte metabolic reprogrammingImmune cell metabolic pathways

Modulation of intracellular metabolic flux (e.g., glycolysis, oxidative phosphorylation, fatty acid oxidation) through the pharmacological targeting of nutrient sensors (mTOR, AMPK) or rate-limiting enzymes (GAPDH, LDHA) to alter immune cell phenotype and function.