Fueling Function Over Expansion in T Cells
Vertebrates generate millions of unique T cell receptors during T cell development, ensuring that the immune system can recognize any number of potential pathogens.
A compromise for this extraordinary molecular diversity is that the T cell population of a given individual contains only a handful of cells that can recognize any particular foreign invader.
To solve this problem, T cells can undergo extraordinary proliferation in response to infection (1). Upon activation, they adopt specialized metabolic programs, such as aerobic glycolysis [the Warburg effect (2–5)], which has long been thought to meet the biosynthetic and bioenergetic requirements associated with rapid expansion (2). But a recent study by Chang et al. (6) raises questions about this model and suggests instead that aerobic glycolysis is necessary for T cell effector function rather than proliferation.
Role of Glyoxalase 1 (Glo1) and methylglyoxal (MG) in behavior: recent advances and mechanistic insights
Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs), oxidative stress, and apoptosis.
The concentration of MG is elevated under high-glucose conditions, such as diabetes.
As such, GLO1 and MG have been implicated in the pathogenesis of diabetic complications.
Recently, findings have linked GLO1 to numerous behavioral phenotypes, including psychiatric diseases (anxiety, depression, schizophrenia, and autism) and pain.
This review highlights GLO1’s association with behavioral phenotypes, describes recent discoveries that have elucidated the underlying mechanisms, and identifies opportunities for future research.