Metabolic control of T-cell immunity via epigenetic mechanisms

摘要

Metabolism has been increasingly considered to play an important role in inflammation and immunity via modulating cellular signaling and transcriptional networks.1 Dysregulation of metabolic enzymes or mediators is increasingly linked to clinical diseases,such as type I diabetes,gliomas and breast cancer.2,3 Numerous metabolic sensors,such as AMP-mediated protein kinase,mammalian target of rapamycin complex1 and hypoxia-induced factor 1α(HIF-1α),have been shown to regulate immunological responses,such as T-cell activation and macrophage polarization,via modulating the property and activity of signaling pathways.4,5 Moreover,emerging evidence suggests that intermediates from multiple metabolic pathways are important in orchestrating transcriptional and epigenetic programs.This interaction between metabolic and epigenetic pathways is crucial for coordinating cellular immunological events in response to extracellular stimuli,such as infection,injury and stress,leading to varied biological and pathological outcomes.