Abstract
Dendritic cells (DCs) are canonical antigen presenting cells of the immune system and serve as a bridge between innate and adaptive immune responses. When DCs are activated by a stimulus through toll-like receptors (TLRs), DCs undergo a process of maturation defined by cytokine & chemokine secretion, co-stimulatory molecule expression, antigen processing and presentation, and the ability to activate T cells. DC maturation is coupled with an increase in biosynthetic demand, which is fulfilled by a TLR-driven upregulation in glycolytic metabolism. Up-regulation of glycolysis in activated DCs provides these cells with molecular building blocks and cellular energy required for DC activation, and inhibition of glycolysis during initial activation impairs both the survival and effector function of activated DCs. Evidence shows that DC glycolytic upregulation is controlled by two distinct pathways, an early burst of glycolysis that is nitric oxide (NO) -independent, and a sustained commitment to glycolysis in NO-producing DC subsets. This review will address the complex role of NO in regulating DC metabolism and effector function.