Metabolic Plasticity in Dendritic Cell Responses: Implications in Allergic Asthma

Figure 1

Basic preferences of DC metabolism. DCs originates from the common dendritic progenitors (CDPs) in the bone marrow (BM) that use mitochondrial oxidative phosphorylation (OXPHOS) as a key metabolic energy source and have increased mitochondrial biogenesis. These DC-committed progenitors egress the BM and circulate in the bloodstream and tissues as naïve immature DCs that promoted mitochondrial OXPHOS and shifted with the metabolic preferences upon allergen uptake and toll-like receptor (TLR) activation. The early glycolytic surge in activated DCs is primarily mediated via AKT pathways that phosphorylate and activate hexokinase II (the rate-limiting enzyme of the glycolytic pathway), whereas a late-occurring event of increased glycolysis is maintained by activated mTORC-HIF1α and is NO-dependent. NO: nitric oxide; mTORC1: mammalian target of rapamycin complex 1; HIF1α: hypoxia-inducible factor 1-alpha.