Abstract
Dendritic cells (DCs) are the bridge between innate and T cell-dependent adaptive immunity and are promising therapeutic targets for cancer and immune-mediated disorders. Upon stimulation by pathogen or danger-sensing receptors, DCs become activated and poised to induce T cell priming. Recent studies have identified critical roles of metabolic pathways, including glycolysis, oxidative phosphorylation, and fatty acid metabolism, in orchestrating DC function. In this review, we discuss the shared and distinct metabolic programs shaping the functional specification of different DC subsets, including conventional DCs, bone marrow-derived DCs, and plasmacytoid DCs. We also briefly discuss the signaling networks that tune metabolic programs in DC subsets.
Highlights
Dendritic cells (DCs) are an innate immune cell population with the capacity to process and present antigenic peptides on major histocompatibility complex (MHC) molecules to antigenspecific T cells
LPS stimulation through TLR4 promotes the rapid upregulation of glycolysis in GM-CSF-bone marrow-derived DCs (BMDCs) and cDCs by activating Akt, which phosphorylates the glycolytic enzyme HKII, thereby anchoring HKII to the mitochondrial membrane where its activity is enhanced (Figure 3A)
The mTOR-dependent upregulation of HIF1α is critical to upregulate inducible nitric oxide synthase (iNOS) expression in GM-CSF-BMDCs (Lawless et al, 2017), which inhibits OXPHOS as discussed above. mTORC1 promotes glycolysis by regulating Myc expression, as we have found that tuberous sclerosis 1 (Tsc1), a negative regulator of mTOR (Chi, 2012), suppresses glycolytic gene expression and glycolysis in FLT3L-BMDCs through inhibiting Myc expression (Wang et al, 2013)
Summary
Dendritic cells (DCs) are an innate immune cell population with the capacity to process and present antigenic peptides on major histocompatibility complex (MHC) molecules to antigenspecific T cells. GLUCOSE AND MITOCHONDRIAL METABOLISM IN THE FUNCTIONAL REGULATION OF GM-CSF-BMDCs AND cDCs
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