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Toll-like receptor stimulation reprograms metabolism in human dendritic cells (DCs). Plasmacytoid DCs utilize glutaminolysis for oxidative phosphorylation, while myeloid DCs rely on glycolysis via mitophagy for activation.

Keywords:
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Area of Science:

  • Immunology
  • Cell Biology
  • Metabolic pathways

Background:

  • Toll-like receptor (TLR) agonists are crucial for immune activation, requiring significant metabolic reprogramming.
  • Understanding metabolic adaptation in distinct human dendritic cell (DC) subsets upon TLR stimulation is essential for elucidating immune responses.

Purpose of the Study:

  • To investigate the distinct mechanisms regulating metabolic adaptation in human blood DC subsets (CD1c+ myeloid DCs and plasmacytoid DCs) following TLR stimulation.
  • To determine the role of mitochondrial dynamics and specific metabolic pathways in DC activation.

Main Methods:

  • Analysis of gene expression related to oxidative phosphorylation and glutamine metabolism in DCs.
  • Assessment of mitochondrial content, intracellular glutamine levels, and autophagy.
  • Investigation of mitophagy, glycolysis, and mitochondrial fusion/fragmentation dynamics.
  • Functional assays measuring DC activation upon inhibition of specific metabolic pathways.

Main Results:

  • TLR stimulation upregulated oxidative phosphorylation and glutamine metabolism in plasmacytoid DCs (pDCs) in an autophagy-dependent manner, increasing mitochondrial content.
  • TLR-induced glutaminolysis fueled oxidative phosphorylation, and its inhibition prevented pDC activation.
  • Conversely, TLR stimulation decreased mitochondrial content and oxidative phosphorylation while inducing glycolysis in CD1c+ myeloid DCs (mDCs).
  • BNIP3-dependent mitophagy was triggered in mDCs, regulating AMPKα1 activity and facilitating glycolysis and activation.

Conclusions:

  • TLR stimulation differentially regulates mitochondrial dynamics and metabolic pathways in distinct human DC subsets.
  • Plasmacytoid DCs rely on autophagy-driven glutaminolysis to fuel oxidative phosphorylation for activation.
  • CD1c+ myeloid DCs utilize BNIP3-dependent mitophagy to induce glycolysis and subsequent activation.