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Human Dendritic Cell Subsets Undergo Distinct Metabolic Reprogramming for Immune Response

Basit, Farhan ; Mathan, Till ; Sancho, David ; de Vries, I Jolanda M

Frontiers in immunology, 2018-11, Vol.9, p.2489-2489 [Periódico revisado por pares]

Switzerland: Frontiers Research Foundation

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  • Título:
    Human Dendritic Cell Subsets Undergo Distinct Metabolic Reprogramming for Immune Response
  • Autor: Basit, Farhan ; Mathan, Till ; Sancho, David ; de Vries, I Jolanda M
  • Assuntos: CD1c+ mDC ; Dendritic cells ; Glutamine metabolism ; glutaminolysis ; Immune response ; Immunology ; mitochondrial dynamics ; mitophagy ; OXPHOS ; pDC ; Toll-like receptors
  • É parte de: Frontiers in immunology, 2018-11, Vol.9, p.2489-2489
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
    Reviewed by: Duojiao Wu, Fudan University, China; Eyal Amiel, University of Vermont, United States; Johan Garaude, INSERM U1211-Rares Diseases Genetics and Metabolism, France
    This article was submitted to Antigen Presenting Cell Biology, a section of the journal Frontiers in Immunology
    Edited by: Bart Everts, Leiden University Medical Center, Netherlands
  • Descrição: Toll-like receptor (TLR) agonists induce metabolic reprogramming, which is required for immune activation. We have investigated mechanisms that regulate metabolic adaptation upon TLR-stimulation in human blood DC subsets, CD1c myeloid DCs (mDCs) and plasmacytoid DCs (pDCs). We show that TLR-stimulation changes expression of genes regulating oxidative phosphorylation (OXPHOS) and glutamine metabolism in pDC. TLR-stimulation increases mitochondrial content and intracellular glutamine in an autophagy-dependent manner in pDC. TLR-induced glutaminolysis fuels OXPHOS in pDCs. Notably, inhibition of glutaminolysis and OXPHOS prevents pDC activation. Conversely, TLR-stimulation reduces mitochondrial content, OXPHOS activity and induces glycolysis in CD1c mDC. Inhibition of mitochondrial fragmentation or promotion of mitochondrial fusion impairs TLR-stimulation induced glycolysis and activation of CD1c mDCs. TLR-stimulation triggers BNIP3-dependent mitophagy, which regulates transcriptional activity of α . BNIP3-dependent mitophagy is required for induction of glycolysis and activation of CD1c mDCs. Our findings reveal that TLR stimulation differentially regulates mitochondrial dynamics in distinct human DC subsets, which contributes to their activation.
  • Editor: Switzerland: Frontiers Research Foundation
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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