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Human Dendritic Cell Subsets Undergo Distinct Metabolic Reprogramming for Immune Response

Frontiers in immunology, 2018-11, Vol.9, p.2489-2489 [Tạp chí có phản biện]

COPYRIGHT 2018 Frontiers Research Foundation ;Copyright © 2018 Basit, Mathan, Sancho and de Vries. 2018 Basit, Mathan, Sancho and de Vries ;ISSN: 1664-3224 ;EISSN: 1664-3224 ;DOI: 10.3389/fimmu.2018.02489 ;PMID: 30455688

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  • Nhan đề:
    Human Dendritic Cell Subsets Undergo Distinct Metabolic Reprogramming for Immune Response
  • Tác giả: Basit, Farhan ; Mathan, Till ; Sancho, David ; de Vries, I Jolanda M
  • Chủ đề: CD1c+ mDC ; Dendritic cells ; Glutamine metabolism ; glutaminolysis ; Immune response ; Immunology ; mitochondrial dynamics ; mitophagy ; OXPHOS ; pDC ; Toll-like receptors
  • Là 1 phần của: Frontiers in immunology, 2018-11, Vol.9, p.2489-2489
  • Mô tả: 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.
  • Nơi xuất bản: Switzerland: Frontiers Research Foundation
  • Ngôn ngữ: English
  • Số nhận dạng: ISSN: 1664-3224
    EISSN: 1664-3224
    DOI: 10.3389/fimmu.2018.02489
    PMID: 30455688
  • Nguồn: Open Access: DOAJ Directory of Open Access Journals
    Freely Accessible Journals
    Open Access: PubMed Central
    ROAD: Directory of Open Access Scholarly Resources
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