ArticleFrontiers in immunology2019
Dendritic Cells Require PINK1-Mediated Phosphorylation of BCKDE1α to Promote Fatty Acid Oxidation for Immune Function.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 48 citations in OpenAlex.
- Glycolysis in the tumor microenvironment shapes dendritic cell function and antitumor immunity.Frontiers in immunology · 2026Review
- PINK1 dysfunction in hepatocellular carcinoma fosters immune evasion and disease progression by promoting neutrophil infiltration.Journal for immunotherapy of cancer · 2025Article
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- Regulation of dendritic cell biology by amino acids and their transporters.Frontiers in immunology · 2025Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- AMPK activation induces RALDH+ tolerogenic dendritic cells by rewiring glucose and lipid metabolism.The Journal of cell biology · 2024Article
- Article
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- PTEN-induced putative kinase 1 regulates mitochondrial quality control and is essential for the maturation of human induced pluripotent stem cell-derived cardiomyocytes.Genes & diseases · 2023Article
- Quantitative proteomic and phosphoproteomic analysis reveal the relationship between mitochondrial dysfunction and cytoskeletal remodeling in hiPSC-CMs deficient in PINK1.Journal of translational medicine · 2023Article
- Lipid metabolism in dendritic cell biology.Immunological reviews · 2023Review
- Immunometabolic reprogramming, another cancer hallmark.Frontiers in immunology · 2023Review
- Metabolic regulation of dendritic cell activation and immune function during inflammation.Frontiers in immunology · 2023Review
- Pathological and protective roles of dendritic cells inFrontiers in cellular and infection microbiology · 2022Review
- Fa(c)t checking: How fatty acids shape metabolism and function of macrophages and dendritic cells.European journal of immunology · 2021Review
- Article
- Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-GlcNAcylation, Acetyl-CoA and Melatonergic Pathway in Regulating Dynamic Metabolic Interactions across Cell Types-Tumour Microenvironment and Metabolism.International journal of molecular sciences · 2020Review
- Pan-Cancer Analysis of the Mitophagy-Related Protein PINK1 as a Biomarker for the Immunological and Prognostic Role.Frontiers in oncology · 2020Article
- Shaping of Dendritic Cell Function by the Metabolic Micro-Environment.Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cell (DCs) activation by Toll-like receptor (TLR) agonist induces robust metabolic rewiring toward glycolysis. Recent findings in the field identified mechanistic details governing these metabolic adaptations. However, it is unknown whether a switch to glycolysis from oxidative phosphorylation (OXPHOS) is a general characteristic of DCs upon pathogen encounter. Here we show that engagement of different TLR triggers differential metabolic adaptations in DCs. We demonstrate that LPS-mediated TLR4 stimulation induces glycolysis in DCs. Conversely, activation of TLR7/8 with protamine-RNA complex, pRNA, leads to an increase in OXPHOS. Mechanistically, we found that pRNA stimulation phosphorylates BCKDE1α in a PINK1-dependent manner. pRNA stimulation increased branched-chain amino acid levels and increased fatty acid oxidation. Increased FAO and OXPHOS are required for DC activation. PINK1 deficient DCs switch to glycolysis to maintain ATP levels and viability. Moreover, pharmacological induction of PINK1 kinase activity primed immunosuppressive DC for immunostimulatory function. Our findings provide novel insight into differential metabolic adaptations and reveal the important role of branched-chain amino acid in regulating immune response in DC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.