Immunometabolism governs dendritic cell and macrophage function
By Luke A. O'Neill, Edward J. Pearce. Journal of Experimental Medicine, 2016
1,528 citations recorded by the source corpus.
In this review, O’Neill and Pearce discuss recent intriguing findings on metabolic changes regulating the function of macrophages and dendritic cells.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/c434e9fa202337341adfa86caf0c8135518028de
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Citations in the corpus
- Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “IL-2-induced ACLY phosphorylation and ACLY activation are required for T-cell proliferation, and inhibition of ACLY by SB204990 induces G1/S cell cycle arrest and suppresses the accumulation of histone acetylation levels in IL-2-treated T cells (Osinalde et al., 2016).”
- Glutamine: Metabolism and Immune Function, Supplementation and Clinical Translation (2018, background): “Due to this mechanism, M1 macrophages exhibit a quick increase in ATP formation that is required for the host defence response [113,118,119].”
- Macrophage Polarization. (2017, background): “METABOLISM AND MACROPHAGE POLARIZATION Biochemical pathway regulation and output are integral to polarization (87, 88).”
- CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer. (2019, background): “Tumor growth is typically supported by aerobic glycolysis, the same metabolic lifestyle used by efficient Teff cells (100, 113, 114).”
- Dendritic Cells and Cancer Immunity (2016, background): “Metabolic reprograming within DCs themselves is also important during TLR-mediated activation and could mediate dysfunction within tumors [62], as was recently demonstrated for activation of the ER stress response factor XBP1 and the ensuing accumulation of intracellular lipids [63].”
- Phagocytosis: An Immunobiologic Process. (2016, background): “However, topics of historic interest, such as the metabolic aspects of phagocytosis, should be integrated with current metabolomics (O’Neill and Pearce, 2016), and we still lack knowledge of the Immunity 44, March 15, 2016 ª2016 Elsevier Inc. 471 relationships between mononuclear phagocytes and…”
- Repurposing mitochondria from ATP production to ROS generation drives a pro-inflammatory phenotype in macrophages that depends on succinate oxidation by complex II (2016, background): “A hallmark of the pro-inflammatory phenotype of macrophages is their switch away from ATP production by oxidative phosphorylation to glycolytic metabolism (O’Neill and Pearce, 2016; Tannahill et al., 2013).”