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Review Series 10.1172/JCI124613

Immunometabolism of pro-repair cells

Benjamin D. Singer and Navdeep S. Chandel

Division of Pulmonary and Critical Care Medicine, Department of Biochemistry and Molecular Genetics, and Simpson Querrey Center for Epigenetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.

Address correspondence to: Navdeep S. Chandel, Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, 240 E. Huron Street, McGaw Pavilion, M-300, Chicago, Illinois 60611, USA. Phone: 312.503.2549; Email: nav@northwestern.edu.

Find articles by Singer, B. in: JCI | PubMed | Google Scholar |

Division of Pulmonary and Critical Care Medicine, Department of Biochemistry and Molecular Genetics, and Simpson Querrey Center for Epigenetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.

Address correspondence to: Navdeep S. Chandel, Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, 240 E. Huron Street, McGaw Pavilion, M-300, Chicago, Illinois 60611, USA. Phone: 312.503.2549; Email: nav@northwestern.edu.

Find articles by Chandel, N. in: JCI | PubMed | Google Scholar |

First published May 13, 2019 - More info

Published in Volume 129, Issue 7 on July 1, 2019
J Clin Invest. 2019;129(7):2597–2607. https://doi.org/10.1172/JCI124613.
© 2019 American Society for Clinical Investigation
First published May 13, 2019 - Version history

Immune cell populations determine the balance between ongoing damage and repair following tissue injury. Cells responding to a tissue-damaged environment have significant bioenergetic and biosynthetic needs. In addition to supporting these needs, metabolic pathways govern the function of pro-repair immune cells, including regulatory T cells and tissue macrophages. In this Review, we explore how specific features of the tissue-damaged environment such as hypoxia, oxidative stress, and nutrient depletion serve as metabolic cues to promote or impair the reparative functions of immune cell populations. Hypoxia, mitochondrial DNA stress, and altered redox balance each contribute to mechanisms regulating the response to tissue damage. For example, hypoxia induces changes in regulatory T cell and macrophage metabolic profiles, including generation of 2-hydroxyglutarate, which inhibits demethylase reactions to modulate cell fate and function. Reactive oxygen species abundant in oxidative environments cause damage to mitochondrial DNA, initiating signaling pathways that likewise control pro-repair cell function. Nutrient depletion following tissue damage also affects pro-repair cell function through metabolic signaling pathways, specifically those sensitive to the redox state of the cell. The study of immunometabolism as an immediate sensor and regulator of the tissue-damaged environment provides opportunities to consider mechanisms that facilitate healthy repair of tissue injury.

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