Review Series 10.1172/JCI124619
1Immunology and Metabolism, LIMES Institute, University of Bonn, Bonn, Germany.
2Platform for Single Cell Genomics and Epigenomics at the German Center for Neurodegenerative Diseases and the University of Bonn, Bonn, Germany.
3Genomics and Immunoregulation, LIMES Institute, University of Bonn, Bonn, Germany.
Address correspondence to: Katarzyna Placek, Joachim L. Schultze, or Anna C. Aschenbrenner, LIMES Institut, Carl-Troll-Straße 31, 53115 Bonn, Germany. Phone: 49.228.73.62742; Email: kplacek@uni-bonn.de (KP). Phone: 49.228.73.62787; Email: j.schultze@uni-bonn.de (JLS). Phone: 49.228.73.62792; Email: a.aschenbrenner@uni-bonn.de (ACA).
Authorship note: All authors contributed equally to this work.
Find articles by Placek, K. in: JCI | PubMed | Google Scholar
1Immunology and Metabolism, LIMES Institute, University of Bonn, Bonn, Germany.
2Platform for Single Cell Genomics and Epigenomics at the German Center for Neurodegenerative Diseases and the University of Bonn, Bonn, Germany.
3Genomics and Immunoregulation, LIMES Institute, University of Bonn, Bonn, Germany.
Address correspondence to: Katarzyna Placek, Joachim L. Schultze, or Anna C. Aschenbrenner, LIMES Institut, Carl-Troll-Straße 31, 53115 Bonn, Germany. Phone: 49.228.73.62742; Email: kplacek@uni-bonn.de (KP). Phone: 49.228.73.62787; Email: j.schultze@uni-bonn.de (JLS). Phone: 49.228.73.62792; Email: a.aschenbrenner@uni-bonn.de (ACA).
Authorship note: All authors contributed equally to this work.
Find articles by Schultze, J. in: JCI | PubMed | Google Scholar
1Immunology and Metabolism, LIMES Institute, University of Bonn, Bonn, Germany.
2Platform for Single Cell Genomics and Epigenomics at the German Center for Neurodegenerative Diseases and the University of Bonn, Bonn, Germany.
3Genomics and Immunoregulation, LIMES Institute, University of Bonn, Bonn, Germany.
Address correspondence to: Katarzyna Placek, Joachim L. Schultze, or Anna C. Aschenbrenner, LIMES Institut, Carl-Troll-Straße 31, 53115 Bonn, Germany. Phone: 49.228.73.62742; Email: kplacek@uni-bonn.de (KP). Phone: 49.228.73.62787; Email: j.schultze@uni-bonn.de (JLS). Phone: 49.228.73.62792; Email: a.aschenbrenner@uni-bonn.de (ACA).
Authorship note: All authors contributed equally to this work.
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Aschenbrenner, A.
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First published July 22, 2019 - More info
Immune cells are pivotal in the reaction to injury, whereupon, under ideal conditions, repair and resolution phases restore homeostasis following initial acute inflammation. Immune cell activation and reprogramming require transcriptional changes that can only be initiated if epigenetic alterations occur. Recently, accelerated deciphering of epigenetic mechanisms has extended knowledge of epigenetic regulation, including long-distance chromatin remodeling, DNA methylation, posttranslational histone modifications, and involvement of small and long noncoding RNAs. Epigenetic changes have been linked to aspects of immune cell development, activation, and differentiation. Furthermore, genome-wide epigenetic landscapes have been established for some immune cells, including tissue-resident macrophages, and blood-derived cells including T cells. The epigenetic mechanisms underlying developmental steps from hematopoietic stem cells to fully differentiated immune cells led to development of epigenetic technologies and insights into general rules of epigenetic regulation. Compared with more advanced research areas, epigenetic reprogramming of immune cells in injury remains in its infancy. While the early epigenetic mechanisms supporting activation of the immune response to injury have been studied, less is known about resolution and repair phases and cell type–specific changes. We review prominent recent findings concerning injury-mediated epigenetic reprogramming, particularly in stroke and myocardial infarction. Lastly, we illustrate how single-cell technologies will be crucial to understanding epigenetic reprogramming in the complex sequential processes following injury.
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