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Riksen, N. P., & Netea, M. G. (2021). Immunometabolic control of trained immunity. Mol. Aspects Med. Added by: Dr. Enrique Feoli (03/02/2021, 01:07) Last edited by: Dr. Enrique Feoli (03/02/2021, 01:14) |
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| Resource type: Journal Article DOI: 10.1016/j.mam.2020.100897 BibTeX citation key: Riksen2021 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Trained immunity Creators: Netea, Riksen Collection: Mol. Aspects Med. |
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| Abstract |
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Innate immune cells can adopt long-term inflammatory phenotypes following brief encounters with exogenous (microbial) or endogenous stimuli. This phenomenon is named trained immunity and can improve host defense against (recurrent) infections. In contrast, trained immunity can also be maladaptive in the context of chronic inflammatory disorders, such as atherosclerosis. Key to future therapeutic exploitation of this mechanism is thorough knowledge of the mechanisms driving trained immunity, which can be used as pharmacological targets. These mechanisms include profound changes in intracellular metabolism, which are closely intertwined with epigenetic reprogramming at the level of histone modifications. Glycolysis, glutamine replenishment of the tricarboxylic acid cycle with accumulation of fumarate, and the mevalonate pathway have all been identified as critical pathways for trained immunity in monocytes and macrophages. In this review, we provide a state-of-the-art overview of how these metabolic pathways interact with epigenetic programs to develop trained immunity.
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| Notes |
Schematic overview of the intracellular mechanisms operating in monocytes/macrophages to build trained immunity. Depicted are the extracellular exogenous and endogenous triggers, the various metabolic pathways that are activated with their most important metabolites, and the bidirectional interaction with epigenetic enzymes in the nucleus.
Schematic representation of the various cell types that are able to build trained immunity or comparable inflammatory memory characteristics, including monocytes, macrophages, myeloid progenitor cells, NK cells, dendritic cells, microglia, endothelial cells, and vascular smooth muscle cells. Trained immunity can either improve host defense against infections or cancer, or be maladaptive in situations of chronic inflammation. Therefore, suppression of trained immunity might be beneficial in situations of chronic inflammatory diseases, such as atherosclerosis, or transplant rejection. On the other hand, boosting trained immunity might improve host defense against infections and might be beneficial in patients with cancer. Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
