期刊
CELL REPORTS
卷 31, 期 3, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2020.107548
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资金
- European Research Council (ERC) [833247]
- Spinoza grant of the Netherlands Organisation for Scientific Research
- European Research Area Cardiovascular Disease (ERA-CVD) - Dutch Heart Foundation (JTC2018, project MEMORY) [2018T093]
- European Union Horizon 2020 Research and Innovation Program [667837]
- INCONTROL grant from the Heart Foundation Netherlands [CVON2012-03, CVON2018-27]
- Competitiveness Operational Programme grant of the Romanian Ministry of European Funds (HINT) [P_37_762, MySMIS 103587]
- Radboud University Medical Center Hypatia Grant
- VENI grant from the Netherlands Organisation for Scientific Research (NWO) [016.176.006]
- European Union's Seventh Framework Programme (FP7/2007-2013) [282510 BLUEPRINT]
Trained immunity confers a sustained augmented response of innate immune cells to a secondary challenge, via a process dependent on metabolic and transcriptional reprogramming. Because of its previous associations with metabolic and transcriptional memory, as well as the importance of H3 histone lysine 4 monomethylation (H3K4me1) to innate immune memory, we hypothesize that the Set7 methyltransferase has an important role in trained immunity induced by beta-glucan. Using pharmacological studies of human primary monocytes, we identify trained immunity-specific immunometabolic pathways regulated by Set7, including a previously unreported H3K4me1-dependent plasticity in the induction of oxidative phosphorylation. Recapitulation of beta-glucan training in vivo additionally identifies Set7-dependent changes in gene expression previously associated with the modulation of myelopoiesis progenitors in trained immunity. By revealing Set7 as a key regulator of trained immunity, these findings provide mechanistic insight into sustained meta- bolic changes and underscore the importance of characterizing regulatory circuits of innate immune memory.
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