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Corrigendum Open Access | 10.1172/jci.insight.159640

miR–9-5p regulates immunometabolic and epigenetic pathways in β-glucan–trained immunity via IDH3α

Haibo Su, Zhongping Liang, ShuFeng Weng, Chaonan Sun, Jiaxin Huang, TianRan Zhang, Xialian Wang, Shanshan Wu, Zhi Zhang, Yiqi Zhang, Qing Gong, and Ying Xu

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Published March 22, 2022 - More info

Published in Volume 7, Issue 6 on March 22, 2022
JCI Insight. 2022;7(6):e159640. https://doi.org/10.1172/jci.insight.159640.
© 2022 immunometabolic et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published March 22, 2022 - Version history
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miR–9-5p regulates immunometabolic and epigenetic pathways in β-glucan–trained immunity via IDH3α
Haibo Su, … , Qing Gong, Ying Xu
Haibo Su, … , Qing Gong, Ying Xu
Research Article Immunology Inflammation

miR–9-5p regulates immunometabolic and epigenetic pathways in β-glucan–trained immunity via IDH3α

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Abstract

Trained immunity, induced by β-glucan in monocytes, is mediated by activating metabolic pathways that result in epigenetic rewiring of cellular functional programs; however, molecular mechanisms underlying these changes remain unclear. Here, we report a key immunometabolic and epigenetic pathway mediated by the miR–9-5p-isocitrate dehydrogenase 3α (IDH3α) axis in trained immunity. We found that β-glucan–trained miR–9-5p–/– monocytes showed decreased IL-1β, IL-6, and TNF-α production after LPS stimulation. Trained miR–9-5p–/– mice produced decreased levels of proinflammatory cytokines upon rechallenge in vivo and had worse protection against Candida albicans infection. miR–9-5p targeted IDH3α and reduced α-ketoglutarate (α-KG) levels to stabilize HIF-1α, which promoted glycolysis. Accumulating succinate and fumarate via miR–9-5p action integrated immunometabolic circuits to induce histone modifications by inhibiting KDM5 demethylases. β-Glucan–trained monocytes exhibited low IDH3α levels, and IDH3α overexpression blocked the induction of trained immunity by monocytes. Monocytes with IDH3α variants from autosomal recessive retinitis pigmentosa patients showed a trained immunity phenotype at immunometabolic and epigenetic levels. These findings suggest that miR–9-5p and IDH3α act as critical metabolic and epigenetic switches in trained immunity.

Authors

Haibo Su, Zhongping Liang, ShuFeng Weng, Chaonan Sun, Jiaxin Huang, TianRan Zhang, Xialian Wang, Shanshan Wu, Zhi Zhang, Yiqi Zhang, Qing Gong, Ying Xu

×

Original citation: JCI Insight. 2021;6(9):e144260. https://doi.org/10.1172/jci.insight.144260

Citation for this corrigendum: JCI Insight. 2022;7(6):e159640. https://doi.org/10.1172/jci.insight.e159640

Information on data availability was omitted from Methods. The correct information is below.

Data availability

Raw data were deposited in the National Genomics Data Center’s Genome Sequence Archive (GSA CRA005771, CRA005786, HRA001843, and HRA001860).

The authors regret the error.

Footnotes

See the related article at miR–9-5p regulates immunometabolic and epigenetic pathways in β-glucan–trained immunity via IDH3α.

Version history
  • Version 1 (March 22, 2022): Electronic publication

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