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. 2020 Mar 4;30(4):300–314. doi: 10.1038/s41422-020-0291-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — By modulating various metabolic pathways of proinflammatory immune cells we can promote a more anti-inflammatory phenotype. Small molecules such as DMM, TEPP-46, Rapamycin, 2DG, DMF and Hyaluronic acid all promote the development of anti-inflammatory Treg cells and M2 macrophages, whilst suppressing differentiation of the more inflammatory Th17 cells and M1 macrophages, which most likely contributes to the efficacious outcomes when using these in models of inflammatory disease.