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. 2023 Jan 16;9:9. doi: 10.1038/s41420-023-01310-7

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© The Author(s) 2023

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 — This regulatory effect is controlled by many factors. For example, IL-33 binds to ST receptors on the Treg surface to promote IL-13 secretion, which subsequently induces apoptosis of alveolar macrophages and prevents further inflammation. On the other hand, netrin 1 and kynurenine both promote M2 macrophage polarization. Netrin 1 binds to A2b receptors on Tregs to induce IL-10 secretion. Kynurenine binds to AHRs and modulates transcription in Tregs, increasing the production of IL-8. Furthermore, the production of IFNγ, which inhibits M2 polarization, is inhibited by Tregs. As a result, Tregs can both prevent injury and promote tissue repair by regulating macrophage function. Kyn kynurenine, IFNγ interferon γ, IL interleukin, SREBP1 sterol regulatory element binding protein 1.