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. 2023 Feb 9;9:53. doi: 10.1038/s41420-023-01347-8

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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. 2 — IL-2 as well as its complexes accelerate Tregs expressing CD39 in the liver, thereby inhibiting the multiplication of CD8⁺ T cells and its function of generating TNF-α and osteopontin, which can reduce biliary fibrosis. Tregs can regulate the pro-fibrotic roles of Th2 cells and Ly-6C^highCCR2^high inflammatory monocytes/macrophages that secrete IL-4 and TGF-β respectively, interestingly, IL-10 secreted by Tregs may regulate them. Tregs can regulate the TGF-β-IDO signalling pathway to enhance the function of hAMSC that repress liver fibrosis. Tregs promoting the expression of amphiregulin can inhibit the development of fibrosis by promoting the proliferation of hepatocytes. In CCL4-induced liver fibrosis, rapamycin has an effective protective effect on the liver. Rapamycin significantly increased the functional activity of CD4⁺CD25⁺ Tregs and enhanced the inhibitory ability of Tregs on HSCs activation. Tregs can repress MCP-1 which plays an important role in liver fibrosis by activating HSC production. Tregs can directly repress CD4⁺ T cell expression that reduces IFN-γ activated HSCs. Tregs also directly promote amphiregulin to repress liver fibrosis. Footnote: interleukin (IL), regulatory cells (Treg), transforming growth factor-α (TGF-α), T helper cell (Th), indoleamine 2,3-dioxygenase (IDO), human amniotic mesenchymal stromal cell (hAMSC), carbon tetrachloride(CCL4), hepatic stellate cells (HSCs), monocyte chemotactic protein-1 (MCP-1), Interferon-γ (IFN-γ).