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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. 1 — Liver fibrosis is primarily induced by HSCs that promote TGF-β based production of myofibroblasts that stimulate ECM-driven fibrogenesis. Tregs can also activate HSCs to promote fibrosis through the TGF-β pathway. Treg can induce HSCs via the expression of IL-8. Treg cells with CD4⁺CD25⁺Foxp3⁺ can be selectively expanded by HSCs in an IL-2–dependent pattern. Tregs can directly suppress NK cells from degranulating in the role of IL-8, TGF-β1, and CTLA-4 signalling pathways. Footnote: hepatic stellate cells (HSCs), transforming growth factor-β (TGF-β), extracellular matrix (ECM), matrix metalloproteinase (MMP), regulatory cells (Treg), kupffer call (KC), interleukin-2 (IL-2), natural killer cell (NK cell), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4).