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. 2022 May 31;44(4):429–444. doi: 10.1007/s00281-022-00949-1

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© The Author(s) 2022, corrected publication 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — MAIT cells’ fibrogenic potential and their role in liver homeostasis and tissue repair. MAIT cells can be triggered via their TCR and/or cytokine receptors. The mode of MAIT cell activation influences their impact on fibrogenesis. TCR activation leads to the secretion of anti-fibrotic effector molecules, including IL-22 and IFN-γ; both cytokines have been shown to inhibit HSC activation. TCR-triggered MAIT cells were also shown to produce proteins involved in tissue repair. Inflammatory cytokine-dependent activation drives a strong secretion of fibrogenic cytokines. IL-7, generated by hepatocytes under inflammatory conditions, twists MAIT cells towards IL-17 secretion, while IL-18/IL-12, produced by myeloid cells, orchestrates a strong TNF/IFN-γ response. The presence of TNF and IL-17 further promotes the secretion of pro-inflammatory cytokines IL-6 and IL-8 by macrophages and hepatic stellate cells (HCSs)/hepatic myofibroblasts (HMFs). This cytokine milieu will stimulate the secretion of collagen and tissue inhibitor of metalloproteinases 1 (TIMP1) by activated myofibroblasts. In addition, evidence is accumulating towards a role of TL1A in the secretion of TNF by MAIT cells and also in liver fibrogenesis. Finally, in presence of pro-inflammatory conditions, MAIT cells can secrete IL-26, recently shown to activate HSCs. See text for references