ArticleNature communications2023
MAIT cell inhibition promotes liver fibrosis regression via macrophage phenotype reprogramming.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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Who cites it
57 citing papers in PubMed.
- Review
- Single Cell Multi-Omics Revealing the Important Role of MR1 Mediated MAIT Cells in Maintaining Rejection for Liver Transplantation.Cell proliferation · 2026Article
- Mitochondrial Dysfunction in Metabolic-Syndrome-Related MASLD/MASH: Metabolic Mechanisms and Therapeutic Perspectives.Metabolites · 2026Review
- Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026Review
- Depletion of NAT10 in T cells attenuates metabolic dysfunction-associated steatohepatitis in mice.Hepatology communications · 2026Article
- Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation.Journal of translational medicine · 2026Review
- Inflammatory and resolution stages of hepatic injury: imaging with USPIO-enhanced MRI in mice.European radiology experimental · 2026Article
- M2 macrophage-derived apoptotic vesicles alleviate liver fibrosis via miR-1224-5p-mediated inhibition of the SP1/TGF-β pathway in hepatic stellate cells.Journal of nanobiotechnology · 2026Article
- TGFBI promotes liver fibrosis through remodeling the profibrotic microenvironment by a positive feedback regulatory loop.Communications biology · 2026Article
- Mucosal-associated invariant T cells and the gut-kidney axis: a review.Clinical kidney journal · 2026Review
- Multi-Target Intervention of Traditional Chinese Medicine in Metabolic Dysfunction-Associated Steatohepatitis: Comprehensive Treatment Strategies from Lipotoxicity to Immune Regulation.International journal of general medicine · 2026Review
- The immunometabolic nature of MASH: framing immune cells within metabolic dysfunction.Frontiers in immunology · 2026Review
- Protective role of mucosa-associated invariant T cells in sepsis-related liver injury.Frontiers in immunology · 2026Article
- CCL20-CCR6 axis mediates mucosal-associated invariant T-M2 macrophage crosstalk to drive immune dysregulation in liver cirrhosis.Frontiers in immunology · 2026Article
- "From inflammation to fibrosis: a proposed role of mucosal-associated invariant T cells in lichen sclerosus - a conceptual framework".Frontiers in immunology · 2026Review
- Immune cells in liver injury: from pathogenic mechanisms to immunotherapy.Frontiers in immunology · 2026Review
- Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026Review
- Primary Human Tissue Models for Metabolic Dysfunction-Associated Liver Disease - toward Streamlining Drug Discovery with Patient-Derived Assays.Advanced biology · 2025Review
- Mucosal-Associated Invariant T Cells: Origins, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Mechanotransduction in Shaping Immunity: Pathways, Crosstalk, and Pathophysiological Relevance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent data have shown that liver fibrosis can regress even at later stages of cirrhosis and shifting the immune response from pro-inflammatory towards a resolutive profile is considered as a promising option. The immune regulatory networks that govern the shift of the inflammatory phenotype and thus potential reversal of liver fibrosis are lesser known. Here we show that in precision-cut human liver slices obtained from patients with end-stage fibrosis and in mouse models, inhibiting Mucosal-Associated Invariant T (MAIT) cells using pharmacological or antibody-driven approaches, limits fibrosis progression and even regresses fibrosis, following chronic toxic- or non-alcoholic steatohepatitis (NASH)-induced liver injury. Mechanistic studies, combining RNA sequencing, in vivo functional studies (performed in male mice) and co-culture experiments indicate that disruption of the MAIT cell-monocyte/macrophage interaction results in resolution of fibrosis both by increasing the frequency of restorative Ly6C
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