ArticleNature communications2017
The microbiota maintain homeostasis of liver-resident γδT-17 cells in a lipid antigen/CD1d-dependent manner.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 189 citations in OpenAlex.
- Gut microbiota-driven IL-17A production by hepatic γδ T cells enhances neutrophil defense against systemicVirulence · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Incretin and Glucagon Signalling in MASLD and MASH: Integrating Metabolic Pathways With Disease Progression.Diabetes, obesity & metabolism · 2026Review
- Multi-omics integration reveals ANXA6-high γδ T cell-endothelial communication as a potential link between periodontitis and MASLD.NPJ systems biology and applications · 2026Article
- Regulatory T cells safeguard liver health during metabolic-associated steatohepatitis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Gut microbiota-derived metabolites and host interactions in fibrotic diseases: mechanisms, cross-organ signatures, and therapeutic opportunities.Frontiers in microbiology · 2026Review
- Modulation of Inflammation-Driven Hepatocarcinogenesis: The Hepatic Immune Microenvironment, Gut-Liver Axis, and Neuroregulation.Journal of hepatocellular carcinoma · 2026Review
- γδ T cell receptor recognition of CD1d in a lipid-independent manner.Nature communications · 2025Article
- Dual roles of T cells in metabolic dysfunction-associated steatohepatitis pathogenesis and liver fibrosis: From inflammation to therapeutic targets.Hepatology communications · 2025Review
- Roles of short-chain fatty acids in metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated steatohepatitis.World journal of hepatology · 2025Review
- Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025Review
- Cannabinoid-2 receptor depletion promotes non-alcoholic fatty liver disease in mice via disturbing gut microbiota and tryptophan metabolism.Acta pharmacologica Sinica · 2025Article
- Identification of potential metabolic biomarkers and immune cell infiltration for metabolic associated steatohepatitis by bioinformatics analysis and machine learning.Scientific reports · 2025Article
- Article
- Chronic hepatitis B virus infection imbalances short-chain fatty acids and amino acids in the liver and gut via microbiota modulation.Gut pathogens · 2025Article
- Diverse Subsets of γδT Cells and Their Specific Functions Across Liver Diseases.International journal of molecular sciences · 2025Review
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- Early-life homeostatic differentiation of thymus-resident B cells into memory B cells.Frontiers in immunology · 2025Article
- Unveiling the gut-liver axis: the behind-the-scenes "manipulator" of human immune function.Frontiers in immunology · 2025Review
- Identification of regulatory cell death-related genes during MASH progression using bioinformatics analysis and machine learning strategies.Frontiers in immunology · 2025Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microbiota control regional immunity using mechanisms such as inducing IL-17A-producing γδ T (γδT-17) cells in various tissues. However, little is known regarding hepatic γδT cells that are constantly stimulated by gut commensal microbes. Here we show hepatic γδT cells are liver-resident cells and predominant producers of IL-17A. The microbiota sustain hepatic γδT-17 cell homeostasis, including activation, survival and proliferation. The global commensal quantity affects the number of liver-resident γδT-17 cells; indeed, E. coli alone can generate γδT-17 cells in a dose-dependent manner. Liver-resident γδT-17 cell homeostasis depends on hepatocyte-expressed CD1d, that present lipid antigen, but not Toll-like receptors or IL-1/IL-23 receptor signalling. Supplementing mice in vivo or loading hepatocytes in vitro with exogenous commensal lipid antigens augments the hepatic γδT-17 cell number. Moreover, the microbiota accelerate nonalcoholic fatty liver disease through hepatic γδT-17 cells. Thus, our work describes a unique liver-resident γδT-17 cell subset maintained by gut commensal microbes through CD1d/lipid antigens.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.