ArticleScientific reports2016
Enterogenous bacterial glycolipids are required for the generation of natural killer T cells mediated liver injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
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- The landscape of gut microbiota in hepatocarcinogenesis: a comprehensive review of pathogenesis and therapeutic interventions.International journal of surgery (London, England) · 2026Review
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- Transcriptomic and lipidomic analysis of aging-associated inflammatory signature in mouse liver.Inflammation and regeneration · 2025Article
- Invariant Natural Killer T lymphocytes as natural sensors for microbes: a two-edged sword in liver diseases.Frontiers in immunology · 2025Review
- Berberine alleviates concanavalin A-induced autoimmune hepatitis in mice by modulating the gut microbiota.Hepatology communications · 2024Article
- The significance of gut microbiota in the etiology of autoimmune hepatitis: a narrative review.Frontiers in cellular and infection microbiology · 2024Review
- CSF-1R+ Macrophages Control the Gut Microbiome-Enhanced Liver Invariant NKT Function through IL-18.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Immune modulation of gut microbiota and its metabolites in chronic hepatitis B.Frontiers in microbiology · 2023Review
- Opposing Roles of DCs and iNKT Cells in the Induction of Foxp3 Expression by MLN CD25International journal of molecular sciences · 2022Article
- Multi-Omics Analysis Reveals the Protection of Gasdermin D in Concanavalin A-Induced Autoimmune Hepatitis.Microbiology spectrum · 2022Article
- Role of Intestinal Microbes in Chronic Liver Diseases.International journal of molecular sciences · 2022Review
- Tet2 deficiency drives liver microbiome dysbiosis triggering Tc1 cell autoimmune hepatitis.Cell host & microbe · 2022Article
- The Gut Microbiota: A Novel Player in Autoimmune Hepatitis.Frontiers in cellular and infection microbiology · 2022Review
- Extrahepatic factors in hepatic immune regulation.Frontiers in immunology · 2022Review
- Repeated α-GalCer Administration Induces a Type 2 Cytokine-Biased iNKT Cell Response and Exacerbates Atopic Skin Inflammation in Vα14Biomedicines · 2021Article
- Intestinal Permeability Is a Mechanical Rheostat in the Pathogenesis of Liver Cirrhosis.International journal of molecular sciences · 2021Review
- Fecal Microbiota Transplantation Controls Progression of Experimental Autoimmune Hepatitis in Mice by Modulating the TFR/TFH Immune Imbalance and Intestinal Microbiota Composition.Frontiers in immunology · 2021Article
- Gut Microbiota and Chemical-Induced Acute Liver Injury.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycolipids are potent activator of natural killer T (NKT) cells. The relationship between NKT cells and intestinal bacterial glycolipids in liver disorders remained unclear. We found that, in sharp contrast to specific pathogen-free (SPF) mice, germ-free (GF) mice are resistant to Concanavalin A (ConA)-induced liver injury. ConA treatment failed to trigger the activation of hepatic NKT cells in GF mice. These defects correlated with the sharply reduced levels of CD1d-presented glycolipid antigens in ConA-treated GF mice compared with SPF counterparts. Nevertheless, CD1d expression was similar between these two kinds of mice. The absence of intestinal bacteria did not affect the incidence of αGalCer-induced liver injury in GF mice. Importantly, we found the intestinal bacteria contain glycolipids which can be presented by CD1d and recognized by NKT cells. Furthermore, supplement of killed intestinal bacteria was able to restore ConA-mediated NKT cell activation and liver injury in GF mice. Our results suggest that glycolipid antigens derived from intestinal commensal bacteria are important hepatic NKT cell agonist and these antigens are required for the activation of NKT cells during ConA-induced liver injury. These finding provide a mechanistic explanation for the capacity of intestinal microflora to control liver inflammation.
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