ArticleHepatology (Baltimore, Md.)2010
Accumulation of natural killer T cells in progressive nonalcoholic fatty liver disease.
Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 1 of them a synthesis that pooled it.
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Who cites it
175 citing papers in PubMed, 1 synthesis or guideline pooled it, 275 citations in OpenAlex.
- Prevalence and Significance of Antinuclear Antibodies in Biopsy-Proven Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis.Disease markers · 2022Pooled it
- Circulating microparticles as disease-specific biomarkers of severity of inflammation in patients with hepatitis C or nonalcoholic steatohepatitis.Gastroenterology · 2012Trial
- When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH.Inflammation · 2026Review
- The immunometabolic nature of MASH: framing immune cells within metabolic dysfunction.Frontiers in immunology · 2026Review
- Modulation of Inflammation-Driven Hepatocarcinogenesis: The Hepatic Immune Microenvironment, Gut-Liver Axis, and Neuroregulation.Journal of hepatocellular carcinoma · 2026Review
- Paired snRNA-seq and scRNA-seq analysis of MASLD patients to identify early-stage markers for disease progression.Hepatology communications · 2025Article
- Article
- Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025Review
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Comprehensive profiling of candidate biomarkers and immune infiltration landscape in metabolic dysfunction-associated steatohepatitis.Metabolism open · 2025Article
- Immune cells in metabolic associated fatty liver disease: Global trends and hotspots (2004-2024).World journal of hepatology · 2025Article
- Coinfection with HIV-1 skews iNKT cells toward TCR anergy and limited expansion potential in people with hepatitis C.Frontiers in immunology · 2025Article
- Association of antinuclear antibody positivity with liver disease severity in pediatric metabolic dysfunction-associated steatotic liver disease.Frontiers in pediatrics · 2025Article
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- Evaluation of autoimmune phenomena in patients with nonalcoholic fatty liver disease on the basis of liver pathology.World journal of hepatology · 2024Article
- Role of gut microbiota and immune cells in metabolic-associated fatty liver disease: clinical impact.Hepatology international · 2024Review
- Innate Immunity and MASLD.Biomolecules · 2024Review
- Linking fatty liver diseases to hepatocellular carcinoma by hepatic stellate cells.Journal of the National Cancer Center · 2024Review
- Causal associations of immunophenotypes with metabolic dysfunction-associated fatty liver disease and mediating pathways: a Mendelian randomization study.Therapeutic advances in chronic disease · 2024Article
- Active role of the immune system in metabolic dysfunction-associated steatotic liver disease.Gastroenterology report · 2024Review
115 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
Abstract
unlabelledLiver inflammation is greater in nonalcoholic steatohepatitis (NASH) than steatosis, suggesting that immune responses contribute to nonalcoholic fatty liver disease (NAFLD) progression. Livers normally contain many natural killer T (NKT) cells that produce factors that modulate inflammatory and fibrogenic responses. Such cells are relatively depleted in steatosis, but their status in more advanced NAFLD is uncertain. We hypothesized that NKT cells accumulate and promote fibrosis progression in NASH. We aimed to determine if livers become enriched with NKT cells during NASH-related fibrosis; identify responsible mechanisms; and assess if NKT cells stimulate fibrogenesis. NKT cells were analyzed in wildtype mice and Patched-deficient (Ptc(+/-)) mice with an overly active Hedgehog (Hh) pathway, before and after feeding methionine choline-deficient (MCD) diets to induce NASH-related fibrosis. Effects of NKT cell-derived factors on hepatic stellate cells (HSC) were examined and fibrogenesis was evaluated in CD1d-deficient mice that lack NKT cells. NKT cells were quantified in human cirrhotic and nondiseased livers. During NASH-related fibrogenesis in wildtype mice, Hh pathway activation occurred, leading to induction of factors that promoted NKT cell recruitment, retention, and viability, plus liver enrichment with NKT cells. Ptc(+/-) mice accumulated more NKT cells and developed worse liver fibrosis; CD1d-deficient mice that lack NKT cells were protected from fibrosis. NKT cell-conditioned medium stimulated HSC to become myofibroblastic. Liver explants were 2-fold enriched with NKT cells in patients with non-NASH cirrhosis, and 4-fold enriched in patients with NASH cirrhosis.
conclusionHh pathway activation leads to hepatic enrichment with NKT cells that contribute to fibrosis progression in NASH.
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Registered trials
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.