ArticleHepatology (Baltimore, Md.)2016
NKp46(+) natural killer cells attenuate metabolism-induced hepatic fibrosis by regulating macrophage activation in mice.
Article in Hepatology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
What it found
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Who cites it
94 citing papers in PubMed, 133 citations in OpenAlex.
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- Unconventional functions of natural killer cells in homeostasis and disease.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- The dual roles of natural killer cells in liver immunity and tolerance: Implications for health and disease.Hepatology communications · 2026Review
- CD36 aggravates ferroptosis in NK cells and dampens their anti-fibrotic activity in the liver.Frontiers in immunology · 2026Article
- Immune System and Hepatic Stellate Cells' Crosstalk in Liver Fibrosis: Pathways and Therapeutic Potential.Journal of immunology research · 2026Review
- Role of miRNA signalling in the pathogenesis of MASLD.Frontiers in pharmacology · 2026Review
- TIGIT impairs NK cell antifibrotic activity through the IFNγ-IFI30 axis in schistosomiasis-induced liver fibrosis.Frontiers in immunology · 2026Article
- Interleukin-18 binding protein protects against metabolic steatohepatitis.Hepatology communications · 2025Article
- From model to man: Understanding Tregs' dual role in MASLD.JHEP reports : innovation in hepatology · 2025Article
- MPTP mediated Ox-mtDNA release inducing macrophage pyroptosis and exacerbating MCD-induced MASH via promoting the ITPR3/CaJournal of translational medicine · 2025Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- Dissecting the mechanisms of MASLD fibrosis in the era of single-cell and spatial omics.The Journal of clinical investigation · 2025Review
- CD44 in Group 1 Innate Lymphoid Cells Impacts the Development and Progression of Steatohepatitis.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025Review
- Causal role of immune cells in primary liver cancer: a mendelian randomization study.BMC cancer · 2025Article
- Immune cell phenotypes as causal factors in liver disease progression revealed by Mendelian randomization.Scientific reports · 2025Article
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- High intake of n-6 polyunsaturated fatty acid exacerbates non-alcoholic steatohepatitis by the involvement of multiple metabolic pathways.Frontiers in nutrition · 2025Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledNonalcoholic steatohepatitis (NASH) affects 3%-5% of the U.S. population, having severe clinical complications to the development of fibrosis and end-stage liver diseases, such as cirrhosis and hepatocellular carcinoma. A critical cause of NASH is chronic systemic inflammation promoted by innate immune cells, such as liver macrophages (Mϕ) and natural killer (NK) cells. However, little is known about how the crosstalk between Mϕ and NK cells contributes to regulate NASH progression to fibrosis. In this report, we demonstrate that NKp46(+) cells play an important role in preventing NASH progression to fibrosis by regulating M1/M2 polarization of liver Mϕ. Using a murine model of NASH, we demonstrate that DX5(+)NKp46(+) NK cells are increased during disease and play a role in polarizing Mϕ toward M1-like phenotypes. This NK's immunoregulatory function depends on the production of interferon-gamma (IFN-γ), but not by granzyme-mediated cytolytic activity. Notably, depletion of NKp46(+) cells promotes the development of fibrosis with increased expression of profibrogenic genes as well as skewed M2 Mϕ phenotypes in hepatic tissues.
conclusionsNK cell-derived IFN-γ may be essential for maintaining a balanced inflammatory environment that promotes tissue integrity and limiting NASH progression to fibrosis.
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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.