ArticleHepatology (Baltimore, Md.)2014
IL-17 signaling accelerates the progression of nonalcoholic fatty liver disease in mice.
Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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Who cites it
161 citing papers in PubMed, 238 citations in OpenAlex.
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- Biocompatible Quaternized Chitosan-Whey Protein Nanofibrous Porous Microspheres for Multi-Functional Synergistic Regulation of the Gut-Liver Axis in the Treatment of Metabolic Dysfunction-Associated Steatotic Liver Disease.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Bixin and Montelukast Combination Mitigates the Progression of MASLD to Cytokine-Driven Inflammatory Stress in an In Vitro Fluid-Dynamic Model.ACS omega · 2026Article
- MASH-Associated T Cell Activation and Neuroinflammation: Evidence for a Hepatosystemic Immune Axis.Seminars in liver disease · 2026Review
- Ambient temperature regulates CD4iScience · 2026Article
- Segmented filamentous bacteria are worldwide human gut commensals.Nature communications · 2026Article
- Low Serum Adiponectin May Identify MASLD as a Comorbidity in Patients with Moderate-to-Severe Psoriasis.Psoriasis (Auckland, N.Z.) · 2026Article
- Local and systemic cytokine signatures for outcome prediction after transarterial chemoembolization in hepatocellular carcinoma.Theranostics · 2026Article
- The immunometabolic nature of MASH: framing immune cells within metabolic dysfunction.Frontiers in immunology · 2026Review
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Modulation of Inflammation-Driven Hepatocarcinogenesis: The Hepatic Immune Microenvironment, Gut-Liver Axis, and Neuroregulation.Journal of hepatocellular carcinoma · 2026Review
- Dual roles of T cells in metabolic dysfunction-associated steatohepatitis pathogenesis and liver fibrosis: From inflammation to therapeutic targets.Hepatology communications · 2025Review
- Sterile inflammation in MASH: emerging role of extracellular RNA and therapeutic strategies.npj metabolic health and disease · 2025Review
- Chronic Waterborne Exposure to Polystyrene Microplastics Induces Kupffer Cell Polarization Imbalance and Hepatic Lipid Accumulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Intriguing Roles of Cytokines in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Narrative Review.Current obesity reports · 2025Review
- Therapeutic effects of adipose tissue-derived mesenchymal stem cells on ER stress in a murine model of metabolic dysfunction-associated steatohepatitis: an in vivo and in vitro study.Stem cell research & therapy · 2025Article
- l-[5-Acta pharmaceutica Sinica. B · 2025Article
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- Protective effects ofFrontiers in microbiology · 2025Article
101 more citing papers are in PubMed but not listed here.
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13 authors at 4 institutions in 1 country.
Funding
Abstract
unlabelledInflammation plays a central pathogenic role in the pernicious metabolic and end-organ sequelae of obesity. Among these sequelae, nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the developed world. The twinned observations that obesity is associated with increased activation of the interleukin (IL)-17 axis and that this axis can regulate liver damage in diverse contexts prompted us to address the role of IL-17RA signaling in the progression of NAFLD. We further examined whether microbe-driven IL-17A regulated NAFLD development and progression. We show here that IL-17RA(-/-) mice respond to high-fat diet stress with significantly greater weight gain, visceral adiposity, and hepatic steatosis than wild-type controls. However, obesity-driven lipid accumulation was uncoupled from its end-organ consequences in IL-17RA(-/-) mice, which exhibited decreased steatohepatitis, nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase enzyme expression, and hepatocellular damage. Neutralization of IL-17A significantly reduced obesity-driven hepatocellular damage in wild-type mice. Further, colonization of mice with segmented filamentous bacteria (SFB), a commensal that induces IL-17A production, exacerbated obesity-induced hepatocellular damage. In contrast, SFB depletion protected from obesity-induced hepatocellular damage.
conclusionThese data indicate that obesity-driven activation of the IL-17 axis is central to the development and progression of NAFLD to steatohepatitis and identify the IL-17 pathway as a novel therapeutic target in this condition.
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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.