ArticleCentral-European journal of immunology2024
Interleukin 17A promotes glycolysis to activate human hepatic stellate cells by mediating the TRAF2/TRAF5/HuR/PFKFB3 axis.
Article in Central-European journal of immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- S100 Calcium-Binding Protein 16 (S100A16) Promotes Hepatic Stellate Cell Activation Via Erb-B2 Receptor Tyrosine Kinase 2 (ERBB2)-mediated Glycolysis to Facilitate Liver Fibrosis.Cell biochemistry and function · 2026Article
- Decoding the ubiquitination-immunity axis in idiopathic pulmonary fibrosis: diagnostic insights and therapeutic implications.Respiratory research · 2026Article
- Glucose metabolism and immune dysregulation - a metabolic lens on lupus pathogenesis.Central-European journal of immunology · 2025Article
- The pivotal role of IL-17A in hepatic stellate cell activation.Central-European journal of immunology · 2024Article
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Authors and funding
5 authors.
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Abstract
Introduction: Biliary atresia (BA) is an obliterating fibrous inflammatory bile duct disease in infants. Interleukin 17A (IL-17A) is abnormally expressed in patients with BA; however, the mechanism of its expression is unclear. Material and methods: Liver tissues from patients with BA and those with anicteric choledochal cysts (non-BA) were collected. The expression of genes and proteins was determined using RT-qPCR and western blot. Cell biological activities, including viability and proliferation, were evaluated by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2 Results: In BA patients, IL-17A, TRAF2, TRAF5, and PFKFB3 were highly expressed, and IL-17A expression was positively correlated with PFKFB3, TRAF2, and TRAF5 expression, respectively. IL-17A elevated PFKFB3 expression and promoted glycolysis and the proliferation and fibrosis of hepatic stellate cells (HSCs), which were abolished by 2-deoxy-D-glucose (2-DG) and PFKFB3/TRAF2/TRAF5 silencing. Mechanistically, IL-17A promoted the interactions among HuR, TRAF2 and TRAF5 to form the TRAF2/TRAF5/HuR complex, thereby enhancing PFKFB3 expression. Conclusions: IL-17A facilitates glycolysis and HSC fibrosis by promoting TRAF2/TRAF5/HuR complex formation to regulate PFKFB3 expression.
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