ArticleFrontiers in immunology2024
Profibrogenic role of IL-15 through IL-15 receptor alpha-mediated trans-presentation in the carbon tetrachloride-induced liver fibrosis model.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Alterations in Immune Cell Profiles in the Liver in Diabetes Mellitus: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- CRISPLD2 protects against liver inflammation and fibrosis via GRP78 to repress HMGB1/TLR4 axis-mediated STING palmitoylation.Hepatology communications · 2026Article
- IL-15 in alopecia areata: the immune tolerance mechanistic insights and translational perspectives.Frontiers in medicine · 2026Review
- Sex-dependent modulation of acute respiratory distress syndrome byFrontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Background: Inflammatory cytokines play key pathogenic roles in liver fibrosis. IL-15 is a proinflammatory cytokine produced by myeloid cells. IL-15 promotes pathogenesis of several chronic inflammatory diseases. However, increased liver fibrosis has been reported in mice lacking IL-15 receptor alpha chain (IL-15Rα), suggesting an anti-fibrogenic role for IL-15. As myeloid cells are key players in liver fibrosis and IL-15 signaling can occur independently of IL-15Rα, we investigated the requirement of IL-15 and IL-15Rα in liver fibrosis. Methods: We induced liver fibrosis in Results: Both Conclusion: Our findings indicate that IL-15 exerts its profibrogenic role in the liver by promoting macrophage activation and that this requires trans-presentation of IL-15 by IL-15Rα.
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