ArticleJHEP reports : innovation in hepatology2025
LSECtin attenuates hepatic Th17 expansion in a murine model of cirrhosis and signals through the LAG-3 receptor.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- LAG3 checkpoint function and its mechanism of action in therapeutic targeting.Nature reviews. Immunology · 2026Review
- Epigenetic drug control of Clec4g/LSECtin expression reduces fibrosis burden in cirrhosis.Hepatology communications · 2026Article
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Authors and funding
12 authors.
Funding
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Abstract
Background & Aims: LSECtin downregulation during cirrhosis progression is associated with adaptive T-cell expansion. We analyzed the molecular mechanism for LSECtin modulation of Th17 proliferation in an experimental cirrhosis model. Methods: A transgenic mouse model of Clec4g/LSECtin overexpression (Clec4g KI) was subjected to CCl Results: Densitometred LSECtin expression was significantly downregulated during cirrhosis in wild-type but not Clec4g-KI mice (0.6 ± 0.2 Conclusions: We have established a valuable murine model of LSECtin overexpression to assess its impact on hepatic inflammation during cirrhosis. LAG-3 was identified as the molecular mechanism by which LSECtin attenuates Th17 differentiation. Given LSECtin capacity to modulate the Th profile and decrease proinflammatory cell death, liver-directed molecular approaches to restore its expression may be of therapeutic interest during cirrhosis. Impact and implications: LSECtin downregulation is associated with the expansion of Th17 cell subpopulation during cirrhosis. Findings highlight the crucial role of LSECtin in regulating immune responses and mitigating liver damage in cirrhosis. Restoring LSECtin expression through targeted liver-directed molecular interventions may be of therapeutic relevance in cirrhosis.
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