ArticleClinical and experimental immunology2024
Tim-4 alleviates acute hepatic injury by modulating homeostasis and function of NKT cells.
Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Emerging roles of mitophagy in liver fibrosis: Implications for therapy.Acta pharmacologica Sinica · 2026Review
- Infiltration of TIM4-positive intratumoral macrophages serves as an adverse prognostic factor in breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- Non-parenchymal cells: key targets for modulating chronic liver diseases.Frontiers in immunology · 2025Review
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Authors and funding
10 authors.
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Abstract
T-cell immunoglobulin and mucin domain-containing molecule 4 (Tim-4) is an immune checkpoint molecule, which involves in numerous inflammatory diseases. Tim-4 is mainly expressed on antigen-presenting cells. However, increasing evidence has shown that Tim-4 is also expressed on natural killer T (NKT) cells. The role of Tim-4 in maintaining NKT cell homeostasis and function remains unknown. In this study, we explored the effect of Tim-4 on NKT cells in acute liver injury. This study found that Tim-4 expression on hepatic NKT cells was elevated during acute liver injury. Tim-4 deficiency enhanced IFN-γ, TNF-α expression while impaired IL-4 production in NKT cells. Loss of Tim-4 drove NKT-cell effector lineages to be skewed to NKT1 subset. Furthermore, Tim-4 KO mice were more susceptible to α-Galactosylceramide (α-GalCer) challenge. In conclusion, our findings indicate that Tim-4 plays an important role in regulating homeostasis and function of NKT cells in acute liver injury. Therefore, Tim-4 might become a new regulator of NKT cells and a potential target for the therapy of acute hepatitis.
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