ArticlePLoS pathogens2023
Inhibition of hepatic natural killer cell function via the TIGIT receptor in schistosomiasis-induced liver fibrosis.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Parasite exosomes-derived circulating sja-miR-61 and sja-miR-7-5p as Novel biomarkers for the detection of Schistosoma japonicum infection using TaqMan real-time PCR.PLoS neglected tropical diseases · 2026Article
- Integrated transcriptomic and metabolomic profiling reveals immune-metabolic crosstalk and predictive biomarkers of ligustrazine treatment response in idiopathic pulmonary fibrosis.Journal of translational medicine · 2026Article
- TIGIT impairs NK cell antifibrotic activity through the IFNγ-IFI30 axis in schistosomiasis-induced liver fibrosis.Frontiers in immunology · 2026Article
- TIGIT blockade improves anti-Mycobacterium tuberculosis immunity.PLoS pathogens · 2025Article
- Single-Cell Sequencing Reveals the Heterogeneity of Hepatic Natural Killer Cells and Identifies the Cytotoxic Natural Killer Subset in Schistosomiasis Mice.International journal of molecular sciences · 2025Article
- Beyond schistosomiasis: unraveling co-infections and altered immunity.Clinical microbiology reviews · 2024Review
- Inhibiting Liver Autophagy and Promoting Hepatocyte Apoptosis byTropical medicine and infectious disease · 2024Article
- The Important Roles of Natural Killer Cells in Liver Fibrosis.Biomedicines · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schistosomiasis is a zoonotic parasitic disease. Schistosoma japonicum eggs deposited in the liver tissue induce egg granuloma formation and liver fibrosis, seriously threatening human health. Natural killer (NK) cells kill activated hepatic stellate cells (HSCs) or induce HSC apoptosis and inhibit the progression of liver fibrosis. However, the function of NK cells in liver fibrosis caused by S. japonicum infection is significantly inhibited. The mechanism of this inhibition remains unclear. Twenty mice were percutaneously infected with S. japonicum cercariae. Before infection and 2, 4, 6, and 8 weeks after infection, five mice were euthanized and dissected at each time point. Hepatic NK cells were isolated and transcriptome sequenced. The sequencing results showed that Tigit expression was high at 4-6 weeks post infection. This phenomenon was verified by reverse transcription quantitative PCR (RT-qPCR) and flow cytometry. NK cells derived from Tigit-/- and wild-type (WT) mice were co-cultured with HSCs. It was found that Tigit-/- NK cells induced apoptosis in a higher proportion of HSCs than WT NK cells. Schistosomiasis infection models of Tigit-/- and WT mice were established. The proportion and killing activity of hepatic NK cells were significantly higher in Tigit-/- mice than in WT mice. The degree of liver fibrosis in Tigit-/- mice was significantly lower than that in WT mice. NK cells were isolated from Tigit-/- and WT mice and injected via the tail vein into WT mice infected with S. japonicum. The degree of liver fibrosis in mice that received NK cell infusion reduced significantly, but there was no significant difference between mice that received NK cells from Tigit-/- and WT mice, respectively. Our findings indicate that Tigit knockout enhanced the function of NK cells and reduced the degree of liver fibrosis in schistosomiasis, thus providing a novel strategy for treating hepatic fibrosis induced by schistosomiasis.
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