ArticleTransplant immunology2017
NKT cells are important mediators of hepatic ischemia-reperfusion injury.
Article in Transplant immunology, 2017. 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.
- Feedback Loops Shape Oxidative and Immune Interactions in Hepatic Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Early activation and recruitment of invariant natural killer T cells during liver ischemia-reperfusion: the major role of the alarmin interleukin-33.Frontiers in immunology · 2023Article
- Immune response associated with ischemia and reperfusion injury during organ transplantation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Oral N-acetylcysteine decreases IFN-γ production and ameliorates ischemia-reperfusion injury in steatotic livers.Frontiers in immunology · 2022Article
- Drug delivery nanosystems targeted to hepatic ischemia and reperfusion injury.Drug delivery and translational research · 2021Review
- Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy.Oxidative medicine and cellular longevity · 2019Review
- The Impact of Invariant NKT Cells in Sterile Inflammation: The Possible Contribution of the Alarmin/Cytokine IL-33.Frontiers in immunology · 2018Review
- Expansion of iNKT Cells Promotes Liver Repair Following Hepatic Ischemia Reperfusion Injury.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
introductionIRI results from the interruption then reinstatement of an organ's blood supply, and this poses a significant problem in liver transplantation and resectional surgery. In this paper, we explore the role T cells play in the pathogenesis of this injury. MATERIALS &
methodsWe used an in vivo murine model of warm partial hepatic IRI, genetically-modified mice, in vivo antibody depletion, adoptive cell transfer and flow cytometry to determine which lymphocyte subsets contribute to pathology. Injury was assessed by measuring serum alanine aminotransfersase (ALT) and by histological examination of liver tissue sections.
resultsThe absence of T cells (CD3εKO) is associated with significant protection from injury (p=0.010). Through a strategy of antibody depletion it appears that NKT cells (p=0.0025), rather than conventional T (CD4+ or CD8+) (p=0.11) cells that are the key mediators of injury. DISCUSSION: Our results indicate that tissue-resident NKT cells, but not other lymphocyte populations are responsible for the injury in hepatic IRI. Targeting the activation of NKT cells and/or their effector apparatus would be a novel approach in protecting the liver during transplantation and resection surgery; this may allow us to expand our current criteria for surgery.
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