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Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand on NK Cells Protects From Hepatic Ischemia-Reperfusion Injury

Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand on NK Cells Protects From Hepatic Ischemia-Reperfusion Injury

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Prüfsumme: MD5:ae8f81fea95316f281e3b9e8f229ff75

FAHRNER, René, Markus TROCHSLER, Nadia CORAZZA, Nadine GRAUBARDT, Adrian KEOGH, Daniel CANDINAS, Thomas BRUNNER, Deborah STROKA, Guido BELDI, 2014. Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand on NK Cells Protects From Hepatic Ischemia-Reperfusion Injury. In: Transplantation. 97(11), pp. 1102-1109. ISSN 0041-1337. eISSN 1534-6080

@article{Fahrner2014-06-15Tumor-28321, title={Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand on NK Cells Protects From Hepatic Ischemia-Reperfusion Injury}, year={2014}, doi={10.1097/TP.0000000000000101}, number={11}, volume={97}, issn={0041-1337}, journal={Transplantation}, pages={1102--1109}, author={Fahrner, René and Trochsler, Markus and Corazza, Nadia and Graubardt, Nadine and Keogh, Adrian and Candinas, Daniel and Brunner, Thomas and Stroka, Deborah and Beldi, Guido} }

2014-07-09T14:22:17Z Trochsler, Markus Corazza, Nadia Transplantation ; 97 (2014), 11. - S. 1102-1109 Background<br />Ischemia-reperfusion injury (IRI) significantly contributes to graft dysfunction after liver transplantation. Natural killer (NK) cells are crucial innate effector cells in the liver and express tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a potent inducer of hepatocyte cell death. Here, we investigated if TRAIL expression on NK cells contributes to hepatic IRI.<br /><br />Methods<br />The outcome after partial hepatic IRI was assessed in TRAIL-null mice and contrasted to C57BL/6J wild-type mice and after NK cell adoptive transfer in RAG2/common gamma-null mice that lack T, B, and NK cells. Liver IRI was assessed by histological analysis, alanine aminotransferase, hepatic neutrophil activation by myeloperoxidase activity, and cytokine secretion at specific time points. NK cell cytotoxicity and differentiation were assessed in vivo and in vitro.<br /><br />Results<br />Twenty-four hours after reperfusion, TRAIL-null mice exhibited significantly higher serum transaminases, histological signs of necrosis, neutrophil infiltration, and serum levels of interleukin-6 compared to wild-type animals. Adoptive transfer of TRAIL-null NK cells into immunodeficient RAG2/common gamma-null mice was associated with significantly elevated liver damage compared to transfer of wild-type NK cells. In TRAIL-null mice, NK cells exhibit higher cytotoxicity and decreased differentiation compared to wild-type mice. In vitro, cytotoxicity against YAC-1 and secretion of interferon gamma by TRAIL-null NK cells were significantly increased compared to wild-type controls.<br /><br />Conclusions<br />These experiments reveal that expression of TRAIL on NK cells is protective in a murine model of hepatic IRI through modulation of NK cell cytotoxicity and NK cell differentiation. Brunner, Thomas 2014-06-15 Stroka, Deborah Fahrner, René Brunner, Thomas Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand on NK Cells Protects From Hepatic Ischemia-Reperfusion Injury Graubardt, Nadine Candinas, Daniel Fahrner, René Trochsler, Markus Beldi, Guido Keogh, Adrian Candinas, Daniel eng deposit-license Corazza, Nadia 2014-07-09T14:22:17Z Beldi, Guido Keogh, Adrian Stroka, Deborah Graubardt, Nadine

Dateiabrufe seit 01.10.2014 (Informationen über die Zugriffsstatistik)

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