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Natural Killer T Cells in Liver Ischemia–Reperfusion Injury
Restoration of blood flow to an ischemic organ results in significant tissue injury. In the field of liver transplantation, ischemia–reperfusion injury (IRI) has proven to be a formidable clinical obstacle. In addition to metabolic stress and inflammation, IRI results in profound graft dysfunction a...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5406773/ https://www.ncbi.nlm.nih.gov/pubmed/28368299 http://dx.doi.org/10.3390/jcm6040041 |
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author | Zimmerman, Michael A. Martin, Alicia Yee, Jennifer Schiller, Jennifer Hong, Johnny C. |
author_facet | Zimmerman, Michael A. Martin, Alicia Yee, Jennifer Schiller, Jennifer Hong, Johnny C. |
author_sort | Zimmerman, Michael A. |
collection | PubMed |
description | Restoration of blood flow to an ischemic organ results in significant tissue injury. In the field of liver transplantation, ischemia–reperfusion injury (IRI) has proven to be a formidable clinical obstacle. In addition to metabolic stress and inflammation, IRI results in profound graft dysfunction and loss. The severity of IRI further limits the ability to expand the donor pool by using partial grafts and marginal organs. As such, the inflammatory response to reperfusion of the liver continues to be an area of intense investigation. Among the various leukocytes involved in IRI, new insights suggest that natural killer T (NKT) cells may be a central driver of hepatocellular injury. Herein, we examine recent experimental observations that provide a mechanistic link between NKT cell recruitment to liver and post-perfusion tissue injury. |
format | Online Article Text |
id | pubmed-5406773 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-54067732017-04-27 Natural Killer T Cells in Liver Ischemia–Reperfusion Injury Zimmerman, Michael A. Martin, Alicia Yee, Jennifer Schiller, Jennifer Hong, Johnny C. J Clin Med Review Restoration of blood flow to an ischemic organ results in significant tissue injury. In the field of liver transplantation, ischemia–reperfusion injury (IRI) has proven to be a formidable clinical obstacle. In addition to metabolic stress and inflammation, IRI results in profound graft dysfunction and loss. The severity of IRI further limits the ability to expand the donor pool by using partial grafts and marginal organs. As such, the inflammatory response to reperfusion of the liver continues to be an area of intense investigation. Among the various leukocytes involved in IRI, new insights suggest that natural killer T (NKT) cells may be a central driver of hepatocellular injury. Herein, we examine recent experimental observations that provide a mechanistic link between NKT cell recruitment to liver and post-perfusion tissue injury. MDPI 2017-04-01 /pmc/articles/PMC5406773/ /pubmed/28368299 http://dx.doi.org/10.3390/jcm6040041 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Zimmerman, Michael A. Martin, Alicia Yee, Jennifer Schiller, Jennifer Hong, Johnny C. Natural Killer T Cells in Liver Ischemia–Reperfusion Injury |
title | Natural Killer T Cells in Liver Ischemia–Reperfusion Injury |
title_full | Natural Killer T Cells in Liver Ischemia–Reperfusion Injury |
title_fullStr | Natural Killer T Cells in Liver Ischemia–Reperfusion Injury |
title_full_unstemmed | Natural Killer T Cells in Liver Ischemia–Reperfusion Injury |
title_short | Natural Killer T Cells in Liver Ischemia–Reperfusion Injury |
title_sort | natural killer t cells in liver ischemia–reperfusion injury |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5406773/ https://www.ncbi.nlm.nih.gov/pubmed/28368299 http://dx.doi.org/10.3390/jcm6040041 |
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