Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy

Acute kidney injury caused by ischemia and subsequent reperfusion is associated with a high rate of mortality and morbidity. Ischemia/reperfusion injury in kidney transplantation causes delayed graft function and is associated with more frequent episodes of acute rejection and progression to chronic...

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Main Authors: Aleksandra Kezić, Natasa Stajic, Friedrich Thaiss
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2017/6305439
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author Aleksandra Kezić
Natasa Stajic
Friedrich Thaiss
author_facet Aleksandra Kezić
Natasa Stajic
Friedrich Thaiss
author_sort Aleksandra Kezić
collection DOAJ
description Acute kidney injury caused by ischemia and subsequent reperfusion is associated with a high rate of mortality and morbidity. Ischemia/reperfusion injury in kidney transplantation causes delayed graft function and is associated with more frequent episodes of acute rejection and progression to chronic allograft nephropathy. Alloantigen-independent inflammation is an important process, participating in pathogenesis of injurious response, caused by ischemia and reperfusion. This innate immune response is characterized by the activity of classical cells belonging to the immune system, such as neutrophils, macrophages, dendritic cells, lymphocytes, and also tubular epithelial cells and endothelial cells. These immune cells not only participate in inflammation after ischemia exerting detrimental influence but also play a protective role in the healing response from ischemia/reperfusion injury. Delineating of complex mechanisms of their actions could be fruitful in future prevention and treatment of ischemia/reperfusion injury. Among numerous so far conducted experiments, observed immunomodulatory role of adenosine and adenosine receptor agonists in complex interactions of dendritic cells, natural killer T cells, and T regulatory cells is emphasized as promising in the treatment of kidney ischemia/reperfusion injury. Potential pharmacological approaches which decrease NF-κB activity and antagonize mechanisms downstream of activated Toll-like receptors are discussed.
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spelling doaj-art-327f18cdb03d4132ab5851eccc8b55462025-02-03T05:47:35ZengWileyJournal of Immunology Research2314-88612314-71562017-01-01201710.1155/2017/63054396305439Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for TherapyAleksandra Kezić0Natasa Stajic1Friedrich Thaiss2School of Medicine, University of Belgrade, Belgrade, SerbiaSchool of Medicine, University of Belgrade, Belgrade, SerbiaThird Medical Department of Clinical Medicine, University Hospital Hamburg Eppendorf, Hamburg, GermanyAcute kidney injury caused by ischemia and subsequent reperfusion is associated with a high rate of mortality and morbidity. Ischemia/reperfusion injury in kidney transplantation causes delayed graft function and is associated with more frequent episodes of acute rejection and progression to chronic allograft nephropathy. Alloantigen-independent inflammation is an important process, participating in pathogenesis of injurious response, caused by ischemia and reperfusion. This innate immune response is characterized by the activity of classical cells belonging to the immune system, such as neutrophils, macrophages, dendritic cells, lymphocytes, and also tubular epithelial cells and endothelial cells. These immune cells not only participate in inflammation after ischemia exerting detrimental influence but also play a protective role in the healing response from ischemia/reperfusion injury. Delineating of complex mechanisms of their actions could be fruitful in future prevention and treatment of ischemia/reperfusion injury. Among numerous so far conducted experiments, observed immunomodulatory role of adenosine and adenosine receptor agonists in complex interactions of dendritic cells, natural killer T cells, and T regulatory cells is emphasized as promising in the treatment of kidney ischemia/reperfusion injury. Potential pharmacological approaches which decrease NF-κB activity and antagonize mechanisms downstream of activated Toll-like receptors are discussed.http://dx.doi.org/10.1155/2017/6305439
spellingShingle Aleksandra Kezić
Natasa Stajic
Friedrich Thaiss
Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy
Journal of Immunology Research
title Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy
title_full Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy
title_fullStr Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy
title_full_unstemmed Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy
title_short Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy
title_sort innate immune response in kidney ischemia reperfusion injury potential target for therapy
url http://dx.doi.org/10.1155/2017/6305439
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AT natasastajic innateimmuneresponseinkidneyischemiareperfusioninjurypotentialtargetfortherapy
AT friedrichthaiss innateimmuneresponseinkidneyischemiareperfusioninjurypotentialtargetfortherapy