Innate Immune Response in Kidney Ischemia/Reperfusion Injury

TY - JOUR

T1 - Innate Immune Response in Kidney Ischemia/Reperfusion Injury

T2 - Potential Target for Therapy

AU - Kezić, Aleksandra

AU - Stajic, Natasa

AU - Thaiss, Friedrich

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

KW - Acute Kidney Injury

KW - Animals

KW - Humans

KW - Immunity, Innate

KW - Inflammation

KW - Kidney

KW - Kidney Transplantation

KW - Mice

KW - NF-kappa B

KW - Purinergic P1 Receptor Agonists

KW - Reperfusion Injury

KW - Toll-Like Receptors

KW - Journal Article

KW - Review

U2 - 10.1155/2017/6305439

DO - 10.1155/2017/6305439

M3 - SCORING: Review article

C2 - 28676864

VL - 2017

SP - 6305439

JO - J IMMUNOL RES

JF - J IMMUNOL RES

SN - 2314-8861

ER -