The innate immune response in ischemic acute kidney injury.
The innate immune response in ischemic acute kidney injury.
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DOI：
10.1016/j.clim.2008.08.016
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发表时间：
2009-01
影响因子：
8.6
通讯作者：
Rabb, Hamid
中科院分区：
文献类型：
--
作者：
Jang, Hye Ryoun;Rabb, Hamid
肾缺血再灌注损伤是移植肾和自体肾脏发病的主要原因。缺血再灌注所致的急性肾损伤具有早期、异体抗原非依赖性炎症的特点。天然免疫系统的主要组成部分被激活，并参与急性肾损伤的发病机制，并为移植肾的排斥反应做好准备。与急性肾损伤有关的天然免疫的可溶性成员包括补体系统、细胞因子和趋化因子。Toll样受体(TLRs)也是重要的贡献者。参与急性肾损伤的效应细胞包括经典的先天免疫细胞、中性粒细胞和巨噬细胞。最近的数据出人意料地发现淋巴细胞是早期急性肾损伤反应的参与者。在这篇综述中，我们将重点介绍参与缺血性急性肾损伤发病机制的免疫介质。
Kidney ischemia reperfusion injury is a major cause of morbidity in both allograft and native kidneys. Ischemia reperfusion-induced acute kidney injury is characterized by early, allo-antigen independent inflammation. Major components of the innate immune system are activated and participate in the pathogenesis of acute kidney injury, plus prime the allograft kidney for rejection. Soluble members of innate immunity implicated in acute kidney injury include the complement system, cytokines, and chemokines. Toll-like receptors (TLRs) are also important contributors. Effector cells that participate in ACUTE KIDNEY INJURY include the classic innate immune cells, neutrophils and macrophages. Recent data has unexpectedly identified lymphocytes as participants of early acute kidney injury responses. In this review, we will focus on immune mediators that participate in the pathogenesis of ischemic acute kidney injury.
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影响因子：
19.6
作者：
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通讯作者：
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影响因子：
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作者：
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Buurman, WA
DOI：
10.1152/ajprenal.00378.2004
发表时间：
2005-04-01
影响因子：
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作者：
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通讯作者：
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