缺血性急性肾损伤中的固有免疫反应。
The innate immune response in ischemic acute kidney injury.
作者信息
Jang Hye Ryoun, Rabb Hamid
机构信息
Nephrology Division, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building, Room 965, 720 Rutland Avenue, Baltimore, MD 21205, USA.
出版信息
Clin Immunol. 2009 Jan;130(1):41-50. doi: 10.1016/j.clim.2008.08.016. Epub 2008 Oct 14.
Abstract
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, alloantigen-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.
摘要
肾脏缺血再灌注损伤是同种异体移植肾和自体肾发病的主要原因。缺血再灌注诱导的急性肾损伤的特征是早期、不依赖同种异体抗原的炎症反应。先天性免疫系统的主要成分被激活并参与急性肾损伤的发病机制，同时使移植肾易于发生排斥反应。与急性肾损伤相关的先天性免疫可溶性成分包括补体系统、细胞因子和趋化因子。Toll样受体（TLRs）也是重要的促成因素。参与急性肾损伤的效应细胞包括经典的先天性免疫细胞、中性粒细胞和巨噬细胞。最近的数据意外地发现淋巴细胞是早期急性肾损伤反应的参与者。在本综述中，我们将重点关注参与缺血性急性肾损伤发病机制的免疫介质。
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