Macrophages, dendritic cells, and kidney ischemia-reperfusion injury.
Macrophages, dendritic cells, and kidney ischemia-reperfusion injury.
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DOI：
10.1016/j.semnephrol.2010.03.005
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发表时间：
2010-05
影响因子：
3.3
通讯作者：
Okusa, Mark D.
中科院分区：
文献类型：
--
作者：
Li, Li;Okusa, Mark D.
树突状细胞和巨噬细胞是肾脏先天免疫的关键早期启动者，并协调缺血再灌注损伤后的炎症反应。它们是存在于肾脏中的最丰富的白细胞，并且它们代表了能够直接通过产生促炎细胞因子和其他可溶性炎症介质或间接通过激活效应T淋巴细胞和自然杀伤T细胞在再灌注后诱导“无菌”炎症的异质细胞群。此外，最近的研究表明，肾脏和免疫细胞microRNA控制基因表达，并有能力调节对损伤的初始炎症反应。虽然树突状细胞和巨噬细胞有助于先天性和适应性免疫，损伤和修复，这篇综述将集中在肾脏缺血再灌注损伤的初始先天性反应。
Dendritic cells and macrophages are critical early initiators of innate immunity in the kidney and orchestrate inflammation subsequent to ischemia-reperfusion injury. They are the most abundant leukocyte present in the kidney, and they represent a heterogeneous population of cells that are capable of inducing ‘sterile’ inflammation following reperfusion directly through the production of proinflammatory cytokines and other soluble inflammatory mediators or indirectly through activation of effector T lymphocytes and nature killer T cells. In addition, recent studies indicate that kidney and immune cell microRNAs control gene expression and have the ability to regulate the initial inflammatory response to injury. Although dendritic cells and macrophages contribute to both innate and adaptive immunity and to injury and repair, this review will focus on the initial innate response to kidney ischemia-reperfusion injury.
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影响因子：
19.6
作者：
Awad, Alaa S.;Rouse, Michael;Huang, Liping;Vergis, Amy L.;Reutershan, Joerg;Cathro, Helen P.;Linden, Joel;Okusa, Mark D.
通讯作者：
Okusa, Mark D.
影响因子：
8.6
作者：
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通讯作者：
Rabb, Hamid
影响因子：
15.9
作者：
HOLDSWORTH, SR;NEALE, TJ;WILSON, CB
通讯作者：
WILSON, CB
影响因子：
20.3
作者：
Delneste, Y;Charbonnier, P;Jeannin, P
通讯作者：
Jeannin, P
影响因子：
48
作者：
Buch, T;Heppner, FL;Waisman, A
通讯作者：
Waisman, A