Lymphocyte-specific deletion of IKK2 or NEMO mediates an increase in intrarenal Th17 cells and accelerates renal damage in an ischemia-reperfusion injury mouse model.

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作者： Linlin,Guo ^[1] ; Hannah Heejung,Lee ^[1] ; María de Las Mercedes,Noriega ^[1] ; Hans J,Paust ^[1] ; Gunther,Zahner ^[1] ; Friedrich,Thaiss ^[2]

作者单位： III Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. ^[1] III Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany thaiss@uke.de. ^[2]

关键词 IκB kinase Th17 cells ischemia-reperfusion injury nuclear factor-κB essential modulator nuclear factor-κB transcription factor signalosome complex

主题词动物(Animals);血尿素氮(Blood Urea Nitrogen);趋化因子CCL20(Chemokine CCL20);肌酸酐(Creatinine);疾病模型, 动物(Disease Models, Animal);I-κB激酶(I-kappa B Kinase);细胞内信号肽和蛋白质类(Intracellular Signaling Peptides and Proteins);肾(Kidney);淋巴细胞(Lymphocytes);小鼠(Mice);小鼠, 基因敲除(Mice, Knockout);恶嗪类(Oxazines);吡啶类(Pyridines);再灌注损伤(Reperfusion Injury);Th17细胞(Th17 Cells)

DOI 10.1152/ajprenal.00242.2016

PMID 27582100

发布时间 2018-06-06

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American journal of physiology. Renal physiology

2016年311卷5期

F1005-F1014页

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Lymphocyte-specific deletion of IKK2 or NEMO mediates an increase in intrarenal Th17 cells and accelerates renal damage in an ischemia-reperfusion injury mouse model.

American journal of physiology. Renal physiology

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American journal of physiology. Renal physiology

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Lymphocyte-specific deletion of IKK2 or NEMO mediates an increase in intrarenal Th17 cells and accelerates renal damage in an ischemia-reperfusion injury mouse model.

American journal of physiology. Renal physiology

相似文献

American journal of physiology. Renal physiology

相关期刊

检索历史清除