肾
急性肾损伤
医学
肌酐
淋巴细胞
再灌注损伤
免疫学
血尿素氮
T淋巴细胞
效应器
缺血
药理学
免疫系统
内科学
作者
Ning Song,Yang Xu,Hans‐Joachim Paust,Ulf Panzer,Maria Mercedes de Las Noriega,Lei Guo,Thomas Renné,Jia-Bin Huang,Xianglin Meng,Mingyan Zhao,Friedrich Thaiss
标识
DOI:10.1007/s00018-023-04763-2
摘要
Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI), and experimental work has revealed detailed insight into the inflammatory response in the kidney. T cells and NFκB pathway play an important role in IRI. Therefore, we examined the regulatory role and mechanisms of IkappaB kinase 1 (IKK1) in CD4+T lymphocytes in an experimental model of IRI. IRI was induced in CD4cre and CD4IKK1Δ mice. Compared to control mice, conditional deficiency of IKK1 in CD4+T lymphocyte significantly decreased serum creatinine, blood urea nitrogen (BUN) level, and renal tubular injury score. Mechanistically, lack in IKK1 in CD4+T lymphocytes reduced the ability of CD4 lymphocytes to differentiate into Th1/Th17 cells. Similar to IKK1 gene ablation, pharmacological inhibition of IKK also protected mice from IRI. Together, lymphocyte IKK1 plays a pivotal role in IRI by promoting T cells differentiation into Th1/Th17 and targeting lymphocyte IKK1 may be a novel therapeutic strategy for IRI.
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