Abstract:
:Kidney ischemia-reperfusion injury (IRI) occurs as a result of complex interactions of kidney parenchymal cells and immune cells that are initiated by hypoxic damage of parenchymal cells. In particular, tubular epithelial cells (TECs) not only are susceptible to ischemia but also have an auto-loop system to amplify renal inflammation caused by ischemia and reperfusion. Since endogenous TLR2 ligands released from TECs trigger renal inflammation leading to kidney IRI in an autocrine manner, we hypothesized that local infusion of TLR2 blockers would prevent kidney IRI. In this study, we demonstrated that injection of antagonist anti-TLR2 mAb through the renal vein after cross-clamping significantly reduced the recruitment of NK cells to the kidney after IRI, a phenomenon that is governed by TLR2 signaling in TECs. In addition, intrarenal blocking of TLR2 signaling was shown to inhibit NK cell-mediated neutrophil infiltration and subsequent renal damage. Overall, our simple experiment system will be of help in testing the efficacy of candidate blockers targeting kidney parenchymal cells in inhibition of kidney IRI.
journal_name
J Immunol Methodsjournal_title
Journal of immunological methodsauthors
Kim HJ,Park SJ,Koo S,Cha HJ,Lee JS,Kwon B,Cho HRdoi
10.1016/j.jim.2014.03.014subject
Has Abstractpub_date
2014-05-01 00:00:00pages
146-50eissn
0022-1759issn
1872-7905pii
S0022-1759(14)00088-Xjournal_volume
407pub_type
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