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• W2012173650 abstract "NKG2D, an activating receptor, may trigger NK and CD8+ T cells. Ligands for NKG2D and major histocompability complex class I chain-related antigen (MIC) have been reported to be expressed in rejected human renal allografts. MIC-NKG2D engagement may induce natural killer (NK) cell activation providing T-cell costimulation. We hypothesized that this interaction between innate and adaptive immunity may occur during kidney ischemia-reperfusion injury (IRI).Male C57BL/6 mice after right renal resection were subjected to 35 minutes of left renal ischemia: the ischemic group. Sham-operated mice underwent the same protocol without vascular occlusion. The sham and ischemic kidneys were removed at 2 to 7, 10, 14, or 28 days postoperatively. The normal, sham, and ischemic kidney tissues were collected for reverse-transcriptase polymerase chain reaction, and immunohistochemistry analysis of MIC homologues in mice (Rae-1 and H60).Compared with no expression in sham control and normal kidneys, IRI caused mRNA expression of Rae-1 from 2 to 10 days postoperatively and protein expression of Rae-1 from 2 to 14 days postoperatively in ischemic kidneys. We observed no expression of H60 mRNA or protein in any kidney.H60 transcripts have been reported to be present in the BALB/c background but not in C57BL/6. We found IRI did not cause H60 mRNA on protein expression in C57BL/6 kidneys. Rae-1 was absent in normal C57BL/6 kidneys. The IRI-induced expression of the NKG2D ligand, Rae-1, might activate NK and CD8+ T cells. Our results suggested that MIC may be an important link between innate and adaptive immunity in kidney IRI." @default.
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• W2012173650 date "2006-09-01" @default.
• W2012173650 modified "2023-10-18" @default.
• W2012173650 title "The Effect of Renal Ischemia-Reperfusion Injury on Expression of RAE-1 and H60 in Mice Kidney" @default.
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• W2012173650 doi "https://doi.org/10.1016/j.transproceed.2006.06.013" @default.
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