The effect of renal ischemia-reperfusion injury on expression of RAE-1 and H60 in mice kidney

Introduction. 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). Methods. 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). Results. 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. Conclusion. 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 C5713L/6 kidneys. Rae-1 was absent in normal C5713L/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.