RORγt(+) IL-22-producing NKp46(+) cells protect from hepatic ischemia reperfusion injury in mice
Abstract
NKp46(+) cells are major effector cells in the pathogenesis of hepatic ischemia reperfusion injury (IRI). Nevertheless, the precise role of unconventional subsets like the IL-22-producing NKp46(+) cells (NK22) remains unknown. The purpose of this study was to examine the role of NK22 cells in IRI in transplantation, particularly with respect to regulation by the transcription factor ROR-gamma-t (RORγt). To explore the role of NK22 cells in IRI in the absence of adaptive immunity, B6.RORγt-(gfp/wt)-reporter and B6.RORγt-(gfp/gfp)-knockout (KO) mice on a Rag KO background underwent 90min partial warm ischemia, followed by 24h of reperfusion. Rag KO mice that possess fully functional NKp46(+) cells, and Rag-common-γ-chain-double-KO (Rag-γc-DKO) mice that lack T, B and NKp46(+) cells, were used as controls. We found that Rag-γc-DKO mice lacking NK22 cells show more severe levels of hepatocellular damage (GPT, histological injury) when compared to both Rag-RORγt-reporter and Rag KO mice that possess NK22 cells. Importantly, Rag-RORγt-reporter and Rag KO mice undergoing IRI expressed high protein levels of both IL-22 and GFP (RORγt), suggesting a protective role for RORγt(+) NK22 cells in IRI. Therefore, we tested the hypothesis that...Continue Reading
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