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Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Front+Immunol 2017 ; 8 (ä): ä Nephropedia Template TP
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Suppression of Natural Killer Cell Activity by Regulatory NKT10 Cells Aggravates Alcoholic Hepatosteatosis #MMPMID29163491
Cui K; Yan G; Zheng X; Bai L; Wei H; Sun R; Tian Z
Front Immunol 2017[]; 8 (ä): ä PMID29163491show ga
We and others have found that the functions of hepatic natural killer (NK) cells are inhibited but invariant NKT (iNKT) cells become activated after alcohol drinking, leaving a possibility that there exists interplay between NK cells and iNKT cells during alcoholic liver disease. Here, in a chronic plus single-binge ethanol consumption mouse model, we observed that NK cells and interferon-? (IFN-?) protected against ethanol-induced liver steatosis, as both wild-type (WT) mice treated with anti-asialo GM1 antibody and IFN-?-deficient GKO mice developed more severe alcoholic fatty livers. As expected, IFN-? could directly downregulate lipogenesis in primary hepatocytes in vitro. On the contrary, iNKT cell-deficient J?18?/? or interleukin-10 (IL-10)?/? mice showed fewer alcoholic steatosis, along with the recovered number and IFN-? release of hepatic NK cells, and exogenous IL-10 injection was sufficient to compensate for iNKT cell deficiency. Furthermore, NK cell depletion in J?18?/? or IL-10?/? mice caused more severe hepatosteatosis, implying NK cells are the direct effector cells to inhibit liver steatosis. Importantly, adoptive transfer of iNKT cells purified from normal but not IL-10?/? mice resulted in suppression of the number and functions of NK cells and aggravated alcoholic liver injury in J?18?/? mice, indicating that IL-10-producing iNKT (NKT10) cells are the regulators on NK cells. Conclusion: Ethanol exposure-triggered NKT10 cells antagonize the protective roles of NK cells in alcoholic hepatosteatosis.