Interleukin-22 Ameliorates Neutrophil-Driven Nonalcoholic Steatohepatitis Through Multiple Targets.
Seonghwan HwangYong HeXiaogang XiangWonhyo SeoSeung-Jin KimJing MaTian-Yi RenSeol Hee ParkZhou ZhouDechun FengGeorge KunosBin GaoPublished in: Hepatology (Baltimore, Md.) (2020)
Hepatic overexpression of CXCL1 is sufficient to drive steatosis-to-NASH progression in HFD-fed mice through neutrophil-derived reactive oxygen species and activation of stress kinases, which can be reversed by IL-22 treatment via the induction of metallothionein.