Their results showed that in both hepatitis mouse models, the expression of IL-33 was upregulated and hepatocyte-specific IL-33 expression was downregulated in natural killer cell- (NK-) depleted poly(I:C)-treated mice with severe liver injury, while natural killer T cell- (NKT-) deficient mice exhibited hepatoprotection against poly(I:C)-induced hepatitis accompanied by an increased number of IL-33-expressing hepatocytes compared with wild-type (WT) controls [48]. This evidence concerns the gene IL33 and hepatitis A virus infection.