乙型肝炎病毒感染的结果与复杂的免疫失衡有关；然而，HBV 引起免疫功能障碍的确切机制尚不清楚。HBV 转基因 (HBs-Tg) 小鼠被用来研究两个不同亚群的肝内 NK 细胞：常规 NK (cNK) 和肝驻留 NK (LrNK) 细胞在慢性 HBV 感染期间。cNK 细胞（而非 LrNK 细胞）是衰老 HBs-Tg 小鼠肝脏中大量 NK 细胞数量增加的主要原因。在衰老的 HBs-Tg 小鼠中，肝 cNK 细胞显示出更强的产生 IL-10 的能力，同时 CD69、TIGIT 和 PD-L1 的表达更高，而 NKG2D 的表达更低。与 HBs-Tg 小鼠的脾 cNK 细胞相比，在肝 cNK 细胞中观察到较低的线粒体质量和膜电位以及较少的极化定位。 HBsAg 肝细胞分泌的半乳糖凝集素 3 (Gal-3) 增强，通过 ITGB1 信号传导导致肝 cNK 细胞产生 IL-10。对于人类，LGALS3 和 ITGB1 表达与 IL-10 表达呈正相关，与 HCC 不良临床进展呈负相关。在慢性 HBV 感染期间，Gal-3-ITGB1 信号传导塑造肝脏 cNK 细胞，但不塑造 LrNK 细胞，这可能与随着 HCC 进展。

The outcomes of HBV infections are related to complex immune imbalances; however, the precise mechanisms by which HBV induces immune dysfunction are not well understood.HBV transgenic (HBs-Tg) mice were used to investigate intrahepatic NK cells in two distinct subsets: conventional NK (cNK) and liver-resident NK (LrNK) cells during a chronic HBV infection.The cNK cells, but not the LrNK cells, were primarily responsible for the increase in the number of bulk NK cells in the livers of ageing HBs-Tg mice. The hepatic cNK cells showed a stronger ability to produce IL-10, coupled with a higher expression of CD69, TIGIT and PD-L1, and lower NKG2D expression in ageing HBs-Tg mice. A lower mitochondrial mass and membrane potential, and less polarized localization were observed in the hepatic cNK cells compared with the splenic cNK cells in the HBs-Tg mice. The enhanced galectin-3 (Gal-3) secreted from HBsAg+ hepatocytes accounted for the IL-10 production of hepatic cNK cells via ITGB1 signaling. For humans, LGALS3 and ITGB1 expression is positively correlated with IL-10 expression, and negatively correlated with the poor clinical progression of HCC.Gal-3-ITGB1 signaling shapes hepatic cNK cells but not LrNK cells during a chronic HBV infection, which may correlate with HCC progression.