Hepatic stellate cell (HSC) activation is closely associated with the progression of liver fibrosis.As an important component of the innate immune system,natural killer (NK) cells are enriched in the liver and play a key role in host defense against viral infection and tumor,and their anti-fibrotic effect has also been confirmed.NK cells can reduce liver fibrosis by killing early-activated or senescent HSCs or secreting interferon-γ.This article summarizes related research advances in recent years,and introduces the molecular immunological mechanism of NK cells in regulating HSCs and their potential anti-fibrotic effect based on the function and phenotype of NK cells and HSCs.

Liver nonparenchymal cells play an important role in hepatitis B virus (HBV)-related liver diseases, and the activation of hepatic stellate cells (HSCs) and their interactions with intrahepatic cells are the main cause of liver fibrosis. This article mainly introduces HBV-induced liver inflammation and the interaction between innate immune cells and HSCs and briefly describes the role of monocytes/macrophages and natural killer cells in the activation and killing of HSCs and the immunomodulatory effect of HSCs in the presence of HBV.

Hepatitis B virus (HBV) is a member of hepadnavirus, and HBV infection may not cause direct hepatocyte lesions. Host immune response determines whether the virus can be eliminated and is a major cause of HBV-related liver diseases. Myeloid-derived suppressor cells (MDSCs) are a group of non-lymphoid immune suppressor cells originating from bone marrow and can regulate innate and adaptive immune responses under different pathological conditions. Studies have shown that chronic hepatitis B patients have a significantly higher number of MDSCs in peripheral blood than the healthy population. This article introduces the role of HBV-induced MDSC subsets in persistent HBV infection and liver pathological mechanism.

Chronic hepatitis B induced by HBV infection is a significant risk factor leading to liver cirrhosis and liver cancer. Half a century ago， HBeAg was first discovered in the serum of HBV infected individuals， and although HBeAg does not participate in HBV infection or replication in hepatocytes， studies have shown that it can interfere with the innate and adaptive immune responses of the host and play an important role in immune activation and immunosuppression during chronic HBV infection. HBV has no cytotoxicity to the infected hepatocytes， and the antiviral action and inflammatory response mediated by immune response determine whether HBV is cleared or induces liver inflammation-related diseases. Therefore， this article reviews the formation of HBeAg and its immune activation and immunosuppression mechanisms in chronic HBV infection， with a focus on the different immune effects caused by HBeAg on innate immune and adaptive immune cells， and this article also elaborates on the dual role of HBeAg in inducing immune responses and explores the conversion role of HBeAg in different stages of chronic HBV infection.

Purines are mainly composed of ATP, NAD + , and nucleic acid. In addition to their key intracellular functions, NAD + , ATP, and their hydrolyzed products (including ADP, AMP, and adenosine) are important extracellular signals involved in physiological processes and pathological conditions. Purine signaling plays an important role in immune regulation of liver microenvironment. This article mainly summarizes the regulatory effect of purine signaling on immune cells in the liver and the effect of purine signaling on the progression of liver diseases by regulating the inflammatory and anti-inflammatory responses of immune cells in the liver.