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Published on: February 19, 2019
Immune suppression in chronic hepatitis B infection associated liver disease: A review
Tian-Yang Li1, Yang Yang2, Guo Zhou1
1Infectious Disease, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000, Guangdong Province, China.
Insights
Hepatitis B virus (HBV) infection impairs immune responses, leading to liver diseases like fibrosis and cancer. This review explores HBV-induced immune dysfunction and its role in liver disease progression.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Hepatitis B virus (HBV) infection is a primary cause of chronic liver disease, liver fibrosis, cirrhosis, and hepatocellular cancer (HCC).
- Chronic HBV infection is associated with impaired innate and adaptive immune responses, including dysfunction of monocytes/macrophages, dendritic cells, NK cells, and T cells.
- Suppressive immune cell subsets, such as myeloid-derived suppressive cells (MDSC), NK-reg, and T-reg, play a critical role in liver fibrogenesis and tumorigenesis during HBV infection.
Purpose of the Study:
- To review recent studies on innate and adaptive immune cell dysfunction in chronic HBV infection, liver fibrosis, cirrhosis, and HCC.
- To discuss the potential mechanisms of HBV-induced immunosuppressive cascades and their consequences.
- To aid ongoing research into the pathogenesis of HBV-related hepatic fibrosis and HCC.
Main Methods:
- Literature review of clinical studies and research on immune cell dysfunction in HBV infection.
- Analysis of mechanisms linking HBV-induced immune dysfunction to liver diseases.
- Synthesis of current understanding of immunosuppressive cascades in HBV.
Main Results:
- Chronic HBV infection leads to dysfunction in various innate and adaptive immune cells.
- Specific suppressive immune cell subsets are implicated in the progression of liver fibrosis and HCC.
- The precise mechanisms connecting HBV-induced immune dysfunction to liver disease pathogenesis require further elucidation.
Conclusions:
- Immune cell dysfunction is a critical factor in the development of HBV-related liver diseases.
- Understanding HBV-induced immunosuppression is key to developing effective therapies for liver fibrosis and HCC.
- Further research is needed to fully elucidate the complex interplay between HBV, the immune system, and liver disease progression.
Abstract:
Hepatitis B virus (HBV) infection is one the leading risk factors for chronic hepatitis, liver fibrosis, cirrhosis and hepatocellular cancer (HCC), which are a major global health problem. A large number of clinical studies have shown that chronic HBV persistent infection causes the dysfunction of innate and adaptive immune response involving monocytes/macrophages, dendritic cells, natural killer (NK) cells, T cells. Among these immune cells, cell subsets with suppressive features have been recognized such as myeloid derived suppressive cells(MDSC), NK-reg, T-reg, which represent a critical regulatory system during liver fibrogenesis or tumourigenesis. However, the mechanisms that link HBV-induced immune dysfunction and HBV-related liver diseases are not understood. In this review we summarize the recent studies on innate and adaptive immune cell dysfunction in chronic HBV infection, liver fibrosis, cirrhosis, and HCC, and further discuss the potential mechanism of HBV-induced immunosuppressive cascade in HBV infection and consequences. It is hoped that this article will help ongoing research about the pathogenesis of HBV-related hepatic fibrosis and HBV-related HCC.
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