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The Hepatitis B virus (HBV) causes a range of liver diseases, including acute and chronic hepatitis B (CHB), liver fibrosis, cirrhosis, and liver cancer. As a result, developing new antiviral strategies and drugs is critical for treating clinical liver diseases. Numerous clinical studies have demonstrated a correlation between the secretion levels of specific cytokines in infected patients and the activation of HBV-specific killer T lymphocytes. Consequently, conducting functional studies on diverse cytokines can offer new prospects for candidate targets in the development of anti-hepatitis B therapy.
Figure 1. Important cytokines and chemokines in the pathogenesis of HBV infection and HBV-related diseases. (Zhong S, et al., 2021)
IL-1 is an inflammatory cytokine, including IL-1α and IL-1β. In an in vitro infection model, IL-1β was able to significantly inhibit the RNA levels of different genotypes of HBV. It was further demonstrated that HBV may maintain persistent viral infection by inhibiting the antiviral effect of IL-1β, which may serve as a potential candidate molecule for anti-HBV therapy.
As an important immunomodulatory factor, IL-10 mainly can inhibit the secretion of pro-inflammatory factors, terminate the inflammatory response, and promote the differentiation of B lymphocytes to produce antibodies. During chronic HBV infection, abnormal elevation of IL-10 in serum correlates with HBV DNA load and hepatic inflammation, which may be one of the important causes of HBV chronicity and even promote the progression of fibrosis.
IL-18 is a multifunctional cytokine involved in the regulation of the immune homeostasis of helper T-lymphocytes (Th)1 and 2. Studies have shown that in a mouse model, IL-18 can synergize with IL-12 in inducing IFN-γ production, which in turn inhibits HBV.
IL-33 is widely present in a variety of tissues and cells as an alert signaling protein and can be secreted cytosolically under stress conditions to participate in the body's inflammatory response. IL-33 has been shown to increase the level of humoral immunity against HBV by activating follicular helper T lymphocytes. On the other hand, elevated expression levels of IL-33 and its membrane receptors in viral hepatitis are often associated with the development of liver fibrosis.
The CSF family mainly consists of granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and macrophage colony-stimulating factor (M-CSF). GM-CSF can induce the maturation and differentiation of dendritic cells as well as promote antigen-presenting cell presentation and therefore has been used as an adjuvant to antitumor or antiviral immunotherapy. It was found that HBV transgenic mice pretreated with GM-CSF and then vaccinated with the hepatitis B vaccine could break the state of immune tolerance, activate HBV-specific humoral immunity and CTL response, and promote viral clearance.
IFN has become a widely used antiviral therapeutic agent since its discovery. In in vitro infection experiments, it has been found that high doses of IFNα can effectively inhibit HBV. IFNα ultimately achieves HBV clearance by exerting an immunomodulatory effect and activating the effects of NK cells, HBV-specific B-lymphocytes, and T-lymphocytes.
Chemokines are a class of small molecule proteins that promote the directed movement of leukocytes, endothelial cells, and epithelial cells involved in tumor metastasis, chronic inflammation, and autoimmune diseases. Serum levels of CXC ligands are significantly elevated in HBV acutely infected humans and chimpanzees.
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