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Updated: Apr 28, 2026

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
Published on: September 25, 2019
Controversial issues regarding the roles of IL-10 and IFN-γ in active/inactive chronic hepatitis B
Hossein Khorramdelazad1, Gholamhossein Hassanshahi1, Mohammad Kazemi Arababadi1
1Hossein Khorramdelazad, Gholamhossein Hassanshahi, Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, 7719617996 Rafsanjan, Iran.
Abstract:
According to the important roles played by cytokines in induction of appropriate immune responses against hepatitis B virus (HBV), Dimitropoulou et al have examined the important cytokines in their patients. They showed that the serum levels of interleukin 10 (IL-10) and interferon-γ (IFN-γ) were decreased in patients with HBeAg-negative chronic active hepatitis B compared with the inactive hepatitis B virus carriers (Dimitropoulou et al 2013). The controversy can be considered regarding the decreased serum levels of IFN-γ in the HBeAg-negative chronic active hepatitis B patients. They concluded that subsequent to decreased expression of IFN-γ, the process of HBV proliferation led to liver diseases. Previous studies stated that HBV is not directly cytopathic for the infected hepatocytes and immune responses are the main reason for destruction of hepatocytes (Chisari et al, 2010). Scientists believe that immune responses against HBV are stronger in active forms of chronic HBV infected patients than inactive forms (Zhang et al, 2012). Therefore, the findings from Dimitropoulou et al may deserve further attention and discussion. Additionally, downregulation of IL-10 in chronically active hepatitis B infected patients has also confirmed our claim. IL-10 is an anti-inflammatory cytokine and its expression is increased in inactive forms in order to downregulate immune responses (Arababadi et al, 2012). Thus, based on the results from Dimitropoulou et al, it can be concluded that increased immune responses in chronically active hepatitis B infected patients are related to declined expression of IL-10 and interestingly IFN-γ is not involved in induction of immune responses in these patients.
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