Published online May 15, 2014. doi: 10.4291/wjgp.v5.i2.120
Revised: December 3, 2013
Accepted: April 17, 2014
Published online: May 15, 2014
Processing time: 231 Days and 18.9 Hours
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.
Core tip: Cytokines play a central role in the induction of appropriate immune responses against hepatitis B, as well as the clinical manifestations of the disease. Dimitropoulou et al showed that serum levels of interleukin 10 and interferon-γ decreased in patients with HBeAg-negative chronic active hepatitis B compared with inactive hepatitis B virus (HBV) carriers (Dimitropoulou et al, 2013) and concluded that this can lead to liver disease. However, we challenge their conclusion because we believe that inappropriate host immune responses are the main causes responsible for the clinical manifestations of the disease, but not the actual replication of the HBV particles.