Khorramdelazad Hossein, Hassanshahi Gholamhossein, Arababadi Mohammad Kazemi
Hossein Khorramdelazad, Gholamhossein Hassanshahi, Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, 7719617996 Rafsanjan, Iran.
World J Gastrointest Pathophysiol. 2014 May 15;5(2):120-1. doi: 10.4291/wjgp.v5.i2.120.
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.
根据细胞因子在诱导针对乙型肝炎病毒(HBV)的适当免疫反应中所起的重要作用,迪米特罗普洛等人研究了他们患者体内的重要细胞因子。他们发现,与乙肝病毒非活动携带者相比,HBeAg阴性慢性活动性乙型肝炎患者的白细胞介素10(IL-10)和干扰素-γ(IFN-γ)血清水平降低(迪米特罗普洛等人,2013年)。对于HBeAg阴性慢性活动性乙型肝炎患者IFN-γ血清水平降低这一情况,存在争议。他们得出结论,IFN-γ表达降低后,HBV增殖过程导致了肝脏疾病。先前的研究表明,HBV对受感染的肝细胞并无直接细胞病变作用,免疫反应是肝细胞破坏的主要原因(奇萨里等人,2010年)。科学家们认为,慢性HBV感染患者的活跃形式对HBV的免疫反应比非活跃形式更强(张等人,2012年)。因此,迪米特罗普洛等人的研究结果可能值得进一步关注和讨论。此外,慢性活动性乙型肝炎感染患者中IL-10的下调也证实了我们的观点。IL-10是一种抗炎细胞因子,其在非活跃形式中的表达增加,以下调免疫反应(阿拉巴迪等人,2012年)。因此,根据迪米特罗普洛等人的研究结果,可以得出结论,慢性活动性乙型肝炎感染患者免疫反应增强与IL-10表达下降有关,有趣的是,IFN-γ并未参与这些患者免疫反应的诱导。