Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Hum Immunol. 2014 Jun;75(6):549-54. doi: 10.1016/j.humimm.2014.02.018. Epub 2014 Feb 12.
The current literature describes pivotal mechanisms in which hepatitis B virus (HBV) induces liver diseases including inflammation, cirrhosis and hepatocellular carcinoma (HCC). It appears that differences in genetic and immunological parameters between patients and controls may be responsible for inducing the prolonged forms of the infection. Previous studies demonstrated that Toll-Like Receptors (TLRs) play key roles in viral recognition and inducing appropriate immune responses. Therefore, TLRs can be considered as key sensors for HBV recognition and subsequent induction of immune responses against this virus. It has also been shown that the TLR2 detects several microbial PAMPs either in its homodimer form or in a heterodimer with TLR1 or TLR6 and subsequently activates NF-κB in a MYD88 dependent manner. Therefore, defective TLR2 expression may result in impaired immune responses against HBV which is reported in long-term forms of hepatitis B. This review presents the recent data regarding the status and important roles played by TLR2 in HBV recognition and induction or suppression of immune responses against HBV as well as its roles in the pathogenesis of cirrhosis and HCC in prolonged hepatitis B forms.
目前的文献描述了乙型肝炎病毒 (HBV) 引发肝脏疾病的关键机制，包括炎症、肝硬化和肝细胞癌 (HCC)。似乎患者和对照组之间遗传和免疫参数的差异可能导致感染的持续形式。先前的研究表明，Toll 样受体 (TLR) 在病毒识别和诱导适当免疫反应中发挥关键作用。因此，TLR 可以被视为 HBV 识别和随后诱导针对该病毒的免疫反应的关键传感器。也已经表明，TLR2 以 MYD88 依赖性方式检测其同源二聚体形式或与 TLR1 或 TLR6 形成的异源二聚体中的几种微生物 PAMP，并随后激活 NF-κB。因此，TLR2 表达缺陷可能导致针对 HBV 的免疫反应受损，这在乙型肝炎的长期形式中已有报道。这篇综述介绍了关于 TLR2 在 HBV 识别以及诱导或抑制针对 HBV 的免疫反应中的地位和重要作用的最新数据，以及其在慢性乙型肝炎形式的肝硬化和 HCC 发病机制中的作用。
