title: Can Toll-Like Receptor (TLR) 2 be considered as a new target for immunotherapy against hepatitis B infection?
abstract: 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.
authors: Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
authors: Vahid
authors: V
authors: Bagheri
authors: Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
authors: Azam
authors: A
authors: Askari
authors: Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Electronic address: dr.kazemi@rums.ac.ir.
authors: Mohammad Kazemi
authors: MK
authors: Arababadi
authors: School of Biomolecular and Physical Science, Eskitis Institute for Drug Discovery, Griffith University Nathan, Queensland, Australia.
authors: Derek
authors: D
authors: Kennedy
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000209:etiology / Q000276:immunology / Q000628:therapy* / Q000821:virology; D005786:Gene Expression Regulation; D006515:Hepatitis B virus / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000150:complications / Q000276:immunology / Q000628:therapy* / Q000821:virology; D006801:Humans; D007167:Immunotherapy; D008103:Liver Cirrhosis / Q000209:etiology / Q000276:immunology / Q000628:therapy* / Q000821:virology; D008113:Liver Neoplasms / Q000209:etiology / Q000276:immunology / Q000628:therapy* / Q000821:virology; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000276:immunology; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D055503:Protein Multimerization; D015398:Signal Transduction; D051194:Toll-Like Receptor 1 / Q000235:genetics / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000276:immunology*; D051216:Toll-Like Receptor 6 / Q000235:genetics / Q000276:immunology
chemical_list: C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; C495342:TLR2 protein, human; C495368:TLR6 protein, human; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2; D051216:Toll-Like Receptor 6