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Arch Pathol Lab Med. 2013 Nov;137(11):1674-9. doi: 10.5858/arpa.2012-0415-OA.

Decreased expressions of Toll-like receptor 9 and its signaling molecules in chronic hepatitis B virus-infected patients.

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From the Departments of Internal Medicine (Drs Sajadi and Mirzaei), Biochemistry (Mr Daredor), and Immunology (Ms Moogooi), Faculty of Medicine, the Molecular Medicine Research Center (Dr Hassanshahi and Mr Khorramdelazad), the Department of Nursing, Faculty of Nursing (Dr Ravary), and the Immunology of Infectious Diseases Research Center (Dr Arababadi), Rafsanjan University of Medical Sciences, Rafsanjan, Iran; the Meybod Health Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran (Mr Hosseini); and the School of Biomolecular and Physical Science, Eskitis Institute for Cell and Molecular Therapies, Griffith University, Nathan, Queensland, Australia (Dr Kennedy).



Toll-like receptors (TLRs) play crucial roles in immune responses, especially innate immunity, against viral infections. Toll-like receptor 9 recognizes intracellular viral double-strand DNA, which leads to the activation of nuclear factor B (NF-κB) through the myeloid differentiation primary response 88 (MYD88) pathway. Defects in the expression of TLR9 and its signaling molecules may cause attenuated immune responses against hepatitis B virus.


To determine expression levels of TLR9 messenger RNA along with MYD88, interleukin 1 receptor-associated kinase 1 (IRAK1), tumor necrosis factor receptor-associated factor 6 (TRAF6), and NF-κB in the peripheral blood mononuclear cells obtained from chronic hepatitis B virus (CHB)-infected patients.


In this study, 60 CHB patients and 60 healthy controls were recruited and the expression of TLR9 and its downstream signaling molecules was examined by real-time polymerase chain reaction techniques using β-actin as a housekeeping gene.


Our results showed that expression of TLR9, MYD88, IRAK1, TRAF6, and NF-κB in peripheral blood mononuclear cells of CHB patients was significantly decreased in comparison with healthy controls.


According to our results, it appears that CHB patients are unable to appropriately express genes in the TLR9 pathway, which may impede immune responses against hepatitis B virus infection. These results suggest a mechanism that may partially explain the fact that immune responses are disrupted in CHB patients.

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