Li Kong1, Kun Liu2,3, Yu-Zhuo Zhang2,4, Meng Jin2, Bo-Rong Wu2, Wei-Zhen Wang2, Wei Li5, Yue-Min Nan2, Youhai H Chen6. 1. Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China. kongliyouxiang@sina.com. 2. Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China. 3. Department of Internal Medicine, Laoting Traditional Chinese Medical Hospital, Tangshan, 063600, China. 4. Department of Internal Medicine, Hebei Province Chinese Medicine Research Institute, Shijiazhuang, 053100, China. 5. Department of Experimental Center, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China. 6. Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104, USA.
Abstract
PURPOSE: Hepatitis C virus (HCV) infection causes chronic hepatitis in approximately 80 % of cases. Although it is well recognized that the immune system plays an important role in determining the outcomes of HCV infection, the underlying molecular mechanisms of persistent HCV infection and hepatic injury are incompletely understood. Tumor necrosis factor-α-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is a newly identified negative regulator of innate and adaptive immunity. The goal of the present study is to investigate the potential role of TIPE2 in chronic hepatitis C (CHC) infection. METHODS: We used quantitative real-time reverse transcription polymerase chain reaction to examine the mRNA expression levels of TIPE2, Toll-like receptor (TLR) 2, and TLR4 in peripheral blood mononuclear cells from 60 CHC patients and 30 healthy controls. RESULTS: The TIPE2 mRNA expression was significantly downregulated, whereas that of TLR2 and TLR4 was upregulated in CHC patients compared with healthy controls. TIPE2 mRNA expression levels were negatively correlated with serum ALT, AST, and HCV RNA levels. TIPE2 mRNA expression was also negatively correlated with TLR2 and TLR4 mRNA levels in CHC patients. Moreover, TIPE2 mRNA expression was upregulated, whereas that of TLR2 and TLR4 was downregulated after treatment of patients with interferon-α and ribavirin. CONCLUSIONS: These results indicate that HCV may promote chronic hepatitis by decreasing TIPE2 expression while enhancing TLR signaling.
PURPOSE:Hepatitis C virus (HCV) infection causes chronic hepatitis in approximately 80 % of cases. Although it is well recognized that the immune system plays an important role in determining the outcomes of HCV infection, the underlying molecular mechanisms of persistent HCV infection and hepatic injury are incompletely understood. Tumor necrosis factor-α-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is a newly identified negative regulator of innate and adaptive immunity. The goal of the present study is to investigate the potential role of TIPE2 in chronic hepatitis C (CHC) infection. METHODS: We used quantitative real-time reverse transcription polymerase chain reaction to examine the mRNA expression levels of TIPE2, Toll-like receptor (TLR) 2, and TLR4 in peripheral blood mononuclear cells from 60 CHCpatients and 30 healthy controls. RESULTS: The TIPE2 mRNA expression was significantly downregulated, whereas that of TLR2 and TLR4 was upregulated in CHCpatients compared with healthy controls. TIPE2 mRNA expression levels were negatively correlated with serum ALT, AST, and HCV RNA levels. TIPE2 mRNA expression was also negatively correlated with TLR2 and TLR4 mRNA levels in CHCpatients. Moreover, TIPE2 mRNA expression was upregulated, whereas that of TLR2 and TLR4 was downregulated after treatment of patients with interferon-α and ribavirin. CONCLUSIONS: These results indicate that HCV may promote chronic hepatitis by decreasing TIPE2 expression while enhancing TLR signaling.
Authors: I Mozer-Lisewska; G Dworacki; E Kaczmarek; W Sluzewski; M Kaczmarek; A Woźniak; J Zeromski Journal: Scand J Immunol Date: 2006-04 Impact factor: 3.487
Authors: I Caramalho; L Rodrigues-Duarte; A Perez; S Zelenay; C Penha-Gonçalves; J Demengeot Journal: Scand J Immunol Date: 2011-12 Impact factor: 3.487