title: Downregulation of TIPE2 mRNA expression in peripheral blood mononuclear cells from patients with chronic hepatitis C.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China. kongliyouxiang@sina.com.
authors.forename: Li
authors.initials: L
authors.lastname: Kong
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.|Department of Internal Medicine, Laoting Traditional Chinese Medical Hospital, Tangshan, 063600, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Liu
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.|Department of Internal Medicine, Hebei Province Chinese Medicine Research Institute, Shijiazhuang, 053100, China.
authors.forename: Yu-Zhuo
authors.initials: YZ
authors.lastname: Zhang
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Meng
authors.initials: M
authors.lastname: Jin
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Bo-Rong
authors.initials: BR
authors.lastname: Wu
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Wei-Zhen
authors.initials: WZ
authors.lastname: Wang
authors.affiliation: Department of Experimental Center, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.affiliation: Department of Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Yue-Min
authors.initials: YM
authors.lastname: Nan
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104, USA.
authors.forename: Youhai H
authors.initials: YH
authors.lastname: Chen
keywords: Chronic hepatitis C; TLR2; TLR4; TNFAIP8L2