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  1. NTU Scholars
  2. 醫學院
  3. 臨床醫學研究所
Please use this identifier to cite or link to this item: https://scholars.lib.ntu.edu.tw/handle/123456789/568455
Title: Liver sinusoidal endothelial cell lectin inhibits CTL-dependent virus clearance in mouse models of viral hepatitis
Authors: Liu B.
Wang M.
Wang X.
Zhao D.
Liu D.
Liu J.
PEI-JER CHEN 
Yang D.
He F.
Tang L.
Issue Date: 2013
Publisher: American Association of Immunologists
Journal Volume: 190
Journal Issue: 8
Start page/Pages: 4185-4195
Source: Journal of Immunology
Abstract: 
Liver sinusoidal endothelial cell lectin (LSECtin) was recently reported to suppress intrahepatic T cell immunity and to limit immune-mediated liver injury. However, its role in the outcome and pathogenesis of viral infection has not yet been elucidated. Using a mouse model infected with a hepatotropic adenovirus, we found that the absence of LSECtin led to a higher frequency of intrahepatic effector CTLs. These cells produced higher levels of antiviral cytokines and cytotoxic factors and exhibited an increased expression of the transcription factors T-bet and Runx3. This phenotype observed in the LSECtin-knockout cells mediated a more efficient virus-specific cytotoxity compared with that of wild-type cells. As a consequence, LSECtin deficiency significantly accelerated liver adenovirus clearance. In contrast, LSECtin upregulation in the liver delayed viral clearance; this delayed clearance was accompanied by the downregulation of the antiviral activity of CTLs. We further constructed an immunocompetent mouse model of acute hepatitis B viral infection to demonstrate that LSECtin significantly delayed the clearance of hepatitis B virus from blood and infected hepatocytes by limiting the frequency of hepatitis B virus-specific IFN-γ-producing cells. Consistent with this function, LSECtin was upregulated in the liver of mouse models of viral hepatitis. Taken together, our results suggest that LSECtin may facilitate the reduction of liver inflammation at the cost of delaying virus clearance and that this effect might be hijacked by the virus as an escape mechanism. Copyright ? 2013 by The American Association of Immunologists, Inc.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-84984577786&doi=10.4049%2fjimmunol.1203091&partnerID=40&md5=320c8b4022904dfbcec87755c0d93907
https://scholars.lib.ntu.edu.tw/handle/123456789/568455
ISSN: 0022-1767
DOI: 10.4049/jimmunol.1203091
SDG/Keyword: gamma interferon; lectin; liver sinusoidal endothelial cell lectin; transcription factor RUNX3; transcription factor T bet; unclassified drug; acute hepatitis; Adenovirus; animal cell; animal experiment; animal model; animal tissue; article; controlled study; cytokine production; cytotoxic T lymphocyte; cytotoxicity; down regulation; hepatitis B; liver cell; mouse; nonhuman; priority journal; protein expression; upregulation; viral clearance; virus hepatitis; wild type
[SDGs]SDG3
Appears in Collections:臨床醫學研究所

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