Fibroleukin at fault in viral hepatitis

July 01, 2003

Unlike other virus-induced diseases, acute and chronic liver disease caused by the hepatitis B virus are not the result of direct viral-induced tissue destruction, but rather a consequence of the host immune response to the virus. Two such responses to viral hepatitis B infection are the deposition of fibrin and thrombosis within the small blood vessels of the liver. Activated endothelial cells and macrophages express procoagulants including a novel prothrombinase, Fgl2/fibroleukin, important for the initiation and localization of fibrin deposition. In the July 1 issue of the Journal of Clinical Investigation, Philip Marsden and colleagues from the University of Toronto, Canada, show that mice lacking Fgl2/fibroleukin fail to develop a procoagulant response to infection with hepatitis B. In addition, the authors show that in humans with chronic hepatitis B virus infection, expression of the Fgl2/fibroleukin gene is high and fibrin is deposited in the liver. Collectively, these studies indicate a critical role for Fgl2/fibroleukin in the pathophysiology of viral hepatitis and suggest that inhibition of this prothrombinase may be important for the treatment of inflammatory diseases not only of the liver but also of other tissues.
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TITLE: The Fgl2/fibroleukin prothrombinase contributes to immunologically-mediated thrombosis in experimental and human viral hepatitis

AUTHOR CONTACT:
Philip A. Marsden
University of Toronto, Toronto, Ontario, Canada.
Phone: 416-978-2441
Fax: 416-978-8765
E-mail: p.marsden@utoronto.ca

View the PDF of this article at: http://www.jci.org/cgi/content/full/112/1/58

JCI Journals

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