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JCI table of contents: Dec. 22, 2010
Date:12/22/2010

poor response to treatment. The work of a team of researchers, led by Matthew Albert, at the Institut Pasteur, France, has now provided an explanation for this. Specifically, the team found that CXCL10 in the blood of patients chronically infected with HCV was shorter than normal CXCL10 and could not attract immune cells. Further analysis revealed that this antagonist form of CXCL10 was generated in the blood by cleavage by the protein DPP4. As discussed by Lynn Dustin and Edgar Charles, at The Rockefeller University, New York, in an accompanying commentary, if these data can be successfully validated in larger cohorts of patients it should be possible to identify those patients who will not respond to anti-HCV treatment and spare them from a therapy that has severe side effects.

TITLE: Evidence for an antagonist form of the chemokine CXCL10 in patients chronically infected with HCV

AUTHOR CONTACT:
Matthew L. Albert
Institut Pasteur, Paris, France.
Phone: 33.0.1.45.68.85.45; Fax: 33.0.1.45.68.85.48; E-mail: albertm@pasteur.fr.

View this article at: http://www.jci.org/articles/view/40594?key=48a115adfcdd54a3517b

ACCOMPANYING COMMENTARY
TITLE: Chemokine antagonism in chronic hepatitis C virus infection

AUTHOR CONTACT:
Lynn B. Dustin
The Rockefeller University, New York, New York, USA.
Phone: 212.327.7067; Fax: 212.327.7048; E-mail: dustinl@rockefeller.edu.

View this article at: http://www.jci.org/articles/view/45610?key=382c2266e619a5edac5c


IMMUNOLOGY: Two genetic hits and you are down with autoimmune lymphoproliferative syndrome

Autoimmune lymphoproliferative syndrome (ALPS) is a genetic disease that affect
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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