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Abstract
Immune responses to hepatitis C virus (HCV) fail to clear the virus in most individuals. Why patients who are less likely to clear HCV infection have high plasma levels of CXCL10 (also known as IP-10), a chemokine that directs T cells to sites of infection, has long been unclear. In this issue of the JCI, Casrouge and colleagues shed light on this paradox by showing that CXCL10 in the plasma of many HCV patients is enzymatically processed to produce a CXCL10 receptor antagonist. These findings introduce a role for chemokine antagonism during HCV infection and unveil new avenues for improved HCV diagnosis and therapy.
Authors
Edgar D. Charles, Lynn B. Dustin
Figure 1
Model of chemokine antagonism in the HCV-infected liver.
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CXCL10 produced in the infected liver recruits T cells from the blood to the infected hepatocyte via the liver sinusoid and the space of Disse (left). When processed by DPP4, CXCL10 becomes an antagonist of T cell recruitment (right). In this issue of the JCI , Casrouge and colleagues have shown that levels of this shortened antagonist form of CXCL10 are increased in many patients who fail to clear HCV (4 ), suggesting a role for chemokine antagonism in an ineffective anti-HCV response.
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ISSN: 0021-9738 (print), 1558-8238 (online)