|
|
Blood, 15 August 2005, Vol. 106, No. 4, pp. 1175-1182.
Prepublished online as a Blood First Edition Paper on April 28, 2005; DOI 10.1182/blood-2005-01-0126.
 Previous Article | Next Article 
Submitted January 11, 2005
Accepted April 15, 2005
Plasma chemokine levels correlate with the outcome of antiviral therapy in hepatitis C patients
David Butera, Svetlana Marukian, Amy E Iwamaye, Edgardo Hembrador, Thomas J Chambers, Adrian M Di Bisceglie, Edgar D Charles, Andrew H Talal, Ira M Jacobson, Charles M Rice, and Lynn B Dustin*
Center for the Study of Hepatitis C, Rockefeller University, New York, NY, USA
Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA
Department of Medicine, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, USA
Center for the Study of Hepatitis C, Department of Medicine, Division of Gastroenterology and Hepatology, Weill Medical College of Cornell University, New York, NY, USA
* Corresponding author; email: dustinl{at}rockefeller.edu.
Chronic infection with the hepatitis C virus (HCV) is associated with failures of T cell-mediated immune clearance and with abnormal B cell growth and activation. We examined the levels of chemokines that bind to CXCR3 to determine whether such chemokines might play a role in the failure of the immune system to clear HCV infection. Elevations in CXCL9, CXCL10, and CXCL11 were observed in all HCV patients. CXCR3 expression was increased significantly on peripheral blood B lymphocytes, but not T lymphocytes, from individuals with HCV infection. Chemokine levels were measured in samples collected before, during and after antiviral therapy from a group of 29 patients infected with HCV genotypes 1a (24 patients) and 1b (5 patients). Levels of CXCL10 and CXCL9 decreased following successful antiviral therapy; CXCL11 did not decline significantly during or in the first 6 months after therapy. The baseline level of CXCL10 (measured before the start of antiviral treatment) was greatest in HCV patients who subsequently became nonresponders to therapy. These results suggest that plasma concentrations of immunoreactive CXCL10 may be a predictor of responsiveness or nonresponsiveness to antiviral therapy with pegylated IFN ± ribavirin. This observation has implications for understanding the pathogenesis of HCV infection.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
V. D. Gonzalez, K. Falconer, N. K. Bjorkstrom, K. G. Blom, O. Weiland, H.-G. Ljunggren, A. Alaeus, and J. K. Sandberg
Expansion of Functionally Skewed CD56-Negative NK Cells in Chronic Hepatitis C Virus Infection: Correlation with Outcome of Pegylated IFN-{alpha} and Ribavirin Treatment
J. Immunol.,
November 15, 2009;
183(10):
6612 - 6618.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T Asselah, I Bieche, A Sabbagh, P Bedossa, R Moreau, D Valla, M Vidaud, and P Marcellin
Gene expression and hepatitis C virus infection
Gut,
June 1, 2009;
58(6):
846 - 858.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T Asselah, I Bieche, S Narguet, A Sabbagh, I Laurendeau, M-P Ripault, N Boyer, M Martinot-Peignoux, D Valla, M Vidaud, et al.
Liver gene expression signature to predict response to pegylated interferon plus ribavirin combination therapy in patients with chronic hepatitis C
Gut,
April 1, 2008;
57(4):
516 - 524.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Rotondi, L. Chiovato, S. Romagnani, M. Serio, and P. Romagnani
Role of Chemokines in Endocrine Autoimmune Diseases
Endocr. Rev.,
August 1, 2007;
28(5):
492 - 520.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Rotondi, R. Minelli, F. Magri, P. Leporati, P. Romagnani, M. C. Baroni, R. Delsignore, M. Serio, and L. Chiovato
Serum CXCL10 levels and occurrence of thyroid dysfunction in patients treated with interferon-{alpha} therapy for hepatitis C virus-related hepatitis
Eur. J. Endocrinol.,
April 1, 2007;
156(4):
409 - 414.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. W. Cruise, J. R. Lukens, A. P. Nguyen, M. G. Lassen, S. N. Waggoner, and Y. S. Hahn
Fas Ligand Is Responsible for CXCR3 Chemokine Induction in CD4+ T Cell-Dependent Liver Damage
J. Immunol.,
May 15, 2006;
176(10):
6235 - 6244.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Rosa, G. Saletti, E. De Gregorio, F. Zorat, C. Comar, U. D'Oro, S. Nuti, M. Houghton, V. Barnaba, G. Pozzato, et al.
Activation of naive B lymphocytes via CD81, a pathogenetic mechanism for hepatitis C virus-associated B lymphocyte disorders
PNAS,
December 20, 2005;
102(51):
18544 - 18549.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
