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15 July 2008

Volume 198, Number 2
The Journal of Infectious Diseases 2008;198:213–217
© 2008 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2008/19802-0009$15.00
DOI: 10.1086/589309
BRIEF REPORT

Hepatitis C Virus–Induced Secretion of Inflammatory Chemokines Preferentially Recruits NKG2A+CD8+ T Cells

Jacob Nattermann,

Roman Sherzada,

Agathe Iwan,

Dominik Bogen,

Ina Maria Niederle,

Daniela Schulte,

Eva Mertens,

Hans Dieter Nischalke,

Benjamin Krämer,

Tilman Sauerbruch,

Ludger Leifeld,a and

Ulrich Spenglera

Department of Internal Medicine I, University of Bonn, Germany

In patients with hepatitis C, a loss‐of‐function mutation of chemokine receptor CCR5 (CCR5Δ32) has been shown to be associated with spontaneous viral clearance and lower levels of hepatic inflammation. In the present study, we show that CCR5 is coexpressed with the inhibitory NKG2A receptor on CD8+ T cells. Consequently, CCR5+ T cells were highly susceptible to NKG2A‐mediated inhibition of cytotoxic activity and NKG2A+ lymphocytes were preferentially attracted by CCR5 ligands induced by hepatitis C virus E2 antigen. Thus, CCR5 is likely to exert immunoregulatory effects in hepatitis C virus infection by preferentially recruiting CD8+ T cells bearing the inhibitory NKG2A receptor to the liver.

Received 16 October 2007; accepted 25 January 2008; electronically published 23 May 2008.

Reprints or correspondence: Jacob Nattermann, Department of Internal Medicine I, University of Bonn, Bonn, Germany ().

Cited by

Mathis Heydtmann, David H. Adams. (2009) Chemokines in the immunopathogenesis of hepatitis C infection. Hepatology 49:2, 676-688
Online publication date: 1-Mar-2009.
CrossRef

  • Potential conflicts of interest: none reported.

    Financial support: Deutsche Forschungsgemeinschaft (SFB 704, TP A6 to J.N. and U.S.).

  • These authors contributed equally to this work.

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