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Journal of Virology, January 2007, p. 945-953, Vol. 81, No. 2
0022-538X/07/$08.00+0     doi:10.1128/JVI.01354-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Analysis of CD127 and KLRG1 Expression on Hepatitis C Virus-Specific CD8+ T Cells Reveals the Existence of Different Memory T-Cell Subsets in the Peripheral Blood and Liver{triangledown}

Bertram Bengsch,1 Hans Christian Spangenberg,1 Nadine Kersting,1 Christoph Neumann-Haefelin,1 Elisabeth Panther,1 Fritz von Weizsäcker,1 Hubert E. Blum,1 Hanspeter Pircher,2 and Robert Thimme1*

Department of Medicine II,1 Department of Immunology, Institute of Medical Microbiology, University of Freiburg, Germany2

Received 27 June 2006/ Accepted 22 October 2006

The differentiation and functional status of virus-specific CD8+ T cells is significantly influenced by specific and ongoing antigen recognition. Importantly, the expression profiles of the interleukin-7 receptor alpha chain (CD127) and the killer cell lectin-like receptor G1 (KLRG1) have been shown to be differentially influenced by repetitive T-cell receptor interactions. Indeed, antigen-specific CD8+ T cells targeting persistent viruses (e.g., human immunodeficiency virus and Epstein-Barr virus) have been shown to have low CD127 and high KLRG1 expressions, while CD8+ T cells targeting resolved viral antigens (e.g., FLU) typically display high CD127 and low KLRG1 expressions. Here, we analyzed the surface phenotype and function of hepatitis C virus (HCV)-specific CD8+ T cells. Surprisingly, despite viral persistence, we found that a large fraction of peripheral HCV-specific CD8+ T cells were CD127+ and KLRG1– and had good proliferative capacities, thus resembling memory cells that usually develop following acute resolving infection. Intrahepatic virus-specific CD8+ T cells displayed significantly reduced levels of CD127 expression but similar levels of KLRG1 expression compared to the peripheral blood. These results extend previous studies that demonstrated central memory (CCR7+) and early-differentiated phenotypes of HCV-specific CD8+ T cells and suggest that insufficient stimulation of virus-specific CD8+ T cells by viral antigen may be responsible for this alteration in HCV-specific CD8+ T-cell differentiation during chronic HCV infection.

* Corresponding author. Mailing address: Department of Medicine II, University Hospital Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany. Phone: 49 761 270 3280. Fax: 49 761 270 3372. E-mail: thimme{at}med1.ukl.uni-freiburg.de.

{triangledown} Published ahead of print on 1 November 2006.

Journal of Virology, January 2007, p. 945-953, Vol. 81, No. 2
0022-538X/07/$08.00+0     doi:10.1128/JVI.01354-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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