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Elevated Numbers of FcRIIIA⁺ (CD16⁺) Effector CD8 T Cells with NK Cell-Like Function in Chronic Hepatitis C Virus Infection¹

Niklas K. Björkström^2,*, Veronica D. Gonzalez^*, Karl-Johan Malmberg^*, Karolin Falconer, Annette Alaeus, Greg Nowak, Carl Jorns, Bo-Göran Ericzon, Ola Weiland, Johan K. Sandberg^* and Hans-Gustaf Ljunggren^2,*

^* Center for Infectious Medicine and Department of Medicine, Unit of Infectious Diseases; and Department of Clinical Science, Intervention and Technology, Division of Transplantation Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden

CTL are crucial in the defense against viral infections. In the course of investigating peripheral blood and intrahepatic CD8 T cells in patients with chronic hepatitis C virus (HCV) infection, we observed a significant population of CD8 T cells expressing the FcRIIIA (CD16) receptor. This observation led us to characterize these cells with respect to their phenotype and function in a cohort of patients with chronic HCV infection as well as in healthy blood donors. On average, 10% of peripheral blood CD8 T cells from HCV-infected patients expressed CD16 compared with only a few percent in healthy donors. CD16⁺ CD8 T cells displayed a late-stage effector phenotype with high levels of perforin. These cells exhibited a restricted TCR profile suggesting underlying clonal expansion. Stimulation of CD16 on CD8 T cells evoked a vigorous response similar to that of CD16 stimulation in NK cells. Our data suggest that CD8 T cells, during chronic HCV infection in humans, continue to differentiate beyond defined stages of terminal effector cells, acquiring CD16 and NK cell-like functional properties.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Swedish Foundation for Strategic Research, the Swedish Research Council, the Swedish Cancer Society, the Swedish International Development Cooperation Agency, the Royal Swedish Academy of Sciences, the Cancer Society of Stockholm, the Karolinska Institutet, and the Karolinska University Hospital.

² Address correspondence and reprint requests to Niklas K. Björkström or Dr. Hans-Gustaf Ljunggren, Department of Medicine, Center for Infectious Medicine, F59, Karolinska Institutet, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Sweden. E-mail addresses: Niklas.bjorkstrom{at}ki.se or Hans-gustaf.ljunggren{at}ki.se

³ Abbreviations used in this paper: HCV, hepatitis C virus; ADCC, Ab-dependent cellular cytotoxicity; IHL, intrahepatic lymphocyte; KIR, killer cell Ig-like receptor; NKR, NK cell receptor.