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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4424-4432.
Prepublished online as a Blood First Edition Paper on February 14, 2006; DOI 10.1182/blood-2005-09-3903.
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IMMUNOBIOLOGY
Foxp3+CD4+CD25+ T cells control virus-specific memory T cells in chimpanzees that recovered from hepatitis C
Tobias Manigold,
Eui-Cheol Shin,
Eishiro Mizukoshi,
Kathleen Mihalik,
Krishna K. Murthy,
Charles M. Rice,
Ciriaco A. Piccirillo, and
Barbara Rehermann
From the Immunology Section, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, MD; Laboratory of Hepatitis Viruses, Center for Biologics Evaluation and Research (CBER), Food and Drug Administration (FDA), Bethesda, MD; Department of Virology and Immunology, Southwest Foundation for Biomedical Research, San Antonio, TX; Center for the Study of Hepatitis C, Rockefeller University, New York, NY; Laboratory of Immunology, NIH, Bethesda, MD; and Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada.
Hepatitis C virus (HCV) poses a global health problem because it readily establishes persistent infection and a vaccine is not available. CD4+CD25+ T cells have been implicated in HCV persistence because their frequency is increased in the blood of HCV-infected patients and their in vitro depletion results in increased IFN- production by HCV-specific T cells. Studying a well-characterized cohort of 16 chimpanzees, the sole animal model for HCV infection, we here demonstrate that the frequency of Foxp3+CD4+CD25+ regulatory T cells (TRegs) and the extent of suppression was as high in spontaneously HCV-recovered chimpanzees as in persistently HCV-infected chimpanzees. Foxp3+CD4+CD25+ TRegs suppressed IFN- production, expansion, and activation-induced cell death of HCV-specific T cells after recovery from HCV infection and in persistent HCV infection. Thus, TReg cells control HCV-specific T cells not only in persistent infection but also after recovery, where they may regulate memory T-cell responses by controlling their activation and preventing apoptosis. However, Foxp3+CD4+CD25+ TReg cells of both HCV-recovered and HCV-infected chimpanzees differed from Foxp3+CD4+CD25+TReg cells of HCV-naive chimpanzees in increased IL-2 responsiveness and lower T-cell receptor excision circle content, implying a history of in vivo proliferation. This result suggests that HCV infection alters the population of Foxp3+CD4+CD25+ TReg cells.
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