The Journal of Experimental Medicine
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Published online 21 August 2006 doi:10.1084/jem.20060651
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 9, 2145-2155
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ARTICLE

 Elimination of chronic viral infection by blocking CD27 signaling

Matthias Matter1, Bernhard Odermatt4, Hideo Yagita5, Jean-Marc Nuoffer2, and Adrian F. Ochsenbein1,3

1 Tumor Immunology, Department of Clinical Research, 2 Institute of Clinical Chemistry, and 3 Institute of Medical Oncology, Inselspital, University of Berne, CH-3010 Bern, Switzerland
4 Department of Pathology, University Hospital, 8091 Zurich, Switzerland
5 Department of Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan

CORRESPONDENCE Adrian F. Ochsenbein: adrian.ochsenbein{at}insel.ch

Neutralizing antibody (nAb) responses to lymphocytic choriomeningitis virus (LCMV) in mice and immunodeficiency virus and hepatitis C virus in humans are usually weak and slow to develop. This may be the result of structural properties of the surface glycoprotein, a low frequency of B cells with neutralizing specificity, and the necessity of prolonged affinity maturation of specific nAbs. In this study, we show that during LCMV infection, CD27 signaling on CD4+ T cells enhances the secretion of interferon-{gamma} and tumor necrosis factor-{alpha}. These inflammatory cytokines lead to the destruction of splenic architecture and immunodeficiency with reduced and delayed virus-specific nAb responses. Consequently, infection with the otherwise persistent LCMV strain Docile was eliminated after CD27 signaling was blocked. Our data provide a novel mechanism by which LCMV avoids nAb responses and suggest that blocking the CD27–CD70 interaction may be an attractive strategy to prevent chronic viral infection.

Abbreviations used: HCV, hepatitis C virus; LCMV, lymphocytic choriomeningitis virus; nAb, neutralizing antibody; PNA, peanut agglutinin; VSV, vesicular stomatitis virus.


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