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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Elimination of chronic viral infection by blocking CD27 signaling.

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.[1]


  1. Elimination of chronic viral infection by blocking CD27 signaling. Matter, M., Odermatt, B., Yagita, H., Nuoffer, J.M., Ochsenbein, A.F. J. Exp. Med. (2006) [Pubmed]
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