| First Author | Matter M | Year | 2006 |
| Journal | J Exp Med | Volume | 203 |
| Issue | 9 | Pages | 2145-55 |
| PubMed ID | 16923852 | Mgi Jnum | J:124567 |
| Mgi Id | MGI:3721867 | Doi | 10.1084/jem.20060651 |
| Citation | Matter M, et al. (2006) Elimination of chronic viral infection by blocking CD27 signaling. J Exp Med 203(9):2145-55 |
| abstractText | 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. |
