Elimination of chronic viral infection by blocking CD27 signaling

Matter, Matthias; Odermatt, Bernhard; Yagita, Hideo; Nuoffer, Jean-Marc; Ochsenbein, Adrian F (2006). Elimination of chronic viral infection by blocking CD27 signaling. Journal of experimental medicine, 203(9), pp. 2145-55. New York, N.Y.: Rockefeller University Press 10.1084/jcm.20060651

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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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Medical Oncology
04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Institute of Clinical Chemistry

UniBE Contributor:

Matter, Matthias; Nuoffer, Jean-Marc and Ochsenbein, Adrian

ISSN:

0022-1007

ISBN:

16923852

Publisher:

Rockefeller University Press

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:46

Last Modified:

06 Dec 2013 13:41

Publisher DOI:

10.1084/jcm.20060651

PubMed ID:

16923852

Web of Science ID:

000240288000017

URI:

https://boris.unibe.ch/id/eprint/18998 (FactScience: 1359)

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