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, 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:	05 Dec 2022 14:14
Publisher DOI:	10.1084/jcm.20060651
PubMed ID:	16923852
Web of Science ID:	000240288000017
URI:	https://boris.unibe.ch/id/eprint/18998 (FactScience: 1359)