|
|
Blood, 1 November 2007, Vol. 110, No. 9, pp. 3472-3479.
Prepublished online as a Blood First Edition Paper on July 26, 2007; DOI 10.1182/blood-2007-06-095414.
 Previous Article | Next Article 
Submitted June 13, 2007
Accepted July 23, 2007
Protection from CMV infection in immunodeficient hosts by adoptive transfer of memory B cells
Karin Klenovsek, Florian Weisel, Andrea Schneider, Uwe Appelt, Stipan Jonjic, Martin Messerle, Birgit Bradel-Tretheway, Thomas H Winkler, and Michael Mach*
Institute for Clinical and Molecular Virology, University Hospital Erlangen, Erlangen, Germany
Institute for Biology, Chair of Genetics, Hematopoesis Unit, University Erlangen-Nuremberg, Erlangen, Germany
Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nuremberg, Erlangen, Germany
Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka, Croatia
Hannover Medical School, Hannover, Germany
Dept. of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY, United States
* Corresponding author; email: mlmach{at}viro.med.uni-erlangen.de.
Severe disease associated with cytomegalovirus (CMV) infection is still a major problem in transplant patients. Support of the patients immune defense against the virus is a major goal in transplantation medicine. We have used the murine model of CMV (MCMV) to investigate the potential of a cell-based strategy to support the humoral antiviral immune response. Immunocompetent C57BL/6 mice were infected with MCMV and memory B cells from the immune animals were adoptively transferred into T and B cell deficient RAG-1-/- mice. Following MCMV infection, a virus specific IgG response developed within 4-7 days in the recipient animals. Concomitantly a significant reduction in viral titers and DNA copies in several organs was observed. In addition, the memory B cell transfer provided long term protection from the lethal course of the infection that is invariably seen in immunodeficient animals. Transfer of memory B cells was also effective in protecting from an already ongoing viral infection indicating a therapeutic potential of virus specific memory B cells. T cells were not involved in this process. Our data provide evidence that a cell based strategy to support the humoral immune response can be effective to combat infectious pathogens in severely immunodeficient hosts.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
C. Burkhardt, S. Himmelein, W. Britt, T. Winkler, and M. Mach
Glycoprotein N subtypes of human cytomegalovirus induce a strain-specific antibody response during natural infection
J. Gen. Virol.,
August 1, 2009;
90(8):
1951 - 1961.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Cekinovic, M. Golemac, E. P. Pugel, J. Tomac, L. Cicin-Sain, I. Slavuljica, R. Bradford, S. Misch, T. H. Winkler, M. Mach, et al.
Passive Immunization Reduces Murine Cytomegalovirus-Induced Brain Pathology in Newborn Mice
J. Virol.,
December 15, 2008;
82(24):
12172 - 12180.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. M. Walton, P. Wyrsch, M. W. Munks, A. Zimmermann, H. Hengel, A. B. Hill, and A. Oxenius
The Dynamics of Mouse Cytomegalovirus-Specific CD4 T Cell Responses during Acute and Latent Infection
J. Immunol.,
July 15, 2008;
181(2):
1128 - 1134.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
