The Journal of Experimental Medicine
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Published online 9 February 2004 doi:10.1084/jem.20030091
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 4, 593-602
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Activation of Virus-specific Memory B Cells in the Absence of T Cell Help

Barbara J. Hebeis1, Karin Klenovsek1, Peter Rohwer2, Uwe Ritter3, Andrea Schneider1,4, Michael Mach1, and Thomas H. Winkler4

1 Institute for Clinical and Molecular Virology, Nikolaus Fiebiger Center
2 Department of Medicine III, Nikolaus Fiebiger Center
3 Interdisciplinary Center for Clinical Research (IZKF), Nikolaus Fiebiger Center
4 Institute for Microbiology, Biochemistry and Genetics, Chair of Genetics, Hematopoiesis Unit, University of Erlangen-Nuremberg, D-91054 Erlangen, Germany

Address correspondence to Thomas H. Winkler, Hematopoiesis Unit, Nikolaus Fiebiger Center for Molecular Medicine, University of Erlangen-Nürnberg, Glückstrasse 6, D-91054 Erlangen, Germany. Phone: 49-9131-85-29136; Fax: 49-9131-85-29106; email: twinkler{at}molmed.uni-erlangen.de

Humoral immunity is maintained by long-lived plasma cells, constitutively secreting antibodies, and nonsecreting resting memory B cells that are rapidly reactivated upon antigen encounter. The activation requirements for resting memory B cells, particularly the role of T helper cells, are unclear. To analyze the activation of memory B cells, mice were immunized with human cytomegalovirus, a complex human herpesvirus, and tick-born encephalitis virus, and a simple flavivirus. B cell populations devoid of Ig-secreting plasma cells were adoptively transferred into T and B cell–deficient RAG-1-/- mice. Antigenic stimulation 4–6 d after transfer of B cells resulted in rapid IgG production. The response was long lasting and strictly antigen specific, excluding polyclonal B cell activation. CD4+ T cells were not involved since (a) further depletion of CD4+ T cells in the recipient mice did not alter the antibody response and (b) recipient mice contained no detectable CD4+ T cells 90 d posttransfer. Memory B cells could not be activated by a soluble viral protein without T cell help. Transfer of memory B cells into immunocompetent animals indicated that presence of helper T cells did not enhance the memory B cell response. Therefore, our results indicate that activation of virus-specific memory B cells to secrete IgG is independent of cognate or bystander T cell help.

Key Words: antigen-specific immunity • immunological memory • B lymphocyte memory • cytomegalovirus • adoptive transfer

The online version of this article includes supplemental material.

B. Hebeis' present address is Babraham Institute, Babraham, Cambridge CB2 4AT, UK.

Abbreviations used in this paper: DB, dense body; FDC, follicular DC; gB, glycoprotein B; GC, germinal center; HCMV, human cytomegalovirus; RAG, recombinase-activating gene; RI, relative intensity; TBEV, tick-born encephalitis virus.


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