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International Immunology Advance Access originally published online on February 10, 2009
International Immunology 2009 21(4):339-348; doi:10.1093/intimm/dxp002
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© The Author 2009. Published by Oxford University Press on behalf of The Japanese Society for Immunology. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press and The Japanese Society for Immunology are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Transgenic Bcl-3 slows T cell proliferation

Michael F. J. Bassetti1, Janice White1,2, John W. Kappler1,2,3,4 and Philippa Marrack1,2,4,5

1 Integrated Department of Immunology
2 Howard Hughes Medical Institute and National Jewish Health
3 Department of Pharmacology
4 Department of Medicine
5 Department of Biochemistry and Molecular Genetics, University of Colorado Denver Health Sciences Center, Denver, CO 80206, USA

Correspondence to: P. Marrack; E-mail: marrackp{at}njc.org

Immunological adjuvants, such as bacterial LPS, increase the mRNA levels of the IkB-related NF-{kappa}B transcriptional transactivator, Bcl-3, in activated T cells. Adjuvants also increase the life expectancy of activated T cells, as does over-expression of Bcl-3, suggesting that Bcl-3 is part of the pathway whereby adjuvants affect T cell lifespans. However, previous reports, confirmed here, show that adjuvants also increase the life expectancies of Bcl-3-deficient T cells, making Bcl-3’s role and effects in adjuvant-induced survival uncertain. To investigate the functions of Bcl-3 further, here we confirm the adjuvant-induced expression of Bcl-3 mRNA and show Bcl-3 induction at the protein level. Bcl-3 was expressed in mice via a transgene driven by the human CD2 promoter. Like other protective events, over-expression of Bcl-3 slows T cell activation very early in T cell responses to antigen, both in vitro and in vivo. This property was intrinsic to the T cells over-expressing the Bcl-3 and did not require Bcl-3 expression by other cells such as antigen-presenting cells.

Keywords: activation, memory, proliferation, T cell

Transmitting editor: K. Murphy

Received 1 April 2008, accepted 3 January 2009.


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