This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chilton, P. M. Articles by Mitchell, T. C. Search for Related Content PubMed PubMed Citation Articles by Chilton, P. M. Articles by Mitchell, T. C.

CD8 T Cells Require Bcl-3 for Maximal Gamma Interferon Production upon Secondary Exposure to Antigen

The Institute for Cellular Therapeutics,¹ the Department of Microbiology and Immunology, University of Louisville, Louisville, Kentucky 40202²

Received 28 October 2005/ Returned for modification 5 January 2006/ Accepted 7 April 2006

Adjuvant-induced survival of T cells after antigen activation correlates with increased expression of Bcl-3. Bcl-3 is an NF-B/IB family member and has been implicated in transcriptional regulation in several cell types. We tested the ability of mice deficient in Bcl-3 (Bcl-3 KO) to exhibit T-cell adjuvant-induced survival after challenge with the superantigen staphylococcal enterotoxin B (SEB), using lipopolysaccharide (LPS) as a natural adjuvant. These studies showed that Bcl-3 is required for secondary gamma interferon (IFN-) production by CD8 T cells but not for adjuvant-induced survival effects. Specifically, wild-type and Bcl-3 KO mice exhibited comparable long-term increases in the Vß8⁺ T-cell populations, indicating no lack of survival in response to adjuvant stimulation in the Bcl-3 KO activated T cells. Ectopic expression of the Bcl-3-related molecules IB, IBß, and IB in SEB-activated T cells increased survival during in vitro culture in the absence of adjuvant, suggesting that these IB molecules could exert a survival function in antigen-activated T cells in place of Bcl-3. However, Vß8⁺ CD8 T cells from SEB- plus LPS-treated Bcl-3 KO mice produced less IFN- upon in vitro restimulation than Vß8⁺ CD8 T cells from wild-type mice. Therefore, Bcl-3 plays a unique role in the regulation of IFN- production in this model system.

Editor: J. F. Urban, Jr.

This article has been cited by other articles:

• Dai, R., Phillips, R. A., Ahmed, S. A. (2007). Despite Inhibition of Nuclear Localization of NF-{kappa}B p65, c-Rel, and RelB, 17-beta Estradiol Up-Regulates NF-{kappa}B Signaling in Mouse Splenocytes: The Potential Role of Bcl-3. J. Immunol. 179: 1776-1783 [Abstract] [Full Text]