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

Content Provider	PubMed Central
Author	Chilton, Paula M. Mitchell, Thomas C.
Copyright Year	2006
Abstract	Adjuvant-induced survival of T cells after antigen activation correlates with increased expression of Bcl-3. Bcl-3 is an NF-κB/IκB 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-γ) 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 Vβ8+ 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 IκBα, IκBβ, and IκBɛ in SEB-activated T cells increased survival during in vitro culture in the absence of adjuvant, suggesting that these IκB molecules could exert a survival function in antigen-activated T cells in place of Bcl-3. However, Vβ8+ CD8 T cells from SEB- plus LPS-treated Bcl-3 KO mice produced less IFN-γ upon in vitro restimulation than Vβ8+ CD8 T cells from wild-type mice. Therefore, Bcl-3 plays a unique role in the regulation of IFN-γ production in this model system.
Related Links	http://dx.doi.org/10.1128/iai.01749-05
Ending Page	4189
Page Count	10
Starting Page	4180
File Format	PDF
ISSN	00199567
e-ISSN	10985522
Journal	Infection and Immunity
Issue Number	7
Volume Number	74
Language	English
Publisher	American Society for Microbiology
Publisher Date	2006-07-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Immunology Microbiology Parasitology Infectious Diseases Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Parasitology Immunology Microbiology

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