Previous Article | Next Article ![]()
Infection and Immunity, June 2007, p. 3150-3159, Vol. 75, No. 6
0019-9567/07/$08.00+0 doi:10.1128/IAI.00581-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118,1 Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 021182
Received 7 April 2006/ Returned for modification 7 June 2006/ Accepted 3 March 2007
Cholera toxin (CT) is one of the most effective and widely studied mucosal adjuvants. Although the ADP-ribosylating A subunit has been implicated in augmenting immune responses, the receptor-binding B subunit (CT-B) has greater immunogenicity and may be a repository of adjuvant activity without potential toxicity. In order to elucidate mechanisms of immune modulation by CT-B alone, primary B cells and macrophages were assessed for responses to CT-B in vitro, as measured by the expression of cell surface markers, cellular signaling events, and cytokine secretion. Increased phosphorylation of multiple signaling molecules, including Erk1/2 and p38, was detected. CT-B also induced transactivation of the transcription elements cyclic AMP-responsive element and NF-
B, the latter of which was inhibited by phosphotyrosine inhibition. While specific inhibition of MEK1/2 did not reduce CT-B induction of cell surface marker expression, it did attenuate CT-B-mediated interleukin-6 secretion. These data show that CT-B induces a set of signaling events related to cellular activation, surface molecule expression, and cytokine production that has potential implications for elucidating CT-B adjuvant activity in the absence of enzymatically active holotoxin.
Published ahead of print on 12 March 2007.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»