Induction of Cell Signaling Events by the Cholera Toxin B Subunit in Antigen-Presenting Cells
| Autor: | Lee M. Wetzler, Aletta C. Schnitzler, Jennifer M. Burke |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Cholera Toxin
Cell signaling medicine.medical_treatment Immunology Antigen-Presenting Cells Cell Communication Biology medicine.disease_cause Microbiology Mice Transactivation Immune system medicine Animals Secretion Antigen-presenting cell B-Lymphocytes Cellular Microbiology: Pathogen-Host Cell Molecular Interactions Cholera toxin Cell biology Mice Inbred C57BL Infectious Diseases Cytokine Parasitology Cytokine secretion Signal Transduction |
| Zdroj: | Infection and Immunity. 75:3150-3159 |
| ISSN: | 1098-5522 0019-9567 |
| DOI: | 10.1128/iai.00581-06 |
| Popis: | 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-κB, 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. |
| Databáze: | OpenAIRE |
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