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(Journal of Leukocyte Biology. 2002;72:962-969.)
© 2002 by Society for Leukocyte Biology

Pertussis toxin and the adenylate cyclase toxin from Bordetella pertussis activate human monocyte-derived dendritic cells and dominantly inhibit cytokine production through a cAMP-dependent pathway

Kenneth C. Bagley*,{dagger}, Sayed F. Abdelwahab*,{ddagger}, Robert G. Tuskan*, Timothy R. Fouts* and George K. Lewis*,{ddagger}

* Division of Vaccine Research, Institute of Human Virology, University of Maryland Biotechnology Institute, and Departments of
{dagger} Microbiology and Immunology and
{ddagger} Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore

Correspondence: George K. Lewis, Ph.D., Division of Vaccine Research, Institute of Human Virology, University of Maryland at Baltimore, 725 W. Lombard Street, Baltimore, MD 21201. E-mail: lewisg{at}umbi.umd.edu

Pertussis toxin (PT) and adenylate cyclase toxin (AT) are AB enterotoxins produced by Bordetella pertussis. PT is a powerful mucosal adjuvant whose cellular target and mechanism of action are unknown; however, emerging evidence suggests that dendritic cells (DC) may be a principal adjuvant target of PT. Here, we investigate the mechanism underlying the effects of these toxins on human monocyte-derived DC (MDDC) in vitro. We found that the effects of PT and AT on MDDC, including maturation, are mediated by cyclic adenosine monophosphate (cAMP). In this regard, adenosine 5'-diphosphate-ribosylation-defective derivatives of PT failed to induce maturation of MDDC, whereas dibutyryl-cAMP (d-cAMP) and Forskolin mimic the maturation of MDDC and dominant inhibition of cytokine production induced by these toxins. Also, cAMP-dependent kinase inhibitors blocked the ability of PT, AT, d-cAMP, and Forskolin to activate MDDC. Taken together, these results show that the effects of PT and AT on MDDC are mediated strictly by cAMP.

Key Words: adjuvant • cholera toxin • enterotoxin




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