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Decrease in cAMP levels modulates adhesion to fibronectin and immunostimulatory ability of human dendritic cells
Author(s) -
Burzyn Dalia,
Jancic Carolina C.,
Zittermann Sandra,
Keller Sarmiento María I.,
Fainboim Leonardo,
Rosenstein Ruth E.,
Chuluyan H. Eduardo
Publication year - 2002
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.72.1.93
Subject(s) - adhesion , fibronectin , tumor necrosis factor alpha , microbiology and biotechnology , biology , dendritic cell , intracellular , phosphodiesterase , monocyte , ibmx , endocrinology , immunology , biochemistry , chemistry , receptor , extracellular matrix , immune system , enzyme , forskolin , organic chemistry
The aim of the present study was to analyze the early events elicited by tumor necrosis factor α (TNF‐α) on monocyte‐derived dendritic cells (moDC) adhesion to fibronectin (FN) and the involvement of cAMP in the signal transduction mechanism. The intracellular concentration of cAMP and moDC adhesion to FN decreased after TNF‐α treatment. An inverted dose‐dependency for TNF‐α effect was observed for adhesion and cAMP levels. The presence of a phosphodiesterase (PDE) inhibitor (IBMX) and cAMP analogs (8Br‐cAMP, Db‐cAMP) reversed the observed TNF‐α effects. The role of cAMP was analyzed further by examining the cAMP levels in nonadhered and adhered, TNF‐α‐treated moDC. Nonadhered moDC showed lower cAMP levels compared with adhered moDC. Furthermore, nonadhered moDC showed higher IL‐12 content and allostimulatory ability compared with adhered moDC. The higher allostimulatory capacity was abolished in the presence of cAMP analogs and a PDE inhibitor. These results suggest that cAMP levels correlate with TNF‐α‐induced changes of moDC adhesion and allostimulatory capacity.