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*
Laboratory of Experimental Surgery, Surgical Department, S. Raffaele Scientific Institute, Milan, Italy;
Department of Immunology and Cell Biology, "Mario Negri" Institute, Milan, Italy;
Laboratory of Analysis, San Luigi Centre, S. Raffaele Scientific Institute, Milan, Italy; and
§
University of Milan, Milan, Italy
Because dendritic cells (DC) play a major role in the initiation of
T cell-mediated immunity, we studied the effects of glucocorticoids,
well-known inhibitors of the immune and inflammatory response, on the
differentiation and maturation of human DC. DC were differentiated from
human monocytes by culture with GM-CSF and IL-4 for 7 days with and
without dexamethasone (Dex). Cells treated with Dex (10-8
M) (Dex-DC) developed a characteristic dendritic morphology; however,
membrane phenotype analysis demonstrated that they were not fully
differentiated. Dex-DC expressed low levels of CD1a and, unlike
untreated cells, high levels of CD14 and CD16. Molecules involved in Ag
presentation (CD40, CD86, CD54) were also impaired. In contrast,
molecules involved in Ag uptake (mannose receptor, CD32) and cell
adhesion (CD11/CD18, CD54) were up-regulated. After exposure to TNF-
or CD40 ligand, Dex-DC expressed lower levels of CD83 and CD86 than
untreated cells. Dex-DC showed a higher endocytic activity, a lower APC
function, and a lower capacity to secrete cytokines than untreated
cells. Overall, these results indicate that DC differentiated in the
presence of Dex are at a more immature stage. Moreover, Dex also
partially blocked terminal maturation of already differentiated DC. In
conclusion, our data suggest that glucocorticoids may act at the very
first step of the immune response by modulating DC differentiation,
maturation, and function.
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