Article: article from journal or magazin.
Monocyte differentiation toward regulatory dendritic cells is not affected by respiratory syncytial virus-induced inflammatory mediators.
American Journal of Respiratory Cell and Molecular Biology
Airway epithelial cells were shown to drive the differentiation of monocytes into dendritic cells (DCs) with a suppressive phenotype. In this study, we investigated the impact of virus-induced inflammatory mediator production on the development of DCs. Monocyte differentiation into functional DCs, as reflected by the expression of CD11c, CD123, BDCA-4, and DC-SIGN and the capacity to activate T cells, was similar for respiratory syncytial virus (RSV)-infected and mock-infected BEAS-2B and A549 cells. RSV-conditioned culture media resulted in a partially mature DC phenotype, but failed to up-regulate CD80, CD83, CD86, and CCR7, and failed to release proinflammatory mediators upon Toll-like receptor (TLR) triggering. Nevertheless, these DCs were able to maintain an antiviral response by the release of Type I IFN. Collectively, these data indicate that the airway epithelium maintains an important suppressive DC phenotype under the inflammatory conditions induced by infection with RSV.
Antigens, CD/biosynthesis, Antigens, CD80/biosynthesis, Antigens, CD86/biosynthesis, Cell Line, Tumor, Dendritic Cells/cytology, Epithelial Cells/cytology, Flow Cytometry/methods, Humans, Immunoglobulins/biosynthesis, Inflammation/metabolism, Inflammation Mediators/metabolism, Membrane Glycoproteins/biosynthesis, Monocytes/cytology, Monocytes/immunology, Phenotype, Receptors, CCR7/biosynthesis, Respiratory Syncytial Viruses/metabolism, Toll-Like Receptors/metabolism
Last modification date