Monocyte differentiation toward regulatory dendritic cells is not affected by respiratory syncytial virus-induced inflammatory mediators

Am J Respir Cell Mol Biol. 2011 May;44(5):655-64. doi: 10.1165/rcmb.2010-0136OC. Epub 2010 Jul 1.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD / biosynthesis
  • B7-1 Antigen / biosynthesis
  • B7-2 Antigen / biosynthesis
  • CD83 Antigen
  • 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

Substances

  • Antigens, CD
  • B7-1 Antigen
  • B7-2 Antigen
  • Immunoglobulins
  • Inflammation Mediators
  • Membrane Glycoproteins
  • Receptors, CCR7
  • Toll-Like Receptors