Measles virus modulates chemokine release and chemotactic responses of dendritic cells

J Gen Virol. 2009 Apr;90(Pt 4):909-914. doi: 10.1099/vir.0.008581-0. Epub 2009 Mar 4.


Interference with dendritic cell (DC) maturation and function is considered to be central to measles virus (MV)-induced immunosuppression. Temporally ordered production of chemokines and switches in chemokine receptor expression are essential for pathogen-driven DC maturation as they are prerequisites for chemotaxis and T cell recruitment. We found that MV infection of immature monocyte-derived DCs induced transcripts specific for CCL-1, -2, -3, -5, -17 and -22, CXCL-10 and CXCL-11, yet did not induce CXCL-8 (interleukin-8) and CCL-20 at the mRNA and protein level. Within 24 h post-infection, T cell attraction was not detectably impaired by these cells. MV infection failed to promote the switch from CCR5 to CCR7 expression and this correlated with chemotactic responses of MV-matured DC cultures to CCL-3 rather than to CCL-19. Moreover, the chemotaxis of MV-infected DCs to either chemokine was compromised, indicating that MV also interferes with this property independently of chemokine receptor modulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation
  • Cell Line
  • Cells, Cultured
  • Chemokines / biosynthesis*
  • Chemokines / genetics
  • Chemotaxis / physiology*
  • Dendritic Cells / cytology
  • Dendritic Cells / immunology*
  • Dendritic Cells / metabolism
  • Dendritic Cells / virology*
  • Humans
  • Lymphocyte Activation
  • Measles virus / pathogenicity*
  • T-Lymphocytes / immunology


  • Chemokines