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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.008581-0
Journal of General Virology 2009;90:909.

A more recent version of this article appeared on April 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.008581-0
© 2009 Society for General Microbiology
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Measles virus modulates chemokine release and chemotactic responses of dendritic cells

Marion Abt1, Evelyn Gassert1 and Sibylle Schneider-Schaulies2,3

1 Institute for Virology and Immunology;
2 Universität Würzburg

3 E-mail: s-s-s{at}vim.uni-wuerzburg.de

Interference with dendritic cell (DC) maturation and function is considered as 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 prerequisite for chemotaxis and T cell recruitment. We found that MV infection of immature monocyte-derived DCs induced CCL1, -2, -3, -5, -17 and -22, CXCL-10 and CXCL-11-specific transcripts yet barely CXCL-8 (IL-8) and CCL-20 on mRNA and protein level. Within 24 hrs post infection, this does not detectably impair T cell attraction by these cells. MV-infection failed to promote the switch from CCR5 to CCR7 expression and this correlated with chemotactic responses of MV-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 interferes with this property also independently of chemokine receptor modulation.

Received 6 November 2008; accepted 7 December 2008.




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