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Originally published as JGV in Press, 10.1099/vir.0.008581-0 on March 4, 2009 J Gen Virol 90 (2009), 909-914; DOI 10.1099/vir.0.008581-0

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Short Communication

Measles virus modulates chemokine release and chemotactic responses of dendritic cells

Marion Abt, Evelyn Gassert and Sibylle Schneider-Schaulies

Institute for Virology and Immunobiology, University of Würzburg, Versbacher Str. 7, D-97078 Würzburg, Germany

Correspondence
Sibylle Schneider-Schaulies
s-s-s{at}vim.uni-wuerzburg.de

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.

Full materials and methods and a supplementary table are available with the online version of this paper.






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