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Originally published online as doi:10.1189/jlb.0307181 on September 26, 2007

Published online before print September 26, 2007
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(Journal of Leukocyte Biology. 2008;83:56-63.)
© 2008 by Society for Leukocyte Biology

Human cytomegalovirus-derived protein UL18 alters the phenotype and function of monocyte-derived dendritic cells

Claudia S. Wagner*,1, Lilian Walther-Jallow*, Eva Buentke{dagger}, Hans-Gustaf Ljunggren*, Adnane Achour* and Benedict J. Chambers*

* Center for Infectious Medicine, Department of Medicine, Karolinska University Hospital Huddinge, and
{dagger} Cancer Center Karolinska, Department of Oncology and Pathology, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden

1 Correspondence: Center for Infectious Medicine, F59, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden. E-mail: claudia.wagner{at}ki.se

ABSTRACT

Human cytomegalovirus (HCMV) encodes the MHC class I-like molecule UL18, which binds with high affinity to the leukocyte Ig-like receptor-1 (LIR-1), an inhibitory receptor commonly expressed on myeloid cells and subsets of NK and T cells. The exact role of UL18 is not known, in particular in relation to its proposed role in HCMV immune escape. Given the ubiquitous expression of LIR-1 on dendritic cells (DCs), we hypothesized that UL18 may affect DC function. To study the effects of UL18 on DC, we made use of UL18 fusion proteins. We demonstrate that UL18 fusion proteins inhibit the chemotaxis of DCs. Furthermore, UL18 interfered with CD40 ligand-induced maturation of DCs, resulting in reduced allogeneic T cell proliferation. Finally, we demonstrate that UL18 proteins up-regulate the expression of the maturation marker CD83 on immature monocyte-derived DCs and induce cytokine production. The capacity of UL18 to affect the function and the phenotype of DCs suggests a novel role for this HCMV-derived protein.

Key Words: MHC class I homologue • host/pathogen interaction • cell trafficking • cell surface molecules • immune modulation




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