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Blood, 15 April 2002, Vol. 99, No. 8, pp. 2913-2921
IMMUNOBIOLOGY
Human cytomegalovirus inhibits maturation and impairs function
of monocyte-derived dendritic cells
Magdalena Moutaftsi,
Anja
M. Mehl,
Leszek K. Borysiewicz, and
Zsuzsanna Tabi
From the Section of Infection and Immunity, University
of Wales College of Medicine, Cardiff, United Kingdom, and the Imperial
College School of Medicine, London, United Kingdom.
Dendritic cells (DCs) play a pivotal role in the generation
of virus-specific cytotoxic T-cell responses, but some viruses can
render DCs inefficient in stimulating T cells. We studied whether
infection of DCs with human cytomegalovirus (HCMV) results in a
suppression of DC function which may assist HCMV in establishing persistence. The effect of HCMV infection on the phenotype and function
of monocyte-derived DCs and on their ability to mature following
infection with an endothelial cell-adapted clinical HCMV isolate were
studied. HCMV infection induced no maturation of DCs; instead, it
efficiently down-regulated the expression of surface major
histocompatibility complex (MHC) class I, CD40, and CD80 molecules.
Slight down-regulation of MHC class II and CD86 molecules was also
observed. Lipopolysaccharide (LPS)-induced maturation of infected DCs
was strongly inhibited, as indicated by lower levels of surface
expression of MHC class I, class II, costimulatory, and CD83 molecules.
The down-regulation or inhibition of these surface markers occurred
only in HCMV antigen-positive DCs. DCs produced no interleukin 12 (IL-12) and only low levels of tumor necrosis factor alpha (TNF- )
upon HCMV infection. Furthermore, cytokine production upon stimulation
with LPS or CD40L was significantly impaired. Inhibition of cytokine
production did not depend on viral gene expression as UV-irradiated
HCMV resulted in the same effect. Proliferation and cytotoxicity of T
cells specific to a recall antigen presented by DCs were also reduced
when DCs were HCMV infected. This study shows that HCMV inhibits DC
function, revealing a powerful viral strategy to delay or prevent the
generation of virus-specific cytotoxic T cells.
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