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Human Herpesvirus 6B Induces Phenotypic Maturation Without IL‐10 and IL‐12p70 Production in Dendritic Cells
Author(s) -
Bertelsen L. B.,
Petersen C. C.,
KofodOlsen E.,
Øster B.,
Höllsberg P.,
Agger R.,
Hokland M.
Publication year - 2010
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2010.02389.x
Subject(s) - cd80 , cd86 , biology , phenotype , immune system , virus , dendritic cell , cd40 , virology , immunology , t cell , in vitro , gene , cytotoxic t cell , genetics
Human herpesvirus 6B (HHV‐6B) is the causative agent of the common childhood febrile illness, exanthema subitum. The virus is predominantly regarded as a T‐cell tropic virus, although in reality it has the ability to infect a wide variety of cell types including monocytes, macrophages and dendritic cells (DC). Although DC are important immune regulators, the modulating effects of HHV‐6B on DC are controversial. Here, we examine the phenotypic and functional consequences of HHV‐6B infection of DC. The addition of HHV‐6B to immature DC led to expression of the nuclear viral p41 protein and cell surface expression of the viral glycoprotein gp60/110 consistent with HHV‐6B infection. Nevertheless, HHV‐6B did not induce noticeable cytopathogenic effects or cell death in infected DC. Importantly, HHV‐6B infection induced a partial phenotypic maturation of immature DC as demonstrated by a substantial increase in the expression of HLA‐DR, CD86 and CD40, whereas only a minor increase in CD80 and CD83 was observed. This phenotypic maturation was, however, not followed by functional maturation, because HHV‐6B infection did not induce IL‐10 and IL‐12p70 production in immature DC. However, infected DC were still able to react to bacteria‐derived stimuli such as lipopolysaccaharide by an even more pronounced production of IL‐10 and IL‐12p70 when compared to that of uninfected DC.