title: Human herpesvirus 6B induces phenotypic maturation without IL-10 and IL-12p70 production in dendritic cells.
abstract: 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.
authors.affiliation: Department of Medical Microbiology and Immunology, Aarhus University, Aarhus C, Denmark.
authors.forename: L B
authors.initials: LB
authors.lastname: Bertelsen
authors.forename: C C
authors.initials: CC
authors.lastname: Petersen
authors.forename: E
authors.initials: E
authors.lastname: Kofod-Olsen
authors.forename: B
authors.initials: B
authors.lastname: Oster
authors.forename: P
authors.initials: P
authors.lastname: Höllsberg
authors.forename: R
authors.initials: R
authors.lastname: Agger
authors.forename: M
authors.initials: M
authors.lastname: Hokland
mesh_terms: D015703:Antigens, CD / Q000276:immunology; D018122:B7-1 Antigen / Q000276:immunology; D051940:B7-2 Antigen / Q000276:immunology; D019013:CD40 Antigens / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology* / Q000648:ultrastructure / Q000821:virology*; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000276:immunology; D015654:Herpesvirus 6, Human / Q000276:immunology*; D006801:Humans; D007136:Immunoglobulins / Q000276:immunology; D016130:Immunophenotyping; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000276:immunology; D018664:Interleukin-12 / Q000096:biosynthesis* / Q000276:immunology; D008562:Membrane Glycoproteins / Q000276:immunology; D018613:Microscopy, Confocal; D019349:Roseolovirus Infections / Q000097:blood / Q000276:immunology* / Q000821:virology; D000097802:CD83 Antigen
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D019013:CD40 Antigens; D006684:HLA-DR Antigens; D007136:Immunoglobulins; D016753:Interleukin-10; D018664:Interleukin-12; D008562:Membrane Glycoproteins; D000097802:CD83 Antigen