Abstract
Human herpesvirus 6 (HHV-6) has a tropism for T lymphocytes and monocytes/macrophages, suggesting that HHV-6 infection affects the immunosurveillance system. In the present study, we investigated the HHV-6-induced phenotypic and functional alterations of dendritic cells (DCs), which are professional antigen-presenting cells. HHV-6 infection of monocyte-derived immature DCs appeared to induce the up-regulation of CD80, CD83, CD86, and HLA class I and class II molecules, suggesting that HHV-6 infection induces the maturation of DCs. In addition, the antigen capture capacity of DCs was found to decrease following infection with HHV-6. In contrast to up-regulation of mature-DC-associated surface molecules on HHV-6-infected DCs, their capacity for presentation of alloantigens and exogenous virus antigens to T lymphocytes decreased significantly from that of uninfected DCs. In contrast, there appeared to be no reduction in the capacity for presentation of an HLA class II-binding peptide to the peptide-specific CD4(+) T lymphocytes. These data indicate that HHV-6 infection induces phenotypic alterations and impairs the antigen presentation capacity of DCs. The present data also suggest that the dysfunction of HHV-6-infected DCs is attributable mainly to impairment of the antigen capture and intracellular antigen-processing pathways.
Highlights
Human herpesvirus 6 (HHV-6) was first isolated in 1986 from patients with lymphoproliferative disorders and AIDS [34]
These data confirm the previous report that both HHV-6A and HHV-6B can infect and replicate in immature dendritic cells (DCs) [4]
It has recently been reported that the apoptosis-inducing ligand CD95L (FasL) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) are up-regulated in human cytomegalovirus (HCMV)-infected DCs, thereby enabling HCMV-infected DCs to delete activated T lymphocytes [29]
Summary
Human herpesvirus 6 (HHV-6) was first isolated in 1986 from patients with lymphoproliferative disorders and AIDS [34]. Up-regulation of CD4, resulting in susceptibility to human immunodeficiency virus type 1 (HIV-1) infection, has been reported to occur in HHV-6A-infected CD4Ϫ T lymphocytes and natural killer cells [23, 25, 27]. It has recently been reported that transcriptional down-regulation of CXCR4 is induced by HHV-6A and HHV-6B infections [14, 46] These data suggest that HHV-6 infection causes immunodeficiency due to dysfunction of T lymphocytes, the immunobiological effect of HHV-6 infection on other immunocompetent cells has not been precisely examined. DCs have the ability to activate the immune response by capturing antigens in peripheral tissues and migrating to secondary lymphoid organs, where they sensitize naive T lymphocytes to the antigens.
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