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Production by Enveloped Virus and Lipopolysaccharide in Human Plasmacytoid Dendritic Cells1
* University of Medicine and Dentistry of New Jersey-New Jersey Medical School, and
Graduate School of Biomedical Sciences, Newark, NJ 07103
Human plasmacytoid dendritic cells (PDC) are a major source of IFN-
upon exposure to enveloped viruses and TLR-7 and TLR-9 ligands. Although IFN regulatory factor-7 (IRF-7) is known to play an essential role in virus-activated transcription of IFN- genes, the molecular mechanisms of IFN- production in human PDC remain poorly understood. We and others have recently reported high constitutive levels of IRF-7 expression in PDC as compared with other PBMC. In this study, we demonstrate that both LPS and HSV up-regulate the expression of IRF-7 in PDC, and that this enhancement of IRF-7 is dependent on NF-
B activation. The NF-B inhibitors MG132 and pyrrolidinedithiocarbamate efficiently inhibited the induction of IRF-7 by HSV or LPS, and also down-regulated the constitutive expression of IRF-7 in PDC and blocked the HSV-induced production of IFN-. In addition, we found that nuclear translocation of IRF-7 occurred rapidly in response to HSV stimulation, but not in response to LPS, which is consistent with the stimulation of IFN- production by virus and not by LPS. Although LPS by itself was not able to induce IFN- production, it led to rapid up-regulation of TLR-4 on PDC and increased the magnitude and accelerated the kinetics of HSV-induced IFN- production in PDC, providing a mechanism that might be operative in a scenario of mixed infection. In contrast to the current concept of IFN- regulation established in cell lines, this study strongly supports the immediate availability of high constitutive levels of IRF-7 expression in PDC, and suggests an activation required for IRF-7 that contributes to IFN- production in virus-stimulated PDC.
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