Human cytomegalovirus suppresses type I interferon secretion by plasmacytoid dendritic cells through its interleukin 10 homolog

W. L William Chang, Peter A Barry, Richard Szubin, Dai Wang, Nicole Baumgarth

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Type I interferons (IFNs) are innate cytokines with potent antiviral and immunoregulatory activities. It remains unclear how human cytomegalovirus (HCMV) can establish persistence in the face of these strongly antagonistic cytokines. In this study, we confirm that IFN-α efficiently suppresses the penetration of HCMV into susceptible cells, including monocytes, the major cell population in peripheral blood that is highly susceptible to HCMV infection. We further demonstrate that the HCMV-derived interleukin 10 (IL-10) homolog functions similar to cellular IL-10 and broadly inhibits TLR-induced transcriptional activation of IFN-α/β genes in plasmacytoid dendritic cells (PDCs), a major type I IFN-producer in vivo that is highly resistant to HCMV infection in vitro. These results suggest that HCMV subverts innate immunity by suppressing type I IFN production of PDCs during primary viral infection via its IL-10 homolog.

Original languageEnglish (US)
Pages (from-to)330-337
Number of pages8
JournalVirology
Volume390
Issue number2
DOIs
StatePublished - Aug 1 2009

Fingerprint

Interferon Type I
Cytomegalovirus
Interleukin-10
Dendritic Cells
Cytomegalovirus Infections
Interferons
Cytokines
Virus Diseases
Innate Immunity
Transcriptional Activation
Antiviral Agents
Monocytes
Population
Genes

Keywords

  • Human cytomegalovirus
  • Interleukin 10
  • Plasmacytoid dendritic cells
  • Type I interferons

ASJC Scopus subject areas

  • Virology

Cite this

Human cytomegalovirus suppresses type I interferon secretion by plasmacytoid dendritic cells through its interleukin 10 homolog. / Chang, W. L William; Barry, Peter A; Szubin, Richard; Wang, Dai; Baumgarth, Nicole.

In: Virology, Vol. 390, No. 2, 01.08.2009, p. 330-337.

Research output: Contribution to journalArticle

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