Reciprocal regulation of opposing functions characterizes biological systems. We now show that adenovirus-infected plasmacytoid dendritic cells (PDC) inhibit monocyte to myeloid dendritic cell (MDC) differentiation and function, and that adenovirus-infected monocytes inhibit PDC type I interferon secretion. Adenovirus-infected PDC secreted IFN-α, β and ω in an 86:2:1 ratio. PDC type I interferons inhibited MDC differentiation and function (reduced IL-12 secretion, IFN-γ induction, MLR and CD40 expression, and increased CD1a+CD14+ cells). Type I interferon receptor blocking antibody reversed all PDC effects, and recombinant IFN-α, β or ω replicated all effects, except reduced CD40. Adenovirus-infected monocytes suppressed PDC type I interferon secretion, which was reversed with anti-IL-10 neutralizing antibodies. Exogenous IL-10 suppressed PDC type I interferon secretion without reducing PDC viability. Therefore, monocyte IL-10 regulates PDC type I interferon secretion, and PDC type I interferons inhibit MDC differentiation and function. Such reciprocal regulation of potentially opposing influences may help modulate anti-pathogen immunity.

Original languageEnglish
Pages (from-to)3833-3839
Number of pages7
JournalEuropean Journal of Immunology
Issue number12
StatePublished - 2001


  • CD40
  • IL-10
  • Monocyte
  • Plasmacytoid dendritic cell
  • Type I interferon


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