DC are a highly heterogeneous population that plays a critical role in host defense. We previously demonstrated that virus infection induces BM plasmacytoid DC (pDC) differentiation into CD11b+ conventional DC (cDC) upon in vitro culture with Fms-like tyrosine kinase 3 ligand (Flt3L). Here we use immunoglobulin D-J rearrangements and pDC adoptive transfer to provide definitive proof supporting BM pDC conversion into CD11b+ cDC during in vivo viral infection. We show that in vivo BM pDC conversion into CD11b+ cDC relates to enhanced ability to prime virus-specific T cells. Furthermore, we demonstrate that in vivo pDC conversion does not rely on viral infection of BM pDC, but instead is mediated by type I IFN signaling. Finally, by exploiting recently identified pDC-specific Ab, we provide further characterizations of the BM pDC fraction that exhibits this broader developmental plasticity. Collectively, these data indicate that BM pDC actively contribute to the CD11b+ cDC pool during in vivo viral infection and delineates molecular, functional, and phenotypic features of this novel developmental pathway.

Original languageEnglish
Pages (from-to)3388-3394
Number of pages7
JournalEuropean Journal of Immunology
Issue number12
StatePublished - 2008


  • CD11b conventional DC
  • Plasmacytoid DC
  • Type I interferon
  • Virus infection


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