Cross-talk between human dendritic cell subsets influences expression of RNA sensors and inhibits picornavirus infection

M. Kramer, B.M. Schulte, D. Eleveld-Trancikova, M.A. van Hout-Kuijer, Liza W J Toonen, J. Tel, I.J.M. de Vries, F.J.M. van Kuppeveld, B.J.H. Jansen, G.J. Adema

Research output: Contribution to journalArticleAcademicpeer-review

20 Citations (Scopus)


Dendritic cells (DCs) are professional antigen-presenting cells that provide a link between innate and adaptive immunity. Multiple DC subsets exist and their activation by microorganisms occurs through binding of conserved pathogen-derived structures to so-called pattern recognition receptors (PRRs). In this study we analyzed the expression of PRRs responding to viral RNA in human monocyte-derived DCs (moDCs) under steady-state or pro-inflammatory conditions. We found that mRNA and protein levels for most PRRs were increased under pro-inflammatory conditions, with the most pronounced increases in the RIG-like helicase (RLH) family. Additionally, freshly isolated human plasmacytoid DCs (pDCs) displayed significantly higher levels of TLR7, RIG-I, MDA5 and PKR as compared to myeloid DCs and moDCs. Finally, we demonstrate for the first time that cross-talk between TLR-matured or virus-stimulated pDCs and moDCs leads to a type I interferon-dependent antiviral state in moDCs. This antiviral state was characterized by enhanced RLH expression and protection against picornavirus infection. These findings might represent a novel mechanism by which pDCs can preserve the function and viability of myeloid DCs that are attracted to a site with ongoing infection, thereby optimizing the antiviral immune response.

Original languageEnglish
Pages (from-to)360-370
Number of pages11
JournalJournal of Innate Immunity
Issue number4
Publication statusPublished - 2010
Externally publishedYes


  • Cell Communication
  • Cells, Cultured
  • Dendritic Cells
  • Humans
  • Monocytes
  • Picornaviridae
  • Picornaviridae Infections
  • RNA
  • Receptors, Pattern Recognition
  • Journal Article
  • Research Support, Non-U.S. Gov't


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