10.6084/m9.figshare.5121115.v1 Kramer M. Kramer M. Schulte B.M. Schulte B.M. Eleveld-Trancikova D. Eleveld-Trancikova D. van Hout-Kuijer M. van Hout-Kuijer M. Toonen L.W.J. Toonen L.W.J. Tel J. Tel J. de Vries I.J.M. de Vries I.J.M. van Kuppeveld F.J.M. van Kuppeveld F.J.M. Jansen B.J.H. Jansen B.J.H. Adema G.J. Adema G.J. Supplementary Material for: Cross-Talk between Human Dendritic Cell Subsets Influences Expression of RNA Sensors and Inhibits Picornavirus Infection Karger Publishers 2010 Human Dendritic cells Cell activation RNA sensor Cross-talk 2010-03-20 00:00:00 Dataset https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Cross-Talk_between_Human_Dendritic_Cell_Subsets_Influences_Expression_of_RNA_Sensors_and_Inhibits_Picornavirus_Infection/5121115 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.