@article{Puttur20161113,
  abstract = {Summary Cytomegalovirus (CMV) is an opportunistic virus severely infecting immunocompromised individuals. In mice, endosomal Toll-like receptor 9 (TLR9) and downstream myeloid differentiation factor 88 (MyD88) are central to activating innate immune responses against mouse \{CMV\} (MCMV). In this respect, the cell-specific contribution of these pathways in initiating anti-MCMV immunity remains unclear. Using transgenic mice, we demonstrate that TLR9/MyD88 signaling selectively in CD11c+ dendritic cells (DCs) strongly enhances \{MCMV\} clearance by boosting natural killer (NK) cell \{CD69\} expression and IFN-γ production. In addition, we show that in the absence of plasmacytoid \{DCs\} (pDCs), conventional \{DCs\} (cDCs) promote robust \{NK\} cell effector function and \{MCMV\} clearance in a TLR9/MyD88-dependent manner. Simultaneously, cDC-derived IL-15 regulates \{NK\} cell degranulation by TLR9/MyD88-independent mechanisms. Overall, we compartmentalize the cellular contribution of \{TLR9\} and MyD88 signaling in individual \{DC\} subsets and evaluate the mechanism by which cDCs control \{MCMV\} immunity. },
  added-at = {2016-11-03T18:21:33.000+0100},
  author = {Puttur, F and Francozo, M and Solmaz, G and Bueno, C and Lindenberg, M and Gohmert, M and Swallow, M and Tufa, D and Jacobs, R and Lienenklaus, S and Kühl, A A and Borkner, L and Cicin-Sain, L and Holzmann, B and Wagner, H and Berod, L and Sparwasser, T},
  biburl = {https://www.bibsonomy.org/bibtex/2aa9bfddbd099947bd856eae728c1b42d/sparwasser},
  interhash = {cbe18885bb0eabe8335ec937a86a2559},
  intrahash = {aa9bfddbd099947bd856eae728c1b42d},
  journal = {Cell Reports },
  keywords = {sparwasser},
  number = 4,
  pages = {1113 - 1127},
  pubmedurl = {https://www.ncbi.nlm.nih.gov/pubmed/27760315},
  timestamp = {2016-11-03T18:21:33.000+0100},
  title = {Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via \{TLR9\} and MyD88 Signaling },
  volume = 17,
  year = 2016
}