@article{ChhatbarDetjeGrabskietal.2018,
  author    = {Chhatbar, Chintan and Detje, Claudia N. and Grabski, Elena and Borst, Katharina and Spanier, Julia and Ghita, Luca and Elliott, David A. and Jord{\~a}o, Marta Joana Costa and Mueller, Nora and Sutton, James and Prajeeth, Chittappen K. and Gudi, Viktoria and Klein, Michael A. and Prinz, Marco and Bradke, Frank and Stangel, Martin and Kalinke, Ulrich},
  title     = {Type I Interferon Receptor Signaling of Neurons and Astrocytes Regulates Microglia Activation during Viral Encephalitis},
  series = {Cell Reports},
  volume    = {25},
  journal   = {Cell Reports},
  doi       = {10.1016/j.celrep.2018.09.003},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-222456},
  pages     = {118-129},
  year      = {2018},
  abstract  = {In sterile neuroinflammation, a pathological role is proposed for microglia, whereas in viral encephalitis, their function is not entirely clear. Many viruses exploit the odorant system and enter the CNS via the olfactory bulb (OB). Upon intranasal vesicular stomatitis virus instillation, we show an accumulation of activated microglia and monocytes in the OB. Depletion of microglia during encephalitis results in enhanced virus spread and increased lethality. Activation, proliferation, and accumulation of microglia are regulated by type I IFN receptor signaling of neurons and astrocytes, but not of microglia. Morphological analysis of myeloid cells shows that type I IFN receptor signaling of neurons has a stronger impact on the activation of myeloid cells than of astrocytes. Thus, in the infected CNS, the cross talk among neurons, astrocytes, and microglia is critical for full microglia activation and protection from lethal encephalitis.},
  language  = {en}
}