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@ARTICLE{Sinner:259695,
      author       = {Sinner, Pia and Peckert-Maier, Katrin and Mohammadian,
                      Hashem and Kuhnt, Christine and Draßner, Christina and
                      Panagiotakopoulou, Vasiliki and Rauber, Simon and
                      Linnerbauer, Mathias and Haimon, Zhana and Royzman, Dmytro
                      and Kronenberg-Versteeg, Deborah and Ramming, Andreas and
                      Steinkasserer, Alexander and Wild, Andreas B},
      title        = {{M}icroglial expression of {CD}83 governs cellular
                      activation and restrains neuroinflammation in experimental
                      autoimmune encephalomyelitis.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2023-00767},
      pages        = {4601},
      year         = {2023},
      abstract     = {Microglial activation during neuroinflammation is crucial
                      for coordinating the immune response against neuronal
                      tissue, and the initial response of microglia determines the
                      severity of neuro-inflammatory diseases. The CD83 molecule
                      has been recently shown to modulate the activation status of
                      dendritic cells and macrophages. Although the expression of
                      CD83 is associated with early microglia activation in
                      various disease settings, its functional relevance for
                      microglial biology has been elusive. Here, we describe a
                      thorough assessment of CD83 regulation in microglia and show
                      that CD83 expression in murine microglia is not only
                      associated with cellular activation but also with
                      pro-resolving functions. Using single-cell RNA-sequencing,
                      we reveal that conditional deletion of CD83 results in an
                      over-activated state during neuroinflammation in the
                      experimental autoimmune encephalomyelitis model.
                      Subsequently, CD83-deficient microglia recruit more
                      pathogenic immune cells to the central nervous system,
                      deteriorating resolving mechanisms and exacerbating the
                      disease. Thus, CD83 in murine microglia orchestrates
                      cellular activation and, consequently, also the resolution
                      of neuroinflammation.},
      keywords     = {Mice / Animals / Encephalomyelitis, Autoimmune,
                      Experimental / Microglia: metabolism / Neuroinflammatory
                      Diseases / Central Nervous System: metabolism / Macrophages:
                      metabolism / Mice, Inbred C57BL},
      cin          = {AG Deleidi / AG Jucker},
      ddc          = {500},
      cid          = {I:(DE-2719)1210011 / I:(DE-2719)1210001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37528070},
      pmc          = {pmc:PMC10394088},
      doi          = {10.1038/s41467-023-40370-2},
      url          = {https://pub.dzne.de/record/259695},
}