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@ARTICLE{Flle:140340,
      author       = {Fülle, Lorenz and Offermann, Nina and Hansen, Jan Niklas
                      and Breithausen, Björn and Erazo, Anna Belen and Schanz,
                      Oliver and Radau, Luca and Gondorf, Fabian and Knöpper,
                      Konrad and Alferink, Judith and Abdullah, Zeinab and
                      Neumann, Harald and Weighardt, Heike and Henneberger,
                      Christian and Halle, Annett and Förster, Irmgard},
      title        = {{CCL}17 exerts a neuroimmune modulatory function and is
                      expressed in hippocampal neurons.},
      journal      = {Glia},
      volume       = {66},
      number       = {10},
      issn         = {0894-1491},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2020-06662},
      pages        = {2246-2261},
      year         = {2018},
      abstract     = {Chemokines are important signaling molecules in the immune
                      and nervous system. Using a fluorescence reporter mouse
                      model, we demonstrate that the chemokine CCL17, a ligand of
                      the chemokine receptor CCR4, is produced in the murine
                      brain, particularly in a subset of hippocampal CA1 neurons.
                      We found that basal expression of Ccl17 in hippocampal
                      neurons was strongly enhanced by peripheral challenge with
                      lipopolysaccharide (LPS). LPS-mediated induction of Ccl17 in
                      the hippocampus was dependent on local tumor necrosis factor
                      (TNF) signaling, whereas upregulation of Ccl22 required
                      granulocyte-macrophage colony-stimulating factor (GM-CSF).
                      CCL17 deficiency resulted in a diminished microglia density
                      under homeostatic and inflammatory conditions. Further,
                      microglia from naïve Ccl17-deficient mice possessed a
                      reduced cellular volume and a more polarized process tree as
                      assessed by computer-assisted imaging analysis. Regarding
                      the overall branching, cell surface area, and total tree
                      length, the morphology of microglia from naïve
                      Ccl17-deficient mice resembled that of microglia from
                      wild-type mice after LPS stimulation. In line,
                      electrophysiological recordings indicated that CCL17
                      downmodulates basal synaptic transmission at CA3-CA1
                      Schaffer collaterals in acute slices from naïve but not
                      LPS-treated animals. Taken together, our data identify CCL17
                      as a homeostatic and inducible neuromodulatory chemokine
                      affecting the presence and morphology of microglia and
                      synaptic transmission in the hippocampus.},
      keywords     = {Animals / Chemokine CCL17: genetics / Chemokine CCL17:
                      metabolism / Chemokine CCL22: metabolism / Female / Gene
                      Expression / Granulocyte-Macrophage Colony-Stimulating
                      Factor: metabolism / Green Fluorescent Proteins: genetics /
                      Green Fluorescent Proteins: metabolism / Hippocampus:
                      immunology / Hippocampus: pathology / Homeostasis:
                      physiology / Inflammation: metabolism / Inflammation:
                      pathology / Lipopolysaccharides / Male / Mice, Inbred C57BL
                      / Mice, Transgenic / Microglia: immunology / Microglia:
                      pathology / Monocytes: immunology / Monocytes: pathology /
                      Neuroimmunomodulation: physiology / Neurons: immunology /
                      Neurons: pathology / Receptors, CCR4: metabolism / Synaptic
                      Transmission: physiology / Tumor Necrosis Factor-alpha:
                      metabolism / Ccl17 protein, mouse (NLM Chemicals) / Ccl22
                      protein, mouse (NLM Chemicals) / Ccr4 protein, mouse (NLM
                      Chemicals) / Chemokine CCL17 (NLM Chemicals) / Chemokine
                      CCL22 (NLM Chemicals) / Lipopolysaccharides (NLM Chemicals)
                      / Receptors, CCR4 (NLM Chemicals) / Tumor Necrosis
                      Factor-alpha (NLM Chemicals) / enhanced green fluorescent
                      protein (NLM Chemicals) / Green Fluorescent Proteins (NLM
                      Chemicals) / Granulocyte-Macrophage Colony-Stimulating
                      Factor (NLM Chemicals)},
      cin          = {U Preclinical Researchers - Bonn / AG Halle},
      ddc          = {610},
      cid          = {I:(DE-2719)7000005 / I:(DE-2719)1013034},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30277599},
      doi          = {10.1002/glia.23507},
      url          = {https://pub.dzne.de/record/140340},
}