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@ARTICLE{Kreutzfeldt:137048,
      author       = {Kreutzfeldt, Mario and Bergthaler, Andreas and Fernandez,
                      Marylise and Brück, Wolfgang and Steinbach, Karin and Vorm,
                      Mariann and Coras, Roland and Blümcke, Ingmar and Bonilla,
                      Weldy V and Fleige, Anne and Forman, Ruth and Müller,
                      Werner and Becher, Burkhard and Misgeld, Thomas and
                      Kerschensteiner, Martin and Pinschewer, Daniel D and
                      Merkler, Doron},
      title        = {{N}europrotective intervention by interferon-γ blockade
                      prevents {CD}8+ {T} cell-mediated dendrite and synapse
                      loss.},
      journal      = {Journal of experimental medicine},
      volume       = {210},
      number       = {10},
      issn         = {1540-9538},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DZNE-2020-03370},
      pages        = {2087-2103},
      year         = {2013},
      abstract     = {Neurons are postmitotic and thus irreplaceable cells of the
                      central nervous system (CNS). Accordingly, CNS inflammation
                      with resulting neuronal damage can have devastating
                      consequences. We investigated molecular mediators and
                      structural consequences of CD8(+) T lymphocyte (CTL) attack
                      on neurons in vivo. In a viral encephalitis model in mice,
                      disease depended on CTL-derived interferon-γ (IFN-γ) and
                      neuronal IFN-γ signaling. Downstream STAT1 phosphorylation
                      and nuclear translocation in neurons were associated with
                      dendrite and synapse loss (deafferentation). Analogous
                      molecular and structural alterations were also found in
                      human Rasmussen encephalitis, a CTL-mediated human
                      autoimmune disorder of the CNS. Importantly, therapeutic
                      intervention by IFN-γ blocking antibody prevented neuronal
                      deafferentation and clinical disease without reducing CTL
                      responses or CNS infiltration. These findings identify
                      neuronal IFN-γ signaling as a novel target for
                      neuroprotective interventions in CTL-mediated CNS disease.},
      keywords     = {Adolescent / Adult / Animals / CD8-Positive T-Lymphocytes:
                      immunology / Cell Nucleus: metabolism / Child / Dendrites:
                      immunology / Humans / Interferon-gamma: antagonists $\&$
                      inhibitors / Interferon-gamma: metabolism / Lymphocytic
                      Choriomeningitis: immunology / Lymphocytic Choriomeningitis:
                      metabolism / Lymphocytic Choriomeningitis: prevention $\&$
                      control / Lymphocytic choriomeningitis virus: immunology /
                      Mice / Mice, Transgenic / Neurons: immunology / Neurons:
                      metabolism / Neurons: virology / Perforin: genetics /
                      Perforin: metabolism / Phosphorylation / Protein Transport /
                      Receptors, Interferon: genetics / Receptors, Interferon:
                      metabolism / STAT1 Transcription Factor: metabolism / Signal
                      Transduction / Spinal Cord: immunology / Spinal Cord:
                      metabolism / Spinal Cord: pathology / Synapses: immunology /
                      T-Lymphocytes, Cytotoxic: immunology / Young Adult / fas
                      Receptor: genetics / fas Receptor: metabolism / Receptors,
                      Interferon (NLM Chemicals) / STAT1 Transcription Factor (NLM
                      Chemicals) / fas Receptor (NLM Chemicals) / interferon gamma
                      receptor (NLM Chemicals) / Perforin (NLM Chemicals) /
                      Interferon-gamma (NLM Chemicals)},
      cin          = {AG Misgeld},
      ddc          = {610},
      cid          = {I:(DE-2719)1110000-4},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23999498},
      pmc          = {pmc:PMC3782053},
      doi          = {10.1084/jem.20122143},
      url          = {https://pub.dzne.de/record/137048},
}