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@ARTICLE{Keil:128879,
      author       = {M. Keil$^*$ and J. Sonner$^*$ and T. Lanz$^*$ and I.
                      Oezen$^*$ and T. Bunse$^*$ and S. Bittner and H. V. Meyer
                      and S. G. Meuth and W. Wick$^*$ and M. Platten$^*$},
      title        = {{G}eneral control non-derepressible 2 ({GCN}2) in {T} cells
                      controls disease progression of autoimmune
                      neuroinflammation.},
      journal      = {Journal of neuroimmunology},
      volume       = {297},
      issn         = {0165-5728},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DKFZ-2017-04892},
      pages        = {117 - 126},
      year         = {2016},
      abstract     = {Relapsing-remitting multiple sclerosis (MS)(2) is
                      characterized by phases of acute neuroinflammation followed
                      by spontaneous remission. Termination of inflammation is
                      accompanied by an influx of regulatory T cells (Tregs).(3)
                      The molecular mechanisms responsible for directing Tregs
                      into the inflamed CNS tissue, however, are incompletely
                      understood. In an MS mouse model we show that the stress
                      kinase general control non-derepressible 2 (GCN2),(4)
                      expressed in T cells, contributes to the resolution of
                      autoimmune neuroinflammation. Failure to recover from acute
                      inflammation was associated with reduced frequencies of
                      CNS-infiltrating Tregs. GCN2 deficient Tregs displayed
                      impaired migration to a CCL2 gradient. These data suggest an
                      important contribution of the T cell stress response to the
                      resolution of autoimmune neuroinflammation.},
      keywords     = {Annexin A5 (NLM Chemicals) / Cytokines (NLM Chemicals) /
                      Myelin-Oligodendrocyte Glycoprotein (NLM Chemicals) /
                      Peptide Fragments (NLM Chemicals) / myelin oligodendrocyte
                      glycoprotein (35-55) (NLM Chemicals) / Eif2ak4 protein,
                      mouse (NLM Chemicals) / Protein-Serine-Threonine Kinases
                      (NLM Chemicals)},
      cin          = {G808 / B062 / G370 / G160 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)G808-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)G370-20160331 / I:(DE-He78)G160-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27397084},
      doi          = {10.1016/j.jneuroim.2016.05.014},
      url          = {https://inrepo02.dkfz.de/record/128879},
}