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@ARTICLE{Wendeln:139909,
      author       = {Wendeln, Ann-Christin and Degenhardt, Karoline and Kaurani,
                      Lalit and Gertig, Michael and Ulas, Thomas and Jain, Gaurav
                      and Wagner, Jessica and Häsler, Lisa M and Wild, Katleen
                      and Skodras, Angelos and Blank, Thomas and Staszewski, Ori
                      and Datta, Moumita and Pena Centeno, Tonatiuh and Capece,
                      Vincenzo and Islam, Rezaul and Kerimoglu, Cemil and
                      Staufenbiel, Matthias and Schultze, Joachim L and Beyer,
                      Marc and Prinz, Marco and Jucker, Mathias and Fischer,
                      André and Neher, Jonas J},
      title        = {{I}nnate immune memory in the brain shapes neurological
                      disease hallmarks.},
      journal      = {Nature},
      volume       = {556},
      number       = {7701},
      issn         = {0028-0836},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group65848},
      reportid     = {DZNE-2020-06231},
      pages        = {332-338},
      year         = {2018},
      abstract     = {Innate immune memory is a vital mechanism of myeloid cell
                      plasticity that occurs in response to environmental stimuli
                      and alters subsequent immune responses. Two types of
                      immunological imprinting can be distinguished-training and
                      tolerance. These are epigenetically mediated and enhance or
                      suppress subsequent inflammation, respectively. Whether
                      immune memory occurs in tissue-resident macrophages in vivo
                      and how it may affect pathology remains largely unknown.
                      Here we demonstrate that peripherally applied inflammatory
                      stimuli induce acute immune training and tolerance in the
                      brain and lead to differential epigenetic reprogramming of
                      brain-resident macrophages (microglia) that persists for at
                      least six months. Strikingly, in a mouse model of
                      Alzheimer's pathology, immune training exacerbates cerebral
                      β-amyloidosis and immune tolerance alleviates it;
                      similarly, peripheral immune stimulation modifies
                      pathological features after stroke. Our results identify
                      immune memory in the brain as an important modifier of
                      neuropathology.},
      keywords     = {Alzheimer Disease: immunology / Alzheimer Disease:
                      pathology / Amyloidosis: immunology / Amyloidosis: pathology
                      / Animals / Brain: immunology / Brain: pathology / Disease
                      Models, Animal / Epigenesis, Genetic / Female / Gene
                      Expression Regulation: immunology / Humans / Immune
                      Tolerance / Immunity, Innate / Immunologic Memory /
                      Inflammation: genetics / Inflammation: immunology / Male /
                      Mice / Microglia: immunology / Microglia: metabolism /
                      Nervous System Diseases: immunology / Nervous System
                      Diseases: pathology / Stroke: immunology / Stroke:
                      pathology},
      cin          = {AG Jucker / AG Fischer ; AG Fischer / Ext UKT / AG Fuhrmann
                      / Göttingen common / AG Bonn 2 / $R\&D$ PRECISE ; $R\&D$
                      PRECISE / AG Beyer / AG Neher},
      ddc          = {500},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1410002 /
                      I:(DE-2719)5000058 / I:(DE-2719)1011004 / I:(DE-2719)6000014
                      / I:(DE-2719)1440012 / I:(DE-2719)1013031 /
                      I:(DE-2719)1013035 / I:(DE-2719)1210012},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 341
                      - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29643512},
      pmc          = {pmc:PMC6038912},
      doi          = {10.1038/s41586-018-0023-4},
      url          = {https://pub.dzne.de/record/139909},
}