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@ARTICLE{Tiwari:272079,
      author       = {Tiwari, Vini and Prajapati, Bharat and Asare, Yaw and
                      Damkou, Alkmini and Ji, Hao and Liu, Lu and Naser, Nawraa
                      and Gouna, Garyfallia and Leszczyńska, Katarzyna B and
                      Mieczkowski, Jakub and Dichgans, Martin and Wang, Qing and
                      Kawaguchi, Riki and Shi, Zechuan and Swarup, Vivek and
                      Geschwind, Daniel H and Prinz, Marco and Gokce, Ozgun and
                      Simons, Mikael},
      title        = {{I}nnate immune training restores pro-reparative myeloid
                      functions to promote remyelination in the aged central
                      nervous system.},
      journal      = {Immunity},
      volume       = {57},
      number       = {9},
      issn         = {1074-7613},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-01122},
      pages        = {2173 - 2190.e8},
      year         = {2024},
      abstract     = {The reduced ability of the central nervous system to
                      regenerate with increasing age limits functional recovery
                      following demyelinating injury. Previous work has shown that
                      myelin debris can overwhelm the metabolic capacity of
                      microglia, thereby impeding tissue regeneration in aging,
                      but the underlying mechanisms are unknown. In a model of
                      demyelination, we found that a substantial number of genes
                      that were not effectively activated in aged myeloid cells
                      displayed epigenetic modifications associated with
                      restricted chromatin accessibility. Ablation of two class I
                      histone deacetylases in microglia was sufficient to restore
                      the capacity of aged mice to remyelinate lesioned tissue. We
                      used Bacillus Calmette-Guerin (BCG), a live-attenuated
                      vaccine, to train the innate immune system and detected
                      epigenetic reprogramming of brain-resident myeloid cells and
                      functional restoration of myelin debris clearance and lesion
                      recovery. Our results provide insight into aging-associated
                      decline in myeloid function and how this decay can be
                      prevented by innate immune reprogramming.},
      keywords     = {Animals / Immunity, Innate / Mice / Aging: immunology /
                      Remyelination / Microglia: immunology / Microglia:
                      metabolism / Myeloid Cells: immunology / Myeloid Cells:
                      metabolism / Central Nervous System: immunology / Mice,
                      Inbred C57BL / Myelin Sheath: metabolism / Myelin Sheath:
                      immunology / Epigenesis, Genetic / Demyelinating Diseases:
                      immunology / Disease Models, Animal / aging (Other) / innate
                      immunity (Other) / microglia (Other) / myelin (Other) /
                      remyelination (Other)},
      cin          = {AG Simons / Clinical Research (Munich) / AG Gokce / AG
                      Dichgans},
      ddc          = {610},
      cid          = {I:(DE-2719)1110008 / I:(DE-2719)1111015 /
                      I:(DE-2719)1013041 / I:(DE-2719)5000022},
      pnm          = {351 - Brain Function (POF4-351) / 353 - Clinical and Health
                      Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39053462},
      doi          = {10.1016/j.immuni.2024.07.001},
      url          = {https://pub.dzne.de/record/272079},
}