% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@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},
}