Author
Listed:
- Ann-Christin Wendeln
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen
University of Tübingen)
- Karoline Degenhardt
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen
University of Tübingen)
- Lalit Kaurani
(University Medical Center Göttingen
German Center for Neurodegenerative Diseases (DZNE))
- Michael Gertig
(University Medical Center Göttingen
German Center for Neurodegenerative Diseases (DZNE))
- Thomas Ulas
(University of Bonn)
- Gaurav Jain
(German Center for Neurodegenerative Diseases (DZNE)
German Center for Neurodegenerative Diseases (DZNE))
- Jessica Wagner
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen
University of Tübingen)
- Lisa M. Häsler
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen)
- Katleen Wild
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen)
- Angelos Skodras
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen)
- Thomas Blank
(University of Freiburg)
- Ori Staszewski
(University of Freiburg)
- Moumita Datta
(University of Freiburg)
- Tonatiuh Pena Centeno
(German Center for Neurodegenerative Diseases (DZNE)
German Center for Neurodegenerative Diseases (DZNE))
- Vincenzo Capece
(German Center for Neurodegenerative Diseases (DZNE)
German Center for Neurodegenerative Diseases (DZNE))
- Md. Rezaul Islam
(German Center for Neurodegenerative Diseases (DZNE))
- Cemil Kerimoglu
(German Center for Neurodegenerative Diseases (DZNE))
- Matthias Staufenbiel
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen)
- Joachim L. Schultze
(University of Bonn
Platform for Single Cell Genomics and Epigenomics at the University of Bonn and the German Center for Neurodegenerative Diseases)
- Marc Beyer
(German Center for Neurodegenerative Diseases (DZNE))
- Marco Prinz
(University of Freiburg
University of Freiburg)
- Mathias Jucker
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen)
- André Fischer
(University Medical Center Göttingen
German Center for Neurodegenerative Diseases (DZNE))
- Jonas J. Neher
(German Center for Neurodegenerative Diseases (DZNE)
University of Tübingen)
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.
Suggested Citation
Ann-Christin Wendeln & Karoline Degenhardt & Lalit Kaurani & Michael Gertig & Thomas Ulas & Gaurav Jain & Jessica Wagner & Lisa M. Häsler & Katleen Wild & Angelos Skodras & Thomas Blank & Ori Staszews, 2018.
"Innate immune memory in the brain shapes neurological disease hallmarks,"
Nature, Nature, vol. 556(7701), pages 332-338, April.
Handle:
RePEc:nat:nature:v:556:y:2018:i:7701:d:10.1038_s41586-018-0023-4
DOI: 10.1038/s41586-018-0023-4
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Cited by:
- Salyan Bhattarai & Qian Li & Jun Ding & Feng Liang & Ekaterina Gusev & Orsolya Lapohos & Gregory J. Fonseca & Eva Kaufmann & Maziar Divangahi & Basil J. Petrof, 2022.
"TLR4 is a regulator of trained immunity in a murine model of Duchenne muscular dystrophy,"
Nature Communications, Nature, vol. 13(1), pages 1-15, December.
- Moumita Datta & Stefanie M. Hansen & Ori Staszewski, 2020.
"Microglial Expression of Hdac1 and Hdac2 is Dispensable for Experimental Autoimmune Encephalomyelitis (EAE) Progression,"
J, MDPI, vol. 3(4), pages 1-8, October.
- Marius Schwabenland & Omar Mossad & Annika Sievert & Adam G. Peres & Elena Ringel & Sebastian Baasch & Julia Kolter & Giulia Cascone & Nikolaos Dokalis & Andreas Vlachos & Zsolt Ruzsics & Philipp Henn, 2023.
"Neonatal immune challenge poses a sex-specific risk for epigenetic microglial reprogramming and behavioral impairment,"
Nature Communications, Nature, vol. 14(1), pages 1-19, December.
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