Journal Article (Review Article)

DZNE-2024-00586

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Epigenetic control of microglial immune responses.

Scholz, R. (First author)DZNE* ; Brösamle, D.DZNE* ; Yuan, X.DZNE* ; Beyer, M.DZNE* ; Neher, J. J. (Last author)DZNE*

2024
Wiley-Blackwell Oxford

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Please use a persistent id in citations: doi:10.1111/imr.13317

Abstract: Microglia, the major population of brain-resident macrophages, are now recognized as a heterogeneous population comprising several cell subtypes with different (so far mostly supposed) functions in health and disease. A number of studies have performed molecular characterization of these different microglial activation states over the last years making use of 'omics' technologies, that is transcriptomics, proteomics and, less frequently, epigenomics profiling. These approaches offer the possibility to identify disease mechanisms, discover novel diagnostic biomarkers, and develop new therapeutic strategies. Here, we focus on epigenetic profiling as a means to understand microglial immune responses beyond what other omics methods can offer, that is, revealing past and present molecular responses, gene regulatory networks and potential future response trajectories, and defining cell subtype-specific disease relevance through mapping non-coding genetic variants. We review the current knowledge in the field regarding epigenetic regulation of microglial identity and function, provide an exemplary analysis that demonstrates the advantages of performing joint transcriptomic and epigenomic profiling of single microglial cells and discuss how comprehensive epigenetic analyses may enhance our understanding of microglial pathophysiology.

Keyword(s): Microglia: immunology (MeSH) ; Microglia: metabolism (MeSH) ; Epigenesis, Genetic (MeSH) ; Humans (MeSH) ; Animals (MeSH) ; Epigenomics: methods (MeSH) ; Transcriptome (MeSH) ; Immunity: genetics (MeSH) ; Gene Regulatory Networks (MeSH) ; Gene Expression Profiling (MeSH) ; Brain: immunology (MeSH) ; Brain: metabolism (MeSH) ; ATAC‐seq ; ATAC‐seq ; Alzheimer ; ChIP‐seq ; aging ; epigenetics ; microglia ; ChIP‐seq

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Contributing Institute(s):

1. Neuroimmunology and Neurodegenerative Disease (AG Neher (Tübingen))
2. Immunogenomics and Neurodegeneration (AG Beyer)
3. Platform for Single Cell Genomics and Epigenomics (PRECISE)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)
2. 351 - Brain Function (POF4-351) (POF4-351)

Experiment(s):

1. Platform for Single Cell Genomics and Epigenomics at DZNE University of Bonn

Appears in the scientific report 2024

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Database coverage:
; ; ; BIOSIS Previews ; BIOSIS Reviews Reports And Meetings ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DEAL Wiley ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 5 ; JCR ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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