ArticleBrain pathology (Zurich, Switzerland)2020
Deciphering the heterogeneity of myeloid cells during neuroinflammation in the single-cell era.
Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
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- Transthyretin, a novel prognostic marker of POCD revealed by time-series RNA-sequencing analysis.Molecular psychiatry · 2025Article
- Microglia Signatures: A Cause or Consequence of Microglia-Related Brain Disorders?International journal of molecular sciences · 2024Review
- Spatial transcriptomic brain imaging reveals the effects of immunomodulation therapy on specific regional brain cells in a mouse dementia model.BMC genomics · 2024Article
- Meningeal interleukin-17-producing T cells mediate cognitive impairment in a mouse model of salt-sensitive hypertension.Nature neuroscience · 2024Article
- Immune checkpoint inhibitor induced neurocognitive deficits in patients.Brain communications · 2023Article
- Protein Expression of the Microglial Marker Tmem119 Decreases in Association With Morphological Changes and Location in a Mouse Model of Traumatic Brain Injury.Frontiers in cellular neuroscience · 2022Article
- The P2XFrontiers in cellular neuroscience · 2021Article
- The myeloid side of the CNS.Brain pathology (Zurich, Switzerland) · 2020Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Multiple sclerosis (MS) is a disabling neuroinflammatory disease, which is little understood and lacks a sufficient therapeutic regimen. Myeloid cells have repeatedly shown to play a pivotal role in the disease progression. During homeostasis, only the CNS-resident microglia and CNS-associated macrophages are present in the CNS. Neuroinflammation causes peripheral immune cells to infiltrate the CNS contributing to disease progression and neurological sequelae. The differential involvement of the diverse peripheral and resident myeloid cell subsets to the disease pathogenesis and outcome are highly debated and difficult to assess. However, novel technological advances (new mouse models, single-cell RNA-Sequencing, and CYTOF) have improved the depth of immune profiling, which allows the characterization of distinct myeloid subsets. This review provides an overview of current knowledge on the phenotypes and roles of these different myeloid subsets in neuroinflammatory disease and their therapeutic relevance.
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Registered trials
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