ArticleFrontiers in immunology2015
Pathologic and Protective Roles for Microglial Subsets and Bone Marrow- and Blood-Derived Myeloid Cells in Central Nervous System Inflammation.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Markers of microglia in post-mortem brain samples from patients with Alzheimer's disease: a systematic review.Molecular psychiatry · 2018Pooled it
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- Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026Review
- Decoding IFN-mediated immunity and cell dynamics in viral encephalitis: Insights from coxsackievirus B3 infection.iScience · 2026Article
- Microglia in Brain Aging and Age-Related Diseases: Friends or Foes?International journal of molecular sciences · 2025Review
- Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders.Communications biology · 2025Article
- Uncovering a new mechanism of ischemic stroke: a study of the association between γδ T cells and immunoinflammation.Frontiers in immunology · 2025Review
- Alarm Functions of PD-1+ Brain-Resident Memory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Spatial dynamics of mammalian brain development and neuroinflammation by multimodal tri-omics mapping.bioRxiv : the preprint server for biology · 2024Article
- Spatiotemporal dynamics of the CD11cMolecular brain · 2024Article
- Glioblastoma-instructed microglia transition to heterogeneous phenotypic states with phagocytic and dendritic cell-like features in patient tumors and patient-derived orthotopic xenografts.Genome medicine · 2024Article
- IKKβ deletion from CNS macrophages increases neuronal excitability and accelerates the onset of EAE, while from peripheral macrophages reduces disease severity.Journal of neuroinflammation · 2024Article
- Glioblastoma-instructed microglia transition to heterogeneous phenotypic states with phagocytic and dendritic cell-like features in patient tumors and patient-derived orthotopic xenografts.bioRxiv : the preprint server for biology · 2023Article
- Noteworthy perspectives on microglia in neuropsychiatric disorders.Journal of neuroinflammation · 2023Review
- The C-C chemokine receptor 7: An immune molecule that modulates central nervous system function in homeostasis and disease.Brain, behavior, & immunity - health · 2023Review
- Microglia depletion as a therapeutic strategy: friend or foe in multiple sclerosis models?Neural regeneration research · 2023Review
- Myeloid-specific blockade of notch signaling alleviates dopaminergic neurodegeneration in Parkinson's disease by dominantly regulating resident microglia activation through NF-κB signaling.Frontiers in immunology · 2023Article
- Peripherally derived myeloid cells induce disease-dependent phenotypic changes in microglia.Frontiers in cellular neuroscience · 2023Article
- Psychological stress induces depressive-like behavior associated with bone marrow-derived monocyte infiltration into the hippocampus independent of blood-brain barrier disruption.Journal of neuroinflammation · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a series of processes designed for eventual clearance of pathogens and repair of damaged tissue. In the context of autoimmune recognition, inflammatory processes are usually considered to be pathological. This is also true for inflammatory responses in the central nervous system (CNS). However, as in other tissues, neuroinflammation can have beneficial as well as pathological outcomes. The complex role of encephalitogenic T cells in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) may derive from heterogeneity of the myeloid cells with which these T cells interact within the CNS. Myeloid cells, including resident microglia and infiltrating bone marrow-derived cells, such as dendritic cells (DC) and monocytes/macrophages [bone marrow-derived macrophages (BMDM)], are highly heterogeneous populations that may be involved in neurotoxicity and also immunoregulation and regenerative processes. Better understanding and characterization of myeloid cell heterogeneity is essential for future development of treatments controlling inflammation and inducing neuroprotection and neuroregeneration in diseased CNS. Here, we describe and compare three populations of myeloid cells: CD11c(+) microglia, CD11c(-) microglia, and CD11c(+) blood-derived cells in terms of their pathological versus protective functions in the CNS of mice with EAE. Our data show that CNS-resident microglia include functionally distinct subsets that can be distinguished by their expression of CD11c. These subsets differ in their expression of Arg-1, YM1, iNOS, IL-10, and IGF-1. Moreover, in contrast to BMDM/DC, both subsets of microglia express protective interferon-beta (IFNβ), high levels of colony-stimulating factor-1 receptor, and do not express the Th1-associated transcription factor T-bet. Taken together, our data suggest that CD11c(+) microglia, CD11c(-) microglia, and infiltrating BMDM/DC represent separate and distinct populations and illustrate the heterogeneity of the CNS inflammatory environment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.