Cited by 13Neuroinflammation and Neurodegeneration MechanismsMultiple Sclerosis Research StudiesTraumatic Brain Injury and Neurovascular Disturbances

Brain Activation of Monocyte-Lineage Cells: Involvement of Interleukin-6

Shafer, Lisa L., McNulty, John A., Young, M. Rita I.·2002·Neuroimmunomodulation

Abstract

Immune processes such as phagocytosis of debris and antigen presentation can be damaging to the function and survival of brain cells. Understanding what conditions and factors mediate immune processes in the brain is central to ameliorating the pathology associated with brain injury and disease. The elevation of secreted interleukin (IL)-6 is a common feature of brain injury and neurodegenerative pathology. Using organotypic brain slice coculture, the effects of brain-derived soluble factors on immune functions in the BV2 microglial cell line were studied. We have previously shown that brain-derived soluble factors upregulated phagocytic activity and class II major histocompatibility complex (MHC II) expression and altered BV2 morphology in a manner selective for microglia and not peripheral macrophages. The present study used IL-6-neutralizing antibody to show that brain-derived IL-6 was at least partially responsible for the brain coculture-induced upregulation of MHC II expression in the BV2 microglia. Additionally, IL-6 upregulated phagocytic activity and induced morphological changes in the BV2 cells similar to brain coculture. These effects were selective for microglia, as they were not observed in peripheral macrophage cell types. The ability of IL-6-neutralizing antibody to downregulate MHC II expression while maintaining enhanced phagocytic activity could potentially evade an antagonizing immune response associated with brain injury or disease.

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Crossref · 10.1159/000069973

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  • IL-6 supports proliferation of both astrocytes and microglia and enhances microglial phagocytosis.

    “It has been shown to support proliferation of both astrocytes and microglia [151, 152] and enhance microglial phagocytosis [153, 154].”

    From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [153]

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Authors
Shafer, L. L., McNulty, J. A., & Young, M. R. I.
Affiliations
Loyola University Medical Center (US)
Venue
Neuroimmunomodulation
Publisher
S. Karger AG
Published
2002
Volume
10
Issue
5
Pages
295-304
ISSN
  • 1021-7401 (ISSN-L)
  • 1423-0216
OpenAlex
W2018392643
Cited by
13
References
61
Citations by year
2024: 1 · 2018: 1 · 2017: 2 · 2015: 1 · 2013: 1 · 2012: 1
FWCI
0.21
Type
journal article
Language
en
Open access
closed
Locations
  • NeuroImmunoModulation (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
interleukin-6, microglia, BV-2 cells, phagocytosis, MHC class II expression, brain injury, neuroinflammation, macrophages, IL-6 neutralizing antibody, microglial morphology, antigen presentation
MeSH terms
Animals, Histocompatibility Antigens Class II, Brain Injuries, Cells, Cultured, Chemotaxis, Leukocyte, Encephalitis, Female, Gliosis, Macrophages, Mice, Inbred C57BL, Monocytes, Organ Culture Techniques, Phagocytosis, Down-Regulation, Interleukin-6, Up-Regulation, Microglia, Coculture Techniques, Cell Lineage, Cell Shape, Mice

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