CD200 Ligand–Receptor Interaction Modulates Microglial Activation In Vivo and In Vitro: A Role for IL-4
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Deficits in cognitive function are associated with neuroinflammatory changes, typified by activation of glial cells and an alteration of the pro- and anti-inflammatory cytokine balance in the brain. Although there is evidence to suggest that activation of microglia is regulated by interaction with other cell types in the brain, the mechanism(s) involved is poorly understood. Here, we provide evidence that interaction between CD200 and its receptor plays a role in modulating microglial activation under conditions of chronic and acute inflammation of the brain. We report that interleukin-4 (IL-4) plays a central role in modulating expression of CD200 and identify a mechanism by which IL-4 directly controls microglial cell activation. Our findings provide the first demonstration of a role for IL-4 in modulating CD200 expression and suggest a mechanism for regulation of microglial activation in the intact CNS under inflammatory conditions.
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IL-4 treatment of cultured neurons and intracerebroventricular administration of IL-4 markedly increase CD200 expression in hippocampal neurons.
“IL-4 treatment of cultured neurons and intracerebroventricular administration of IL-4 markedly increased CD200 expression in hippocampal neurons (Lyons et al, 2007).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Lyons et al, 2007
Aged rats show reduced neuronal CD200 that is associated with increased microglial MHCII expression.
“Compared with young adults, aged rats showed reduced neuronal CD200 that was associated with the increased microglial MHCII expression (Lyons et al, 2007).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Lyons et al, 2007
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- Authors
- Lyons, A., Downer, E. J., Crotty, S., Nolan, Y. M., Mills, K. H. G., & Lynch, M. A.
- Affiliations
- Trinity College Dublin (IE)
- Trinity College (CA)
- University College Cork (IE)
- Corresponding author
- Lynch, Marina A.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-08-01
- Volume
- 27
- Issue
- 31
- Pages
- 8309-8313
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6673084
- OpenAlex
- W2059844545
- Cited by
- 258
- References
- 22
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 16 · 2023: 6 · 2022: 9 · 2021: 12 · 2020: 15 · 2019: 9 · 2018: 20 · 2017: 14 · 2016: 17 · 2015: 13 · 2014: 19 · 2013: 20 · 2012: 25
- FWCI
- 7.20
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Arrow@dit (Dublin Institute of Technology) (acceptedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion, cc-by-nc-sa)
- Funders
- Science Foundation Ireland
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- CD200, CD200R, microglial activation, IL-4, neuroinflammation, cognitive impairment, glial activation, cytokine balance
- MeSH terms
- Acute Disease, Animals, Chronic Disease, Inflammation, Ligands, Male, Membrane Glycoproteins, Mice, Inbred C57BL, Antigens, CD, Interleukin-4, Rats, Wistar, Microglia, Mice, Rats
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