Granulocyte-Macrophage Colony-Stimulating Factor Induces an Expression Program in Neonatal Microglia That Primes Them for Antigen Presentation
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Neonatal microglial cells respond to GM-CSF and M-CSF by acquiring different morphologies and phenotypes. To investigate the extent and consequences of this process, a global gene expression analysis was performed, with significant changes in transcript levels confirmed by biochemical analyses. Primary murine microglial cells underwent substantial expression reprogramming after treatment with GM-CSF or M-CSF with many differentially expressed transcripts important in innate and adaptive immunity. In particular, many gene products involved in Ag presentation were induced by GM-CSF, but not M-CSF, thus potentially priming relatively quiescent microglia cells for Ag presentation. This function of GM-CSF is distinct from its primary function in cell proliferation and survival.
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Colony-stimulating factors have opposite effects on MHCII, and subsequently on neuroinflammation, in mouse and human microglia.
“Moreover, colony-stimulating factors have been shown to have opposite effects on MHCII, and subsequently, on neuroinflammation, in mouse and human microglia.20, 21”
From Tubular human brain organoids to model microglia-mediated neuroinflammation (2021) · cites this paper as [21]
The Ag presentation section reports that GM-CSF increased class II MHC protein in neonatal mouse microglia, while M-CSF did not; the Discussion links GM-CSF to proinflammatory activity. The paper does not establish opposite MHCII effects in mouse versus human microglia or show that such a difference subsequently changes neuroinflammation. (LLM, conf=0.87)
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- Authors
- Re, F., Belyanskaya, S. L., Riese, R. J., Cipriani, B., Fischer, F. R., Granucci, F., Ricciardi-Castagnoli, P., Brosnan, C., Stern, L. J., Strominger, J. L., & Santambrogio, L.
- Affiliations
- Dana-Farber Cancer Institute (US)
- Brigham and Women's Hospital (US)
- Albert Einstein College of Medicine (US)
- Justus-Liebig-Universität Gießen (DE)
- University of Milano-Bicocca (IT)
- Department of Biotechnology and Bioscience, University of Milano-Bicocca , Milan ,
- Massachusetts Institute of Technology (US)
- Corresponding author
- Re, Fabio
- Santambrogio, Laura
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-09-01
- Volume
- 169
- Issue
- 5
- Pages
- 2264-2273
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2116369972
- Cited by
- 109
- References
- 56
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 4 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 4 · 2015: 4 · 2014: 2 · 2013: 10 · 2012: 4
- FWCI
- 6.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Zenodo (CERN European Organization for Nuclear Research) (other-oa)
- Funders
- National Institutes of Health (5r35ca047554-13, AI48833)
- National Cancer Institute (R35CA47554)
- National Institute of Allergy and Infectious Diseases (R01-AI-48832, R01-AI48833, R01AI048833, R01AI048832)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- GM-CSF, microglia, macrophage colony-stimulating factor, gene expression reprogramming, antigen presentation, microglial activation, innate immunity, adaptive immunity
- MeSH terms
- Animals, Animals, Newborn, Cathepsins, Cells, Cultured, Dendritic Cells, Macrophages, Mice, Inbred Strains, Phagocytosis, Receptors, Immunologic, Biomarkers, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Cytokines, Microglia, Antigen Presentation, Receptors, Cytokine, Chemokines, Receptors, Chemokine, Oligonucleotide Array Sequence Analysis, Matrix Metalloproteinases, Gene Expression Profiling, Mice
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