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Loss of IL-10 Promotes Differentiation of Microglia to a M1 Phenotype
Open accessAbstract
Microglia represent the primary resident immune cells of the central nervous system (CNS) and modulate local immune responses. Depending on their physiological functions, microglia can be classified into pro- (M1) and anti-inflammatory (M2) phenotype. Interleukin (IL)-10 is an important modulator of neuronal homeostasis, with anti-inflammatory and neuroprotective functions, and can be released by microglia. Here, we investigated how IL-10 deficiency affected the M1/2 polarization of primary microglia upon lipopolysaccharide (LPS) stimulation in vitro. Microglia phenotypes were analyzed via flow cytometry. Cytokine and chemokine secretion were examined by ELISA and bead-based multiplex LEGENDplex™. Our results showed that genetic depletion of IL-10 led to elevated M1 like phenotype (CD86+CD206-) under pro-inflammatory conditions associated with increased frequency of IL-6+, TNF-α+ cells and enhanced release of several pro-inflammatory chemokines. Absence of IL-10 led to an attenuated M2 like phenotype (CD86-CD206+) and a reduced secretion of TGF-β1 upon LPS stimulation. In conclusion, IL-10 deficiency may promote the polarisation of microglia into M1-prone phenotype under pro-inflammatory conditions.
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“which is known to inhibit the synthesis of pro-inflammatory cytokines, and may promote the differentiation of microglia into the anti-inflammatory state, classically known as M2 or homeostatic state [40].”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [40]
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Metadata
- Authors
- Laffer, B., Bauer, D., Wasmuth, S., Busch, M., Jalilvand, T. V., Thanos, S., Meyer zu Hörste, G., Loser, K., Langmann, T., Heiligenhaus, A., & Kasper, M.
- Affiliations
- St. Franziskus Hospital (DE)
- University of Münster (DE)
- University of Cologne (DE)
- Corresponding author
- Kasper, Maren
- ORCID
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2019-10-09
- Volume
- 13
- Pages
- 430-430
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC6794388
- OpenAlex
- W2979963107
- Cited by
- 120
- References
- 115
- Citations by year
- 2026: 21 · 2025: 16 · 2024: 14 · 2023: 16 · 2022: 16 · 2021: 20 · 2020: 16
- FWCI
- 5.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- IL-10, microglia, M1 macrophage phenotype, M2 phenotype, microglial polarization, lipopolysaccharide, IL-10 deficiency, CD86, CD206, inflammatory cytokines, TNF-α, interleukin-6, TGF-β1, chemokines, neuroinflammation
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