Cerebral regulatory T cells restrain microglia/macrophage-mediated inflammatory responses via IL-10
Open accessAbstract
Forkhead box P3 (Foxp3) + regulatory T (Treg) cells maintain the immune tolerance and prevent inflammatory responses in the periphery. However, the presence of Treg cells in the CNS under steady state has not been studied. Here, for the first time, we show a substantial TCR αβ + CD4 + Foxp3 + T‐cell population (cerebral Treg cells) in the rat cerebrum, constituting more than 15% of the cerebral CD4 + T‐cell compartment. Cerebral Treg cells showed an activated/memory phenotype and expressed many Treg‐cell signature genes at higher levels than peripheral Treg cells. Consistent with their activated/memory phenotype, cerebral Treg cells robustly restrained the LPS‐induced inflammatory responses of brain microglia/macrophages, suggesting a role in maintaining the cerebral homeostasis by inhibiting the neuroinflammation. In addition, brain astrocytes were the helper cells that sustained Foxp3 expression in Treg cells through IL‐2/STAT5 signaling, showing that the interaction between astrocytes and Treg cells contributes to the maintenance of Treg‐cell identity in the brain. Taken together, our work represents the first study to characterize the phenotypic and functional features of Treg cells in the rat cerebrum. Our data have provided a novel insight for the contribution of Treg cells to the immunosurveillance and immunomodulation in the cerebrum under steady state.
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In SAE, brain-infiltrating Tregs antagonize microglial inflammatory cascades by secreting IL-10 and TGF-β, and suppress astrocytic IL-6 synthesis through the amphiregulin (AREG)-EGFR signaling axis.
“In SAE, brain-infiltrating Tregs antagonize microglial inflammatory cascades by secreting factors like IL-10 and TGF-β, and suppress astrocytic IL-6 synthesis through the amphiregulin (AREG)-EGFR signaling axis [35,36].”
From Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy (2026) · cites this paper as [36]
The Results section on LPS-induced microglia/macrophage responses reports that cerebral Tregs suppress inflammatory cytokines and that IL-10 neutralization attenuates this effect. It does not establish this mechanism specifically in sepsis-associated encephalopathy (SAE), or show Treg secretion of TGF-β or suppression of astrocytic IL-6 through AREG–EGFR. The astrocyte Results instead concern astrocyte-mediated maintenance of Tregs through IL-2/STAT5. Page numbers are unavailable in our copy. (LLM, conf=0.91)
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References 48 · Cited by 185
- Authors
- Xie, L., Choudhury, G. R., Winters, A., Yang, S., & Jin, K.
- Affiliations
- University of North Texas Health Science Center (US)
- Corresponding author
- Jin, Kunlin
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2014-11-24
- Volume
- 45
- Issue
- 1
- Pages
- 180-191
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- PMC
- PMC4293323
- OpenAlex
- W1581792805
- Cited by
- 185
- References
- 48
- Citations by year
- 2026: 15 · 2025: 13 · 2024: 19 · 2023: 25 · 2022: 24 · 2021: 16 · 2020: 19 · 2019: 8 · 2018: 13 · 2017: 12 · 2016: 12 · 2015: 9
- FWCI
- 5.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- US Public Health Service (NS57186)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- Foxp3, CD4+ T cells, microglia/macrophages, neuroinflammation, IL-10, astrocytes, IL-2/STAT5 signaling, lipopolysaccharide-induced inflammation, immune surveillance
- MeSH terms
- Animals, Astrocytes, Cell Communication, Encephalitis, Gene Expression Regulation, Immunologic Memory, Immunologic Surveillance, Interleukin-2, Lipopolysaccharides, Macrophage Activation, Macrophages, Male, Signal Transduction, Interleukin-10, Rats, Sprague-Dawley, T-Lymphocytes, Regulatory, STAT5 Transcription Factor, Rats, Cerebrum, Primary Cell Culture
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