Control of inflammation by integration of environmental cues by regulatory T cells
Open accessAbstract
Tregs have been implicated in control of homeostasis in the immune system and beyond. These cells restrain inflammatory responses to self antigens, commensal microorganisms, allergens, and pathogens and adapt their homeostatic and functional capabilities to a particular environment. In this review, we discuss a general model of integration of environmental cues by Tregs in which specialized Treg homeostatic, migratory, and suppression programs are established in dynamically changing inflammatory environments by maintaining an optimal threshold of activation of transcription factors involved in regulation of the corresponding type of effector immune responses.
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STAT3 and Foxp3 coregulate IL-10 in Tregs through histone acetyl transferase-1/FoxP3-mediated epigenetic modification of the IL-10 promoter, maintaining the ability of Foxp3+ Tregs to inhibit inflammatory Th17 cells.
“STAT3 and Foxp3 appear to coregulate IL10 in T-regs”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Chaudhry and Rudensky, 2013
In “Treg-mediated control of inflammatory responses” (page unavailable), the paper says STAT3 binds Foxp3 and modulates gene expression, and that STAT3 is needed to control Th17 responses. It does not identify IL-10 as a gene they coregulate. The “Overriding inhibitions” section instead describes IL-10-mediated STAT3 activation in Tregs; neither passage supports the claimed acetyltransferase-mediated modification of the IL-10 promoter. (LLM, conf=0.87)
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“…et al., 2011) through histone acetyl transferase-1/FoxP3-mediated epigenetic modification of the IL-10 promoter (Chaudhry et al., 2009, 2011; Chaudhry and Rudensky, 2013), thus maintaining the ability of Foxp31 Tregs to inhibit inflammatory Th17 cells (Chaudhry et al., 2009, 2011; Chaudhry…”
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- Authors
- Chaudhry, A., & Rudensky, A. Y.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2013-03-01
- Volume
- 123
- Issue
- 3
- Pages
- 939-944
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3582113
- OpenAlex
- W2053418050
- Cited by
- 183
- References
- 56
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 5 · 2023: 8 · 2022: 8 · 2021: 18 · 2020: 16 · 2019: 10 · 2018: 12 · 2017: 21 · 2016: 22 · 2015: 23 · 2014: 17 · 2013: 10
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Cancer Research Institute
- Memorial Sloan-Kettering Cancer Center
- National Institutes of Health (10021)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- regulatory T cells, inflammation control, environmental cues, Treg homeostasis, Treg migration, immunosuppression, commensal microorganisms, self-tolerance
- MeSH terms
- Animals, Cell Differentiation, Gene Expression Regulation, Humans, Inflammation, Cytokines, Inflammation Mediators, T-Lymphocytes, Regulatory, STAT Transcription Factors
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