Interleukin-10 Signaling in Regulatory T Cells Is Required for Suppression of Th17 Cell-Mediated Inflammation
Open accessAbstract
Effector CD4+ T cell subsets, whose differentiation is facilitated by distinct cytokine cues, amplify the corresponding type of inflammatory response. Regulatory T (Treg) cells integrate environmental cues to suppress particular types of inflammation. In this regard, STAT3, a transcription factor essential for T helper 17 (Th17) cell differentiation, is necessary for Treg cell-mediated control of Th17 cell responses. Here, we showed that anti-inflammatory interleukin-10 (IL-10), and not proinflammatory IL-6 and IL-23 cytokine signaling, endowed Treg cells with the ability to suppress pathogenic Th17 cell responses. Ablation of the IL-10 receptor in Treg cells resulted in selective dysregulation of Th17 cell responses and colitis similar to that observed in mice harboring STAT3-deficient Treg cells. Thus, Treg cells limit Th17 cell inflammation by serving as principal amplifiers of negative regulatory circuits operating in immune effector cells.
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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 et al., 2011
The Results section (“IL-10R signaling facilitates IL-10 production by Treg cells”; page unavailable) shows that STAT3 binds the Il10 locus and links IL-10R signaling to IL-10 expression in Tregs. The Introduction says STAT3 and Foxp3 cooperatively regulate a subset of genes, but our copy does not establish that IL10 is one of those jointly regulated genes. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIL-10 production has been shown to render Th17 cells less pathogenic in autoimmunity, while co-production of IL-10 and IL-17a may be the indicated response for clearing certain infections like Staphylococcus aureus at mucosal sites.
“Although IL-10 production has been shown33,38,39 to render Th17 cells less pathogenic in autoimmunity, co-production of IL-10 and IL-17a may be the indicated response for clearing certain infections like Staphylococcus aureus at mucosal sites40.”
From Dynamic regulatory network controlling TH17 cell differentiation (2013) · cites this paper as [39]
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- Authors
- Chaudhry, A., Samstein, R. M., Treuting, P., Liang, Y., Pils, M. C., Heinrich, J.-M., Jack, R. S., Wunderlich, F. T., Brüning, J. C., Müller, W., & Rudensky, A. Y.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Max Planck Society (DE)
- Corresponding author
- Rudensky, Alexander Y.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 34
- Issue
- 4
- Pages
- 566-578
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3088485
- OpenAlex
- W1990295999
- Cited by
- 980
- References
- 49
- Citations by year
- 2026: 56 · 2025: 56 · 2024: 66 · 2023: 73 · 2022: 74 · 2021: 89 · 2020: 63 · 2019: 67 · 2018: 59 · 2017: 49 · 2016: 58 · 2015: 50 · 2014: 62 · 2013: 65 · 2012: 60
- FWCI
- 30.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 838 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of General Medical Sciences (GM 07739, T32GM007739)
- National Institute of Allergy and Infectious Diseases (R37AI034206)
- National Institute of Diabetes and Digestive and Kidney Diseases (F30DK091968)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- IL-10, regulatory T cells, Th17 cells, STAT3, IL-10 receptor, interleukin-6, IL-23, colitis, immunosuppression, CD4+ T cell differentiation
- MeSH terms
- Animals, Colitis, Phosphorylation, Signal Transduction, Interleukin-10, Mice, Knockout, Cell Lineage, T-Lymphocytes, Regulatory, STAT3 Transcription Factor, Mice, Receptors, Interleukin-10, Th17 Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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