Regulatory T Cell-Derived Interleukin-10 Limits Inflammation at Environmental Interfaces
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The regulatory T (Treg) cells restrain immune responses through suppressor-function elaboration that is dependent upon expression of the transcription factor Foxp3. Despite a critical role for Treg cells in maintaining lympho-myeloid homeostasis, it remains unclear whether a single mechanism or multiple mechanisms of Treg cell-mediated suppression are operating in vivo and how redundant such mechanisms might be. Here we addressed these questions by examining the role of the immunomodulatory cytokine IL-10 in Treg cell-mediated suppression. Analyses of mice in which the Treg cell-specific ablation of a conditional IL-10 allele was induced by Cre recombinase knocked into the Foxp3 gene locus showed that although IL-10 production by Treg cells was not required for the control of systemic autoimmunity, it was essential for keeping immune responses in check at environmental interfaces such as the colon and lungs. Our study suggests that Treg cells utilize multiple means to limit immune responses. Furthermore, these mechanisms are likely to be nonredundant, in that a distinct suppressor mechanism most likely plays a prominent and identifiable role at a particular tissue and inflammatory setting.
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IL-10 serves a key function in tolerance induction by keeping immune responses in check and preventing self tissue damage.
“IL-10 can serve a key function in tolerance induction by keeping immune responses in check and preventing self tissue damage13–15.”
From The histone deacetylase HDAC11 regulates the expression of interleukin 10 and immune tolerance (2009) · cites this paper as [15]
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- Authors
- Rubtsov, Y. P., Rasmussen, J. P., Chi, E. Y., Fontenot, J., Castelli, L., Ye, X., Treuting, P., Siewe, L., Roers, A., Henderson, W. R., Muller, W., & Rudensky, A. Y.
- Affiliations
- University of Washington (US)
- University of Cologne (DE)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Rudensky, Alexander Y.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2008-04
- Volume
- 28
- Issue
- 4
- Pages
- 546-558
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2030284768
- Cited by
- 1,586
- References
- 55
- Citations by year
- 2026: 70 · 2025: 84 · 2024: 88 · 2023: 83 · 2022: 95 · 2021: 105 · 2020: 96 · 2019: 107 · 2018: 88 · 2017: 95 · 2016: 80 · 2015: 109 · 2014: 90 · 2013: 89 · 2012: 76
- FWCI
- 31.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- University of Alabama
- 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, IL-10, Foxp3, systemic autoimmunity, intestinal inflammation, lung inflammation, environmental interfaces, suppressor mechanisms, immune homeostasis
- MeSH terms
- Animals, Autoimmune Diseases, Colitis, Female, Luminescent Proteins, Lung, Male, Mice, Inbred C57BL, Mice, Transgenic, Organ Specificity, Skin, Interleukin-10, Mice, Knockout, Inflammation Mediators, Integrases, T-Lymphocytes, Regulatory, Mice, Forkhead Transcription Factors
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