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Interleukin-10 and the Interleukin-10 Receptor
Abstract
Interleukin-10 (IL-10), first recognized for its ability to inhibit activation and effector function of T cells, monocytes, and macrophages, is a multifunctional cytokine with diverse effects on most hemopoietic cell types. The principal routine function of IL-10 appears to be to limit and ultimately terminate inflammatory responses. In addition to these activities, IL-10 regulates growth and/or differentiation of B cells, NK cells, cytotoxic and helper T cells, mast cells, granulocytes, dendritic cells, keratinocytes, and endothelial cells. IL-10 plays a key role in differentiation and function of a newly appreciated type of T cell, the T regulatory cell, which may figure prominently in control of immune responses and tolerance in vivo. Uniquely among hemopoietic cytokines, IL-10 has closely related homologs in several virus genomes, which testify to its crucial role in regulating immune and inflammatory responses. This review highlights findings that have advanced our understanding of IL-10 and its receptor, as well as its in vivo function in health and disease.
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“Another key difference between the IL-10R and the IL-6R, besides their differing interactions with SOCS3, is that the IL-10R has two motifs for STAT3 activation while the gp130 subunit of the IL-6R has four, leading to the IL-6R inducing a higher amplitude STAT3 signal [13], [27], [28].”
From A Model for How Signal Duration Can Determine Distinct Outcomes of Gene Transcription Programs (2012) · cites this paper as [27]
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“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 [13]
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Self-citation
Metadata
- Authors
- Moore, K. W., de Waal Malefyt, R., Coffman, R. L., & O'Garra, A.
- Affiliations
- Departments of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology Inc., Palo Alto, California 94304;
- ORCID
- Coffman, Robert L.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2001-04
- Volume
- 19
- Issue
- 1
- Pages
- 683-765
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2161074777
- Cited by
- 6,737
- References
- 676
- Citations by year
- 2026: 141 · 2025: 217 · 2024: 193 · 2023: 228 · 2022: 268 · 2021: 269 · 2020: 222 · 2019: 251 · 2018: 231 · 2017: 249 · 2016: 298 · 2015: 276 · 2014: 312 · 2013: 317 · 2012: 348
- FWCI
- 23.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- IL-10, IL-10 receptor, cytokine signaling, immunomodulation, inflammation, regulatory T cells, immune tolerance, T cell regulation, B cell differentiation, natural killer cells, dendritic cells, hematopoietic cells
- MeSH terms
- Animals, Autoimmune Diseases, Clinical Trials as Topic, Dendritic Cells, Diabetes Mellitus, Type 1, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Gene Expression Regulation, Herpesviridae, Humans, Infections, Inflammation, Lupus Erythematosus, Systemic, Mice, Inbred NZB, Neoplasms, Neutrophils, Primates, Protein-Tyrosine Kinases, Transcription Factors, Transcription, Genetic, Viral Proteins, Signal Transduction, Lymphocyte Subsets, Mice, Inbred NOD, Interleukin-10, Clinical Trials, Phase II as Topic, Receptors, Interleukin, Mice, Knockout, Mice, Receptors, Interleukin-10
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.
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