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Cited by 6,737Cytokine Signaling Pathways and InteractionsT-cell and B-cell ImmunologyIL-33, ST2, and ILC Pathways

Interleukin-10 and the Interleukin-10 Receptor

Moore, Kevin W., de Waal Malefyt, Rene, Coffman, Robert L., O'Garra, Anne·2001·Annual Review of Immunology
DOI 10.1146/annurev.immunol.19.1.683
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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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Crossref · 10.1146/annurev.immunol.19.1.683

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  • IL-10R has two motifs for STAT3 activation while the gp130 subunit of IL-6R has four, leading to IL-6R inducing a higher amplitude STAT3 signal.

    “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]

  • 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 [13]

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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
DOI
10.1146/annurev.immunol.19.1.683
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
  • Health Sciences › Medicine › Oncology › 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

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