Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response
Abstract
Interleukin (IL)-10 performs an irreplaceable role in negatively regulating inflammation, primarily through a mechanism that selectively blocks the expression of pro-inflammatory genes encoding cytokines, chemokines, cell-surface molecules and other molecules involved in the propagation of inflammation. Not surprisingly, IL-10 has attracted interest as a tool to regulate inflammatory diseases. The clinical use of IL-10 as an anti-inflammatory agent has, however, not met expectations. Nevertheless, the signaling pathway used by the IL-10 receptor to generate the anti-inflammatory response is only beginning to be understood and could be a way to regulate inflammation by pharmacological agents.
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The ability of IL-10 to induce signaling via JAK1/STAT3 is primarily restricted to cells of the immune system, such as macrophages and dendritic cells.
“the ability of IL-10 to induce signaling via JAK1/STAT3 appears primarily restricted to cells of the immune system, such as macrophages and dendritic cells”
From Model Based Targeting of IL-6-Induced Inflammatory Responses in Cultured Primary Hepatocytes to Improve Application of the JAK Inhibitor Ruxolitinib (2017) · cites this paper as Murray, 2006
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References 63 · Cited by 436
- Authors
- MURRAY, P.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Corresponding author
- MURRAY, P
- Venue
- Current Opinion in Pharmacology
- Publisher
- Elsevier BV
- Published
- 2006-08
- Volume
- 6
- Issue
- 4
- Pages
- 379-386
- ISSN
- 1471-4892 (ISSN-L)
- OpenAlex
- W1982664065
- Cited by
- 436
- References
- 63
- Citations by year
- 2026: 22 · 2025: 21 · 2024: 17 · 2023: 27 · 2022: 22 · 2021: 28 · 2020: 23 · 2019: 24 · 2018: 16 · 2017: 19 · 2016: 27 · 2015: 15 · 2014: 23 · 2013: 22 · 2012: 27
- FWCI
- 9.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P 30CA 21765, P30CA021765)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- IL-10, STAT3 signaling, anti-inflammatory response, IL-10 receptor signaling, inflammation regulation, inflammatory diseases, cytokine gene expression, chemokines
- MeSH terms
- Animals, Antineoplastic Agents, Dendritic Cells, Humans, Inflammation, Macrophages, Neoplasms, T-Lymphocytes, Toxoplasma, Transcription, Genetic, Vaccinia virus, Signal Transduction, Interleukin-10, STAT3 Transcription Factor, Receptors, Interleukin-10
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