ArticleThe Biochemical journal2001
Negative cross-talk between interleukin-3 and interleukin-11 is mediated by suppressor of cytokine signalling-3 (SOCS-3).
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 44 citations in OpenAlex.
- Role of SOCS and VHL Proteins in Neuronal Differentiation and Development.International journal of molecular sciences · 2023Review
- Roles of IL-11 in the regulation of bone metabolism.Frontiers in endocrinology · 2023Review
- IL-11 prevents IFN-γ-induced hepatocyte death through selective downregulation of IFN-γ/STAT1 signaling and ROS scavenging.PloS one · 2019Article
- SOCS3, a Major Regulator of Infection and Inflammation.Frontiers in immunology · 2014Review
- The role of suppressors of cytokine signalling in human neoplasms.Molecular biology international · 2014Review
- SOCS proteins in development and disease.American journal of clinical and experimental immunology · 2013Article
- IL-10-induced gp130 expression in mouse mast cells permits IL-6 trans-signaling.Journal of leukocyte biology · 2012Article
- Neuropoietin attenuates adipogenesis and induces insulin resistance in adipocytes.The Journal of biological chemistry · 2008Article
- Principles of interleukin (IL)-6-type cytokine signalling and its regulation.The Biochemical journal · 2003Review
- Regulation of IFN-gamma signaling is essential for the cytotoxic activity of CD8(+) T cells.Journal of immunology (Baltimore, Md. : 1950) · 2001Article
- Suppressor of cytokine signaling 3 (SOCS-3) protects beta -cells against interleukin-1beta - and interferon-gamma -mediated toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that addition of interleukin-3 (IL-3) abrogated the B-cell potential of primary colonies supported by IL-11, erythropoietin, IL-7 and steel factor. However, the mechanism by which IL-3 exerts its inhibitory role is not understood. Using a variant of the mouse pro-B cell line Ba/F3 which expresses both IL-3 and IL-11 receptors, we showed that pretreatment of these cells with IL-3 before stimulation by IL-11 suppressed the tyrosine phosphorylation and nuclear translocation of STAT3 (signal transducer and activator of transcription 3). This inhibition occurred within 30 min and required the synthesis of a negative regulator. The onset of IL-3-dependent inhibition was correlated temporally with the appearance of SOCS-3 (suppressor of cytokine signalling-3) protein. In addition, overexpression of SOCS-3 in the pro-B cell line effectively blocked STAT3 activation induced by IL-11. These findings establish that a cytokine (IL-3) that has been shown to modulate its own signal of activation is also able to down-regulate signalling activated by a different cytokine (IL-11). This cross-talk involves activation of the JAK (Janus kinase)/STAT signalling pathway, but not mitogen-activated protein kinase pathways, and is mediated, at least in part, by SOCS-3.
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