SOCS1 Is a Critical Inhibitor of Interferon γ Signaling and Prevents the Potentially Fatal Neonatal Actions of this Cytokine
Open accessAbstract
Mice lacking suppressor of cytokine signaling-1 (SOCS1) develop a complex fatal neonatal disease. In this study, SOCS1-/- mice were shown to exhibit excessive responses typical of those induced by interferon gamma (IFNgamma), were hyperresponsive to viral infection, and yielded macrophages with an enhanced IFNgamma-dependent capacity to kill L. major parasites. The complex disease in SOCS1-/- mice was prevented by administration of anti-IFNgamma antibodies and did not occur in SOCS1-/- mice also lacking the IFNgamma gene. Although IFNgamma is essential for resistance to a variety of infections, the potential toxic action of IFNgamma, particularly in neonatal mice, appears to require regulation. Our data indicate that SOCS1 is a key modulator of IFNgamma action, allowing the protective effects of this cytokine to occur without the risk of associated pathological responses.
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Physiologically, SOCS1 is the main inducible inhibitor of IFNγ signaling and in neonatal mice prevents establishment of a lethal inflammatory disease characterized by heightened circulating IFNγ, fatty degeneration of the liver, and necrosis of the liver and other organs.
“Physiologically, SOCS1 is the main inducible inhibitor of IFN␥ signaling and in neonatal mice prevents the establishment of a lethal inflammatory disease characterized by heightened levels of circulating IFN␥, fatty degeneration of the liver, and necrosis of the liver and other organs (22).”
From The Comparative Roles of Suppressor of Cytokine Signaling-1 and -3 in the Inhibition and Desensitization of Cytokine Signaling (2006) · cites this paper as [22]
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- Authors
- Alexander, W. S., Starr, R., Fenner, J. E., Scott, C. L., Handman, E., Sprigg, N. S., Corbin, J. E., Cornish, A. L., Darwiche, R., Owczarek, C. M., Kay, T. W. H., Nicola, N. A., Hertzog, P. J., Metcalf, D., & Hilton, D. J.
- Affiliations
- The Royal Melbourne Hospital (AU)
- Monash Medical Centre (AU)
- Walter and Eliza Hall Institute of Medical Research (AU)
- Corresponding author
- Hilton, Douglas J
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1999-09
- Volume
- 98
- Issue
- 5
- Pages
- 597-608
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2000583211
- Cited by
- 762
- References
- 68
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 14 · 2023: 17 · 2022: 17 · 2021: 19 · 2020: 21 · 2019: 23 · 2018: 16 · 2017: 22 · 2016: 26 · 2015: 14 · 2014: 33 · 2013: 27 · 2012: 29
- FWCI
- 17.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA22556)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- SOCS1, suppressor of cytokine signaling, interferon-gamma, neonatal lethality, cytokine toxicity, macrophage killing, Leishmania major, viral susceptibility, anti-interferon-gamma antibody, cytokine signaling regulation, neonatal diseases
- MeSH terms
- Suppressor of Cytokine Signaling 1 Protein, Animals, Carrier Proteins, Disease Susceptibility, Interferon-gamma, Leishmaniasis, Lymphopenia, Macrophages, Mice, Inbred C57BL, Mice, Mutant Strains, Repressor Proteins, Semliki forest virus, Signal Transduction, Leishmania major, Alphavirus Infections, Gene Expression Regulation, Developmental, Suppressor of Cytokine Signaling Proteins, Mice
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