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General Nature of the STAT3-Activated Anti-Inflammatory Response
Author(s) -
Karim C. El Kasmi,
Jeff Holst,
Maryaline Coffre,
Lisa A. Mielke,
Antoine De Pauw,
Nouara Lhocine,
Amber M. Smith,
Robert Rutschman,
Deepak Kaushal,
Yuhong Shen,
Takashi Suda,
Raymond P. Donnelly,
Martin G. Myers,
Warren S. Alexander,
Dario A.A. Vignali,
Stephanie S. Watowich,
Matthias Ernst,
Douglas J. Hilton,
Peter J. Murray
Publication year - 2006
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.177.11.7880
Subject(s) - suppressor of cytokine signaling 1 , cytokine , proinflammatory cytokine , socs3 , receptor , stat3 , signal transduction , socs2 , microbiology and biotechnology , cytokine receptor , biology , heterologous , suppressor of cytokine signalling , immunology , inflammation , chemistry , suppressor , biochemistry , gene
Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.

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