General nature of the STAT3-activated anti-inflammatory response

被引:179
作者
El Kasmi, Karim C.
Holst, Jeff
Coffre, Maryaline
Mielke, Lisa
de Pauw, Antoine
Lhocine, Nouara
Smith, Amber M.
Rutschman, Robert
Kaushal, Deepak
Shen, Yuhong
Suda, Takashi
Donnelly, Raymond P.
Myers, Martin G., Jr.
Alexander, Warren
Vignali, Dario A. A.
Watowich, Stephanie S.
Ernst, Matthias
Hilton, Douglas J.
Murray, Peter J.
机构
[1] St Jude Childrens Hosp, Dept Infect Dis, Memphis, TN 38105 USA
[2] St Jude Childrens Hosp, Dept Immunol, Memphis, TN 38105 USA
[3] St Jude Childrens Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA
[4] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3050, Australia
[5] Royal Melbourne Hosp, Ludwig Inst Canc Res, Parkville, Vic 3050, Australia
[6] Rockefeller Univ, Mol Cell Biol Lab, New York, NY 10016 USA
[7] Kanazawa Univ, Canc Res Inst, Ctr Dev Mol Target Drugs, Kanazawa, Ishikawa 920, Japan
[8] US FDA, Ctr Drug Evaluat & Res, Div Therapeut Prot, Bethesda, MD 20892 USA
[9] Univ Michigan, Sch Med, Dept Med, Div Metab Endocrinol & Diabet, Ann Arbor, MI 48109 USA
[10] Univ Texas, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA
关键词
D O I
10.4049/jimmunol.177.11.7880
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:7880 / 7888
页数:9
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