Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5

被引:0
|
作者
Xiang-Ping Yang
Kamran Ghoreschi
Scott M Steward-Tharp
Jaime Rodriguez-Canales
Jinfang Zhu
John R Grainger
Kiyoshi Hirahara
Hong-Wei Sun
Lai Wei
Golnaz Vahedi
Yuka Kanno
John J O'Shea
Arian Laurence
机构
[1] Molecular Immunology and Inflammation Branch,
[2] National Institute of Arthritis,undefined
[3] Musculoskeletal and Skin Diseases,undefined
[4] National Institutes of Health,undefined
[5] Laser Capture Microdissection Core Laboratory of Pathology,undefined
[6] National Cancer Institute,undefined
[7] National Institutes of Health,undefined
[8] Laboratory of Immunology,undefined
[9] National Institute of Allergy and Infectious Diseases,undefined
[10] National Institutes of Health,undefined
[11] Mucosal Immunology Section,undefined
[12] National Institute of Allergy and Infectious Diseases,undefined
[13] National Institutes of Health,undefined
[14] Clinical Immunology Section,undefined
[15] National Eye Institute,undefined
[16] National Institutes of Health,undefined
来源
Nature Immunology | 2011年 / 12卷
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中图分类号
学科分类号
摘要
Loss of IL-2 signaling results in autoimmunity. Laurence and colleagues show that the IL-2–STAT5 axis counteracts STAT3 activation of Il17 to dampen IL-17 production independently of Foxp3.
引用
收藏
页码:247 / 254
页数:7
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