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

关键词：

D O I：

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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

页码：247 / 254

页数：7

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