期刊
NATURE IMMUNOLOGY
卷 14, 期 7, 页码 732-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2633
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资金
- US National Institutes of Health
- Leukemia and Lymphoma Society
- MD Anderson Cancer Center
- Biology of Inflammation Center at Baylor College of Medicine
- American Heart Association
- American Cancer Society
- Shanghai Board of Health Foundation
- Shanghai Jiao Tong University
- Ministry of Education of China
Transcription factors of the STAT family are critical in the cytokine-mediated functional differentiation of CD4(+) helper T cells. Signaling inhibitors of the SOCS family negatively regulate the activation of STAT proteins; however, their roles in the differentiation and function of helper T cells are not well understood. Here we found that the SOCS protein CIS, which was substantially induced by interleukin 4 (IL-4), negatively regulated the activation of STAT3, STAT5 and STAT6 in T cells. CIS-deficient mice spontaneously developed airway inflammation, and CIS deficiency in T cells led to greater susceptibility to experimental allergic asthma. CIS-deficient T cells showed enhanced differentiation into the TH2 and TH9 subsets of helper T cells. STAT5 and STAT6 regulated IL-9 expression by directly binding to the Il9 promoter. Our data thus demonstrate a critical role for CIS in controlling the proallergic generation of helper T cells.
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