Foxp3 controls regulatory T-cell function by interacting with AML1/Runx1

被引：0
|
作者：
Masahiro Ono
Hiroko Yaguchi
Naganari Ohkura
Issay Kitabayashi
Yuko Nagamura
Takashi Nomura
Yoshiki Miyachi
Toshihiko Tsukada
Shimon Sakaguchi
机构：
[1] Institute for Frontier Medical Sciences,Department of Experimental Pathology
[2] and,Department of Dermatology
[3] Graduate School of Medicine,Molecular Oncology Division
[4] Kyoto University,undefined
[5] Kyoto 606-8507,undefined
[6] Japan,undefined
[7] Tumor Endocrinology Project,undefined
[8] and,undefined
[9] ,undefined
[10] National Cancer Center Research Institute,undefined
[11] Chuo-ku,undefined
[12] Tokyo,undefined
[13] 104-0045,undefined
[14] Japan,undefined
[15] Core Research for Evolutional Science and Technology (CREST),undefined
[16] Japan Science and Technology Agency,undefined
[17] Kawaguchi 332-0012,undefined
[18] Japan,undefined
来源：
Nature | 2007年 / 446卷
关键词：
D O I：
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学科分类号：
摘要：
CD25+CD4+ regulatory T cells or 'Tregs' are vital to the immune system, suppressing aberrant or excessive immune responses such as autoimmune disease and allergy. Ono et al. find that Tregs act via the interaction of the transcription factors AML1/Runx1 and Foxp3. This interaction is therefore a potential therapeutic target for controlling immune responses.
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页码：685 / 689
页数：4
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