IκBζ regulates TH17 development by cooperating with ROR nuclear receptors

被引：0

作者：

Kazuo Okamoto

Yoshiko Iwai

Masatsugu Oh-hora

Masahiro Yamamoto

Tomohiro Morio

Kazuhiro Aoki

Keiichi Ohya

Anton M. Jetten

Shizuo Akira

Tatsushi Muta

Hiroshi Takayanagi

机构：

[1] Graduate School of Medical and Dental Sciences,Department of Cell Signaling

[2] Tokyo Medical and Dental University,Department of Microbiology and Immunology

[3] Global Center of Excellence (GCOE) Program,Department of Pediatrics and Developmental Biology

[4] International Research Center for Molecular Science in Tooth and Bone Diseases,Department of Hard Tissue Engineering (Pharmacology)

[5] ,Division of Intramural Research

[6] Japan Science and Technology Agency (JST),undefined

[7] ERATO,undefined

[8] Takayanagi Osteonetwork Project,undefined

[9] Yushima 1-5-45,undefined

[10] Bunkyo-ku,undefined

[11] Tokyo 113-8549,undefined

[12] Japan ,undefined

[13] Medical Top Track Program,undefined

[14] Medical Research Institute,undefined

[15] Tokyo Medical and Dental University,undefined

[16] Yushima 1-5-45,undefined

[17] Bunkyo-ku,undefined

[18] Tokyo 113-8510,undefined

[19] Japan ,undefined

[20] Laboratory of Immune Regulation,undefined

[21] Graduate School of Medicine,undefined

[22] and WPI Immunology Frontier Research Center,undefined

[23] Osaka University,undefined

[24] 2-2,undefined

[25] Yamada-oka,undefined

[26] Suita,undefined

[27] Osaka 565-0871,undefined

[28] Japan,undefined

[29] Graduate School of Medical and Dental Sciences,undefined

[30] Tokyo Medical and Dental University,undefined

[31] Yushima 1-5-45,undefined

[32] Bunkyo-ku,undefined

[33] Tokyo 113-8519,undefined

[34] Japan,undefined

[35] Graduate School of Medical and Dental Sciences,undefined

[36] Tokyo Medical and Dental University,undefined

[37] Yushima 1-5-45,undefined

[38] Bunkyo-ku,undefined

[39] Tokyo 113-8549,undefined

[40] Japan,undefined

[41] Cell Biology Section,undefined

[42] National Institute of Environmental Health Sciences,undefined

[43] National Institutes of Health,undefined

[44] 111 T.W. Alexander Drive Research Triangle Park,undefined

[45] North Carolina 27709,undefined

[46] USA,undefined

[47] Laboratory of Host Defense,undefined

[48] WPI Immunology Frontier Research Center,undefined

[49] Osaka University,undefined

[50] Yamada-oka 3-1,undefined

来源：

Nature | 2010年 / 464卷

关键词：

D O I：

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中图分类号：

学科分类号：

摘要：

The development of interleukin (IL)-17-producing T cells (TH17 cells) is shown to require the transcription factor IκBζ in addition to ROR nuclear receptors. IκBζ cooperates with ROR factors through binding to the upstream conserved non-coding sequence CNS2, and mice deficient for IκBζ are resistant to the induction of experimental autoimmune encephalomyelitis. The work highlights the transcriptional mechanisms involved in TH17 development and suggests novel therapeutic approaches to autoimmune disease.

引用

页码：1381 / 1385

页数：4

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