Regulatory T-cell suppressor program co-opts transcription factor IRF4 to control TH2 responses

被引：0

作者：

Ye Zheng

Ashutosh Chaudhry

Arnold Kas

Paul deRoos

Jeong M. Kim

Tin-Tin Chu

Lynn Corcoran

Piper Treuting

Ulf Klein

Alexander Y. Rudensky

机构：

[1] Howard Hughes Medical Institute,Department of Comparative Medicine

[2] ,Immunology Division

[3] Department of Immunology,undefined

[4] ,undefined

[5] University of Washington,undefined

[6] Seattle,undefined

[7] Washington 98195,undefined

[8] USA,undefined

[9] The Walter and Eliza Hall Institute,undefined

[10] Institute for Cancer Genetics and Herbert Irving Comprehensive Cancer Center,undefined

[11] Columbia University,undefined

[12] New York,undefined

[13] New York 10032,undefined

[14] USA,undefined

[15] Present address: Department of Immunology,undefined

[16] Memorial Sloan-Kettering Cancer Center,undefined

[17] New York,undefined

[18] New York 10021,undefined

[19] USA.,undefined

来源：

Nature | 2009年 / 458卷

关键词：

D O I：

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学科分类号：

摘要：

The X-chromosome-encoded transcription factor Foxp3 is thought to play a key role in the immune response as a regulator of the differentiation and suppressor function of regulatory T cells (Treg cells). Zheng et al. show here that regulatory T cells express the transcription factor IRF4 (interferon regulatory factor-4), which is essential for the differentiation of TH2 effector cells, and that IRF4 expression is dependent on Foxp3. IRF4 depletion in Treg cells induces TH2-driven autoimmune disease, leading the authors to suggest that IRF4 directs a module within Treg cells which selectively suppressesTH2 responses.

引用

页码：351 / 356

页数：5

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