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
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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.
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页码：351 / 356
页数：5
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