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

Ye Zheng, Ashutosh Chaudhry, Arnold Kas, Paul deRoos, Jeong M. Kim, Tin-Tin Chu, Lynn Corcoran, Piper Treuting, Ulf Klein and Alexander Y. Rudensky ()
Additional contact information
Ye Zheng: Howard Hughes Medical Institute,
Ashutosh Chaudhry: Howard Hughes Medical Institute,
Arnold Kas: Howard Hughes Medical Institute,
Paul deRoos: Howard Hughes Medical Institute,
Jeong M. Kim: Howard Hughes Medical Institute,
Tin-Tin Chu: Howard Hughes Medical Institute,
Lynn Corcoran: The Walter and Eliza Hall Institute
Piper Treuting: University of Washington, Seattle, Washington 98195, USA
Ulf Klein: Institute for Cancer Genetics and Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA
Alexander Y. Rudensky: Howard Hughes Medical Institute,

Nature, 2009, vol. 458, issue 7236, 351-356

Abstract: T helper cells: IRF4 in control 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.

Date: 2009
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DOI: 10.1038/nature07674

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