BATF–JUN is critical for IRF4-mediated transcription in T cells

Peng Li (), Rosanne Spolski, Wei Liao, Lu Wang, Theresa L. Murphy, Kenneth M. Murphy and Warren J. Leonard ()
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Peng Li: Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health
Rosanne Spolski: Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health
Wei Liao: Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health
Lu Wang: Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health
Theresa L. Murphy: Washington University School of Medicine
Kenneth M. Murphy: Washington University School of Medicine
Warren J. Leonard: Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health

Nature, 2012, vol. 490, issue 7421, 543-546

Abstract: The pleiotropic transcription factor IRF4 is shown to regulate CD4+ T-cell differentiation and TH17 function through cooperative binding interactions with BATF and JUN family proteins via AP1–IRF4 composite elements (AICEs).

Date: 2012
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DOI: 10.1038/nature11530

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