Article abstract
Nature Immunology 8, 958 - 966 (2007)
Published online: 5 August 2007 | doi:10.1038/ni1500
The development of inflammatory TH-17 cells requires interferon-regulatory factor 4
Anne Brüstle1, Sylvia Heink2, Magdalena Huber1, Christine Rosenplänter1, Christine Stadelmann3, Philipp Yu4, Enrico Arpaia5, Tak W Mak5,6, Thomas Kamradt2 & Michael Lohoff1
Abstract
Interferon-regulatory factor 4 (IRF4) is essential for the development of T helper type 2 cells. Here we show that IRF4 is also critical for the generation of interleukin 17–producing T helper cells (TH-17 cells), which are associated with experimental autoimmune encephalomyelitis. IRF4-deficient (Irf4-/-) mice did not develop experimental autoimmune encephalomyelitis, and T helper cells from such mice failed to differentiate into TH-17 cells. Transfer of wild-type T helper cells into Irf4-/- mice rendered the mice susceptible to experimental autoimmune encephalomyelitis. Irf4-/- T helper cells had less expression of ROR
t and more expression of Foxp3, transcription factors important for the differentiation of TH-17 and regulatory T cells, respectively. Altered regulation of both transcription factors contributed to the phenotype of Irf4-/- T helper cells. Our data position IRF4 at the center of T helper cell development, influencing not only T helper type 2 but also TH-17 differentiation.
- Institut für Medizinische Mikrobiologie und Krankenhaushygiene, 35043 Marburg, Germany.
- Institut für Immunologie, Universitätsklinikum Jena, 07740 Jena, Germany.
- Institut für Neuropathologie, Universität Göttingen, 37075 Göttingen, Germany.
- Institut für Immunologie, 35043 Marburg, Germany.
- Advanced Medical Discovery Institute, University of Toronto, Toronto, Ontario, Canada M5G2C1.
- Departments of Immunology and Medical Biophysics, University of Toronto, Toronto, Ontario, Canada M5G2C1.
Correspondence to: Michael Lohoff1 e-mail: lohoff@med.uni-marburg.de
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