The development of inflammatory T-H-17 cells requires interferon-regulatory factor 4
2007 | journal article. A publication with affiliation to the University of Göttingen.
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- Authors
- Bruestle, Anne; Heink, Sylvia; Huber, Magdalena; Rosenplaenter, Christine; Stadelmann, Christine ; Yu, Philipp; Arpaia, Enrico; Mak, Tak W.; Kamradt, Thomas; Lohoff, Michael
- 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 (T-H-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 T-H-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 gamma t and more expression of Foxp3, transcription factors important for the differentiation of T-H-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 T-H-17 differentiation.
- Issue Date
- 2007
- Status
- published
- Publisher
- Nature Publishing Group
- Journal
- Nature Immunology
- ISSN
- 1529-2908