The development of inflammatory TH-17 cells requires interferon-regulatory factor 4 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-09

AUTHORS

Anne Brüstle, Sylvia Heink, Magdalena Huber, Christine Rosenplänter, Christine Stadelmann, Philipp Yu, Enrico Arpaia, Tak W Mak, Thomas Kamradt, Michael Lohoff

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 RORgammat 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. More... »

PAGES

958-966

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni1500

DOI

http://dx.doi.org/10.1038/ni1500

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1004683401

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17676043


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