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Abstracts (complete list) - Wissenschaft Online

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Anne Brüstle, Sylvia Heink, Magdalena Huber, Christine Rosenplänter, Christine<br />

Stadelmann, Philipp Yu, Enrico Arpaia, Tak W. Mak, Thomas Kamradt, Michael Lohoff<br />

Development of inflammatory Th17 cells requires interferon<br />

regulatory factor 4<br />

The transcription factor IRF4 is essential for T helper 2 (Th2) development. We show<br />

here that IRF4 is also critical for generating Th17 cells, pro-inflammatory cytokineproducing<br />

cells associated with autoimmune diseases like experimental autoimmune<br />

encephalomyelitis (EAE). IRF4-deficient (IRF4-/-) mice did not develop EAE and IRF4-/-<br />

Th cells failed to differentiate into Th17 cells. Transfer of IRF4+/+ Th cells rendered<br />

IRF4-/- mice susceptible to EAE. IRF4-/- Th cells showed reduced expression of RORgt<br />

and increased expression of Foxp3, transcription factors important for Th17 and<br />

regulatory T cell differentiation, respectively. The dysregulation of both factors<br />

contributed to the phenotype of IRF4-/- Th cells . Our data position IRF4 at the center<br />

of Th development, influencing not only Th2 but also Th17 differentiation.

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