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Article
Nature Immunology  4, 380 - 386 (2003)
Published online: 24 February 2003; | doi:10.1038/ni903

Transcriptional profiling identifies Id2 function in dendritic cell development

Christine Hacker1, 5, Ralf D. Kirsch1, 5, Xin-Sheng Ju1, Thomas Hieronymus1, Tatjana C. Gust1, Christiane Kuhl1, 4, Thorsten Jorgas1, Steffen M. Kurz1, Stefan Rose-John2, Yoshifumi Yokota3 & Martin Zenke1

1  Max-Delbrück-Center for Molecular Medicine, MDC, Robert-Rössle-Str. 10, 13092 Berlin, Germany.

2  Department of Biochemistry, Christian-Albrechts-University, Olshausenstr. 40, 24098 Kiel, Germany.

3  Department of Biochemistry, Fukui Medical University, Matsuoka, 910-1193 Fukui, Japan.

4  Present address: Weatherall Institute of Molecular Medicine, Headington, Oxford OX3 9DS, UK.

5  These authors contributed equally to this work.

Correspondence should be addressed to Martin Zenke zenke@mdc-berlin.de
Dendritic cells (DCs) are potent antigen-presenting cells with a pivotal role in antigen-specific immune responses. Here, we found that the helix-loop-helix transcription factor Id2 is up-regulated during DC development in vitro and crucial for the development of distinct DC subsets in vivo. Id2-/- mice lack Langerhans cells (LCs), the cutaneous contingent of DCs, and the splenic CD8alpha+ DC subset is markedly reduced. Mice deficient for transforming growth factor (TGF)-beta also lack LCs, and we demonstrate here that, in DCs, TGF-beta induces Id2 expression. We also show that Id2 represses B cell genes in DCs. These findings reveal a TGF-beta−Id2 signaling pathway in DCs and suggest a mechanism by which Id2 affects the lineage choice of B cell and DC progenitors.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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