Nature Immunology
4, 380 - 386 (2003)
Published online: 24 February 2003; | doi:10.1038/ni903
Transcriptional profiling identifies Id2 function in dendritic cell developmentChristine 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 Zenke11
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.deDendritic 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 CD8 + DC subset is markedly reduced. Mice deficient for transforming growth factor (TGF)- also lack LCs, and we demonstrate here that, in DCs, TGF- induces Id2 expression. We also show that Id2 represses B cell genes in DCs. These findings reveal a TGF-−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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