The Journal of Experimental Medicine
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Published 6 December 2004. doi:10.1084/jem.20041231
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 11, 1503-1509
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Brief Definitive Report

 The ETS Transcription Factor Spi-B Is Required for Human Plasmacytoid Dendritic Cell Development

Remko Schotte1, Maho Nagasawa1, Kees Weijer1,2, Hergen Spits1, and Bianca Blom1

1 Department of Cell Biology and Histology, Academic Medical Center (AMC), University of Amsterdam, 1105 AZ Amsterdam, Netherlands
2 Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands

Address correspondence to Bianca Blom, Department of Cell Biology and Histology, AMC, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, Netherlands. Phone: 31-20-5664966; Fax: 31-20-6974156; email: b.blom{at}amc.uva.nl

A number of transcription factors that act as molecular switches for hematopoietic lineage decisions have been identified. We recently described the ETS transcription factor Spi-B to be exclusively expressed in plasmacytoid dendritic cells (pDCs), but not in myeloid DCs. To assess whether Spi-B is required for pDC development we used an RNA interference knock down approach to specifically silence Spi-B protein synthesis in CD34+ precursor cells. We observed that a knock down of Spi-B mRNA strongly inhibited the ability of CD34+ precursor cells to develop into pDCs in both in vitro assays as well as in vivo upon injection into recombination activating gene 2–/– {gamma} common–/– mice. The observed effects were restricted to the pDC lineage as the differentiation of pro–B cells and CD14+ myeloid cells was not inhibited but slightly elevated by Spi-B knock down. Knock down of the related ETS factor PU.1 also inhibited in vitro development of CD34+ cells into pDCs. However, in contrast to Spi-B, PU.1 knock down inhibited B cell and myeloid cell development as well. These results identify Spi-B as a key regulator of human pDC development.

Key Words: human plasmacytoid dendritic cells • hematopoiesis • RNA interference • Spi-B


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