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International Immunology Advance Access originally published online on November 28, 2007
International Immunology 2008 20(1):155-164; doi:10.1093/intimm/dxm127
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

SAGE library screening reveals ILT7 as a specific plasmacytoid dendritic cell marker that regulates type I IFN production

Minkwon Cho1, Koji Ishida1, Jingtao Chen1, Jun Ohkawa1, Wei Chen2, Sahori Namiki1, Ayumi Kotaki1, Naoko Arai1, Ken-ichi Arai1,3 and Yumiko Kamogawa-Schifter1,3

1 Department of Immunobiology, Ginkgo Biomedical Research Institute, Tokyo, Japan
2 Department of Pediatrics, Division of Hematology, Oncology and Bone Marrow Transplantation, University of Minnesota Cancer Center, Minneapolis, MN, USA
3 Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan

Correspondence to: Y. Kamogawa-Schifter; E-mail: ykamogawa{at}sbigroup.co.jp

Plasmacytoid dendritic cells (pDCs) link innate to acquired immune responses by producing high levels of type I IFN upon infection. In order to identify the specific genes that control pDC, we compared serial analysis of gene expression libraries from human pDCs, herpes simplex virus-stimulated pDCs and monocytes. We found that Ig-like transcript ILT7 is specifically expressed on pDC cell surfaces and is down-regulated when pDC mature in response to viral or bacterial stimulation. ILT7 expression on the cell surface required association with the Fc{epsilon}RI{gamma} adaptor molecule. Although treatment with one anti-ILT7-specific mAb suppressed type I IFN production in response to cytosine-phosphate-guanosice (CpG) stimulation, another anti-ILT7 mAb up-regulated type I IFN production. We conclude that ILT7 is a key regulator of human pDC function.

Keywords: IFN, ILT7, pDC, SAGE

Transmitting editor: T. Saito

Received 13 February 2007, accepted 26 October 2007.


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W. Cao, L. Bover, M. Cho, X. Wen, S. Hanabuchi, M. Bao, D. B. Rosen, Y.-H. Wang, J. L. Shaw, Q. Du, et al.
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