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International Immunology Advance Access originally published online on January 5, 2007
International Immunology 2007 19(2):217-226; doi:10.1093/intimm/dxl138
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Dendritic cells suppress IgE production in B cells

Kunie Obayashi1, Tomomitsu Doi1,2 and Shigeo Koyasu1,2

1 Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
2 Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi-shi, Saitama 332-0012, Japan

Correspondence to: S. Koyasu; E-mail: koyasu{at}sc.itc.keio.ac.jp

Ig class switch recombination (CSR) is triggered by the engagement of CD40 on B cells by CD40 ligand on T cells. In addition, recent studies have shown that dendritic cells (DCs) are able to directly control the CSR of B cells through B lymphocyte stimulator protein [or B cell activation factor belonging to the tumor necrosis factor family] and a proliferation-inducing ligand. We examined in this study the regulatory role of DCs in CSR and demonstrate that DCs selectively suppress IgE production from B cells stimulated by CD40 and IL-4 through two different mechanisms: by direct cell–cell interaction or by soluble factors including transforming growth factor-ß and IFN-{gamma}. In addition, distinct DCs utilize different mechanisms: immature bone marrow-derived dendritic cells (BMDCs) and primary lung DCs strongly inhibit IgE CSR. On the other hand, LPS-induced mature BMDCs lose the ability to inhibit IgE CSR but still suppress IgE production by decreasing IgE protein expression. These results indicate novel regulatory functions of DCs on IgE production.

Keywords: AID, class switch recombination, hyper-IgE, IFN-{gamma}, TGF-ß

Transmitting editor: T. Kurosaki


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