Skip Navigation


International Immunology Advance Access originally published online on January 5, 2007
International Immunology 2007 19(2):217-226; doi:10.1093/intimm/dxl138
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
19/2/217    most recent
dxl138v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (2)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Obayashi, K.
Right arrow Articles by Koyasu, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Obayashi, K.
Right arrow Articles by Koyasu, S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© 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


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Immunol.Home page
M. Bax, J. J. Garcia-Vallejo, J. Jang-Lee, S. J. North, T. J. Gilmartin, G. Hernandez, P. R. Crocker, H. Leffler, S. R. Head, S. M. Haslam, et al.
Dendritic Cell Maturation Results in Pronounced Changes in Glycan Expression Affecting Recognition by Siglecs and Galectins
J. Immunol., December 15, 2007; 179(12): 8216 - 8224.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.