Skip Navigation



International Immunology Advance Access published online on August 31, 2004

International Immunology, doi:10.1093/intimm/dxh150
© 2004 by The Japanese Society for Immunology
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/10/1487    most recent
dxh150v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Ota, T.
Right arrow Articles by Koyasu, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ota, T.
Right arrow Articles by Koyasu, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received March 15, 2004
Accepted July 25, 2004

Article

Auto-reactive B cells against peripheral antigen, desmoglein 3, escape from tolerance mechanism

Takayuki Ota 1, Miyo Aoki-Ota 2, Kazuyuki Tsunoda 3, Kouji Simoda 4, Takeji Nishikawa 2, Masayuki Amagai 2, Shigeo Koyasu 5*

1 Department of Dermatology, Keio University School of Medicine, Tokyo 160-8582, Japan; Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan
2 Department of Dermatology, Keio University School of Medicine, Tokyo 160-8582, Japan
3 Department of Dermatology, Keio University School of Medicine, Tokyo 160-8582, Japan; Department of Dentistry and Oral Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan
4 Laboratory Animal Center, Keio University School of Medicine, Tokyo 160-8582, Japan
5 Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan; Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan

* To whom correspondence should be addressed. E-mail: koyasu{at}sc.itc.keio.ac.jp.


   Abstract

To examine the mechanism of B cell tolerance against natural peripheral self-antigen, we generated transgenic mice expressing IgM specific for desmoglein 3 (Dsg3) from AK7 monoclonal antibody which itself does not induce blisters. Dsg3 is mainly expressed on stratified squamous epithelium and is the target antigen of an autoimmune bullous disease, pemphigus vulgaris. Transgenic B cells reactive to Dsg3 were observed in the spleen and lymph node. Although these B cells are autoreactive, they did not develop into B1 B cells. These B cells were functionally competent and anti-Dsg3 IgM was detected in the serum and on the keratinocyte cell surface. These results indicate that auto-reactive B cells against peripheral antigen (Dsg3) are able to develop in the presence of Dsg3 but are ignored by the immune system.

Keywords: autoimmunity; B1 B cell; pemphigus vulgaris; peripheral tolerance; transgenic mouse.
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
H. Takahashi, M. Kuwana, and M. Amagai
A Single Helper T Cell Clone Is Sufficient to Commit Polyclonal Naive B Cells to Produce Pathogenic IgG in Experimental Pemphigus Vulgaris
J. Immunol., February 1, 2009; 182(3): 1740 - 1745.
[Abstract] [Full Text] [PDF]


Home page
Int ImmunolHome page
T. Ota, M. Aoki-Ota, K. Tsunoda, T. Nishikawa, S. Koyasu, and M. Amagai
Autoreactive B-cell elimination by pathogenic IgG specific for the same antigen: implications for peripheral tolerance
Int. Immunol., October 1, 2008; 20(10): 1351 - 1360.
[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.