Home | My Profile | Contact Us
Research Trends Products  |   order gateway  |   author gateway  |   editor gateway  
Register | Forgot Password

Author Resources
 Author Gateway
 Article submission guidelines

Editor Resources
 Editor/Referee Gateway

 Regional Subscription Agents/Distributors
Current Trends in Immunology   Volumes    Volume 5 
Escherichia coli enterotoxin B subunit reduces CD5+ B cell numbers in the peritoneal cavity in mice and stimulates polyclonal IgM production dependent on its binding to GM1-ganglioside
Toshiyasu Shimizu, Keiko Sasaki, Sadayuki Ochi, Michio Kato, Hideyuki Arimitsu, Yoshio Ichinose, Takashi Yokochi, Takao Tsuji
Pages: 129 - 140
Number of pages: 12
Current Trends in Immunology
Volume 5 

Copyright © 2003 Research Trends. All rights reserved


Intraperitoneal administration of the B subunit of Escherichia coli enterotoxin to mice temporarily decreased the numbers of CD5+CD45+ double-positive cells, CD5+ B cells, in peritoneal cavity. In vitro, CD5+ B cells treated with the B subunit decreased in number like in vivo but did not recover. Functionally, the peritoneal cells stimulated by the B subunit in vitro produced immunoglobulin M (IgM) in a dose- and time-dependent manner. A mutant defective in binding to GM1-ganglioside significantly reduced less number of CD5+ B cell and did not increase production of IgM than the B subunit. Although the apoptosis in CD5+ B cell fraction was not detected, a new fraction containing CD5-CD45- double-negative cells appeared in vitro following by reduction of CD5+ B cells and partially underwent apoptosis.

These results suggest that the B subunit reduces the number of CD5+ B cells and stimulates production of IgM dependent on its binding to GM1-ganglioside. CD5+ B cells stimulated by the B subunit might lose their specific antigens to produce IgM and after die with apoptosis.

Buy this Article


Buy this article
Buy this volume
Subscribe to this title
Shopping Cart

Quick Links
Search Products
Browse in Alphabetical Order : Journals
Browse by Subject Classification : Journals

Ordering Information Ordering Information
Downloadable forms Downloadable Forms