The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Liou, L. B.
Right arrow Articles by Scott, D. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liou, L. B.
Right arrow Articles by Scott, D. W.

The Journal of Immunology, Vol 154, Issue 12 6262-6274, Copyright © 1995 by American Association of Immunologists

ARTICLES

Differential susceptibility to tolerance induction in vitro of splenic B cells from several transgenic mouse lines. Role of B1 cells

LB Liou, A Colosia, RB Corley, SH Clarke and DW Scott
Cancer Center Immunology Division, University of Rochester, NY, USA.

Spleen cells from transgenic mice, whose rearranged Ig receptors reflect the repertoires of B1 (CD5+ and "sister" B cells) or normal B2 cells, were examined for their ability to be rendered unresponsive. By using an anti-Ig tolerance protocol that is independent of receptor specificity, we previously reported that peritoneal B cells, containing primarily CD5+ and "sister" B cells, were not susceptible to unresponsiveness. Herein, we show that splenic B cells from two separate transgenic mouse lines, each expressing a B1-type receptor, are resistant to tolerance induction in vitro. In contrast, splenic B cells from two other transgenic mouse lines with a large representation of conventional B cells were sensitive to anti-lg-mediated unresponsiveness. This difference does not reside in the surface Ig density, cell cycle, or activation stage of these cells, but is reflected in the initial calcium mobilization and tyrosine phosphorylation after surface Ig cross-linking. Therefore, these results support the hypothesis that the antigenic specificity of B cell receptors may drive cells toward the B1 subset, as suggested by Cong et al. (Cong, Y-Z., E. Rabin, and H. H. Wortis. 1991. Int. Immunol. 3:467- 476), and that B1 cell characteristics confer the ability of B cells to withstand in vitro tolerance induction, irrespective of their anatomical location. The possibility that this results from previous antigenic experience is discussed.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
M. J. Chumley, J. M. Dal Porto, and J. C. Cambier
The Unique Antigen Receptor Signaling Phenotype of B-1 Cells Is Influenced by Locale but Induced by Antigen
J. Immunol., August 15, 2002; 169(4): 1735 - 1743.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
C. M. Mueller and D. W. Scott
Distinct Molecular Mechanisms of Fas Resistance in Murine B Lymphoma Cells
J. Immunol., August 15, 2000; 165(4): 1854 - 1862.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
L. W. Arnold, S. K. McCray, C. Tatu, and S. H. Clarke
Identification of a Precursor to Phosphatidyl Choline-Specific B-1 Cells Suggesting That B-1 Cells Differentiate from Splenic Conventional B Cells In Vivo: Cyclosporin A Blocks Differentiation to B-1
J. Immunol., March 15, 2000; 164(6): 2924 - 2930.
[Abstract] [Full Text] [PDF]

Home page
 J. Exp. Med.Home page
C. Tatu, J. Ye, L. W. Arnold, and S. H. Clarke
Selection at Multiple Checkpoints Focuses VH12 B Cell Differentiation toward a Single B-1 Cell Specificity
J. Exp. Med., October 4, 1999; 190(7): 903 - 914.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.