The JI Acurri Cytometers
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
Right arrow Citation Map
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 Stewart, J. J.
Right arrow Articles by Seiden, P. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stewart, J. J.
Right arrow Articles by Seiden, P. E.

The Journal of Immunology, Vol 159, Issue 4 1728-1738, Copyright © 1997 by American Association of Immunologists


ARTICLES

A solution to the rheumatoid factor paradox: pathologic rheumatoid factors can be tolerized by competition with natural rheumatoid factors

JJ Stewart, H Agosto, S Litwin, JD Welsh, M Shlomchik, M Weigert and PE Seiden
Department of Molecular Biology, Princeton University, NJ 08544, USA.

Rheumatoid factors (RF) associated with arthritic joint erosion are only seen transiently, if at all, in nondiseased individuals. Therefore, a tolerance mechanism must exist that prevents pathologic RF B cells from expressing Abs. Surprisingly, it has been shown that pathologic RF B cells are not tolerized by any previously established tolerance mechanism such as deletion, receptor editing, anergy, or prevention of memory establishment. How are pathologic RF cells tolerized? By simulating the RF response with a cellular automaton model immune system, we demonstrate that pathologic RFs can be tolerized by the novel mechanism of "competitive tolerance" with natural, nonpathologic RFs. We then demonstrate that competitive tolerance can be broken when a sequestered pool of expanding B cells are inappropriately subjected to chronic stimulation (as appears to occur in MRL/lpr mice and in patients with rheumatoid arthritis).


This article has been cited by other articles:


Home page
Rheumatology (Oxford)Home page
N. Milosevic-Jovcic, D. Ciric, L. Hajdukovic-Dragojlovic, and V. Mircetic
Differences in the relationship of specificity to titre and functional affinity between circulating Ga- and pan-reactive IgM rheumatoid factors in rheumatoid arthritis
Rheumatology, September 1, 2004; 43(9): 1190 - 1193.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
J. H. Roark, J. B. Bussel, D. B. Cines, and D. L. Siegel
Genetic analysis of autoantibodies in idiopathic thrombocytopenic purpura reveals evidence of clonal expansion and somatic mutation
Blood, July 30, 2002; 100(4): 1388 - 1398.
[Abstract] [Full Text] [PDF]


Home page
J. Exp. Med.Home page
M. R. Ehrenstein, H. T. Cook, and M. S. Neuberger
Deficiency in Serum Immunoglobulin (Ig)M Predisposes to Development of IgG Autoantibodies
J. Exp. Med., April 3, 2000; 191(7): 1253 - 1258.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
X. Dong, W. J. Storkus, and R. D. Salter
Binding and Uptake of Agalactosyl IgG by Mannose Receptor on Macrophages and Dendritic Cells
J. Immunol., November 15, 1999; 163(10): 5427 - 5434.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
R. Jemmerson, J. M. Minnerath, S. M. Hedrick, and S. Oehen
B Cell Tolerance to a Minor, But Not to a Major, Antigenic Surface of the Self Antigen, Cytochrome c
J. Immunol., September 15, 1998; 161(6): 2841 - 2847.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1997 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1997 by The American Association of Immunologists, Inc. All rights reserved.