The Journal of Experimental Medicine
PBL InterferonSource
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rosenberg, Y. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rosenberg, Y. J.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Journal of Experimental Medicine, Vol 150, 1561-1566, Copyright © 1979 by Rockefeller University Press


ARTICLES

Influence of the sex-linked defect in CBA/N mice on autoimmune responses to isologous erythrocytes. Ability to overcome the defect with age

YJ Rosenberg

Normal mice spontaneously develop plaque-forming cells (PFC) specific for antigens on modified self erythrocytes (bromelain-treated mouse erythrocytes [BrMRBC] antigens). Our study demonstrates that the sex- linked defect that results in the inability of CBA/N mice to respond to several T-independent antigens (TI-2 antigens) also regulates the autoantibody response to BrMRBC antigens. Thus, in CBA/N homozygous mice and male F1 offspring of CBA/N-mothered crosses, e.g., (CBA/N X NZB)F1 males, such PFC are absent. To examine whether specific autoreactive B cells are present in defective mice, the latter were stimulated either nonspecifically with the mitogen LPS or by infection with lethal malaria (17XL Plasmodium yoelii) known to induce anti- BrMRBC PFC specifically. The results indicate that modest antibody responses to self antigens could be induced in young (5- to 7-wk old) defective mice and that these responses increased as a function of age. The data is consistent with the view that the defect in CBA/N mice does not result from an absence of functional anti-BrMRBC B cells but rather from low frequencies of the specific precursors, which can be triggered and expanded with age probably by environmental stimulations.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?




  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS