Skip Navigation



International Immunology Advance Access published online on May 30, 2006
International Immunology, doi:10.1093/intimm/dxl047
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
18/7/1127    most recent
dxl047v1
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 Nijnik, A.
Right arrow Articles by Cornall, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nijnik, A.
Right arrow Articles by Cornall, R. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
Received August 12, 2005
Accepted April 26, 2006

Article

Spontaneous B cell hyperactivity in autoimmune-prone MRL mice

Anastasia Nijnik 1, Helen Ferry 1, Graham Lewis 1, Eleni Rapsomaniki 1, Janson C. H. Leung 1, Angelika Daser 1, Teresa Lambe 1, Christopher C. Goodnow 2, and Richard J. Cornall 1 *

1 Henry Wellcome Building of Molecular Physiology, Oxford University, Roosevelt Drive, Oxford, OX3 7BN, UK
2 Australian Cancer Research Foundation Genetics Laboratory, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601, Australia

* To whom correspondence should be addressed.
Richard J. Cornall, E-mail: richard.cornall{at}ccmp.ox.ac.uk


  Abstract

The MRL-lpr/lpr mouse strain is a commonly used model of the human autoimmune disease systemic lupus erythematosus (SLE). Although much is known about the contribution of the lpr Fas mutation to B cell tolerance breakdown, the role of the genetic background of the MRL strain itself is less well explored. In this study, we use the MD4 anti-hen egg lysozyme Ig (IgHEL) transgenic system to explore B cell function in MRL+/+ and non-autoimmune mice. We demonstrate that MRL IgHEL B cells show spontaneous hyperactivity in the absence of self-antigen, which is associated with low total B cell numbers but an expansion of the marginal zone B cell population. However, B cell anergy is normal in the presence of soluble lysozyme [soluble hen egg lysozyme (sHEL)], and MRL IgHEL B cells undergo normal elimination in the presence of sHEL when competing with a polyclonal C57BL/6 B cell repertoire. We conclude that B cell hyperactivity may contribute to the autoimmune phenotype of MRL+/+ and MRL-lpr/lpr strains when it initiates antibody responses to rare or sequestered antigens that are below the threshold for tolerance induction, but that there is no B cell intrinsic defect in anergy in MRL mice.

Keywords: B lymphocytes; systemic lupus erythematosus (SLE); tolerance.
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
A. Lartigue, N. Colliou, S. Calbo, A. Francois, S. Jacquot, C. Arnoult, F. Tron, D. Gilbert, and P. Musette
Critical Role of TLR2 and TLR4 in Autoantibody Production and Glomerulonephritis in lpr Mutation-Induced Mouse Lupus
J. Immunol., November 15, 2009; 183(10): 6207 - 6216.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
Y. Wang, A. Kissenpfennig, M. Mingueneau, S. Richelme, P. Perrin, S. Chevrier, C. Genton, B. Lucas, J. P. DiSanto, H. Acha-Orbea, et al.
Th2 Lymphoproliferative Disorder of LatY136F Mutant Mice Unfolds Independently of TCR-MHC Engagement and Is Insensitive to the Action of Foxp3+ Regulatory T Cells
J. Immunol., February 1, 2008; 180(3): 1565 - 1575.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
J. R. Groom, C. A. Fletcher, S. N. Walters, S. T. Grey, S. V. Watt, M. J. Sweet, M. J. Smyth, C. R. Mackay, and F. Mackay
BAFF and MyD88 signals promote a lupuslike disease independent of T cells
J. Exp. Med., August 6, 2007; 204(8): 1959 - 1971.
[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.