Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Sverremark, E.
Right arrow Articles by Fernández, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sverremark, E.
Right arrow Articles by Fernández, C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 12, No. 4, 431-438, April 2000
© 2000 Japanese Society for Immunology

{kappa}-deficient mice are non-responders to dextran B512: is this unresponsiveness due to specialization of the {kappa} and {lambda} Ig repertoires?

Eva Sverremark1,2, Cecilia Rietz1 and Carmen Fernández1

1 Department of Immunology, The Wenner-Gren Institute, Arrhenius Laboratories for Natural Sciences, Stockholm University, 106 91 Stockholm, Sweden.
2 Division of Clinical Immunology, Karolinska Hospital, 171 76 Stockholm, Sweden

Correspondence to: C. Fernández

In the dextran B512 high-responder strain C57BL, the response to dextran is restricted to the preferential expression of the VHB512 and the V{kappa}OX1 gene combination. The importance of the heavy chain is suggested by the fact that mice with the Ig CH allotype, different from C57BL, are low or non-responders to dextran, but the light chain could also play a role. All anti-dextran B512 mAb described to date (>200) use {kappa} light chains. No anti-dextran antibody using {lambda} has ever been observed. To ascertain if the restriction of the use of V{kappa} genes in response to dextran B512 was more stochastic or due to other factors, we have studied the response to dextran B512 in C57BL/6 mice where the C{kappa} domain has been disrupted (C57BL.C{kappa}T). These mice are unable to express {kappa} light chains and their humoral antibodies bear light chains of the {lambda} type. We found that C{kappa} knockout mice are unable to respond to dextran given in a thymus-independent or -dependent form. The lack of responsiveness is specifically directed to the dextran epitopes since these mice are fully competent to respond to other antigenic structures present in the same immunogenic molecule. These mice are also apparently normal regarding the expression of VH genes. Finally, we tested the response to dextran in C57BL.C{kappa}T mice carrying the lpr mutation that was introduced to favor an increase in the life span and make the response to dextran more easily detectable. The introduction of the lpr mutation was not sufficient to change the pattern of unresponsiveness in the C57BL.C{kappa}T mice. We concluded that there are deficiencies in the light chain repertoire because the V {lambda} light chain could not reconstitute the response to dextran. We discuss the possible mechanisms for this new type of unresponsiveness to dextran B512.

Keywords: dextran B512, Ig repertoire

Transmitting editor: C. Martinez-A


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
BloodHome page
J. Peng, C. Liu, D. Liu, C. Ren, W. Li, Z. Wang, N. Xing, C. Xu, X. Chen, C. Ji, et al.
Effects of B7-blocking agent and/or CsA on induction of platelet-specific T-cell anergy in chronic autoimmune thrombocytopenic purpura
Blood, April 1, 2003; 101(7): 2721 - 2726.
[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.