Skip Navigation

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 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 arrow Search for citing articles in:
ISI Web of Science (14)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Lam, K.-P.
Right arrow Articles by Stall, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lam, K.-P.
Right arrow Articles by Stall, A. M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 5, No. 9, pp. 1011-1022,September 1993
© 1993 Japanese Society for Immunology

A high frequency of hybridomas from M54 µ heavy chain transgenic mice initially co-express transgenic and rearranged endogenous µ genes

Kong-Peng Lam, L. A. Herzenberg1 and A. M. Stall

Department of Microbiology, College of Physicians & Surgeons, Columbia University New York, NY 10032, USA
1 Department of Genetics, Beckman Center B007, Stanford University School of Medicine Stanford, CA 94305-5125, USA

Correspondence to: Correspondence to: A. M. Stall

The M54 transgenic mouse line, which carries the 17.2.25 Ig µ heavy chain gene, rearranges Ig eavy chains and expresses both transgenic and endogenous µ. B cell lineage development is selectively impaired in these mice and cells that simultaneously express transgenic and endogenous µ (‘double-producers’) are common amongst the B cells and plasma cells that do develop. Weaver, Imanlshl-karl, Baltimore and colleagues failed to obtain double-producing hybridomas from M54 mice; however, molecular and serologic studies presented here show that such hybridomas are readily generated. These hybridomas are extremely unstable and rapidly yield variants producing either transgenic or endogenous µ. Therefore the stable cloned lines we obtained, like Weaver et al., were almost all single or non-producers. We also found that the VH gene usage in our hybridomas was skewed towards the JH proximal (VHQ52, VH81X) families, supporting the Idea that the expression of the M54 transgene alters the endogenous lg repertoire.

Keywords: B cell lineages, B-1 cells, CD5 B cells, fluorescence activated cell sorter, gene expression, Ig gene rearrangement, Ly-1 B cells, transgenic mice

Received 12 March 1993, accepted 14 May 1993.


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
L. Yunk, W. Meng, P. L. Cohen, R. A. Eisenberg, and E. T. Luning Prak
Antibodies in a Heavy Chain Knock-In Mouse Exhibit Characteristics of Early Heavy Chain Rearrangement
J. Immunol., July 1, 2009; 183(1): 452 - 461.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
J. J. Kenny, L. J. Rezanka, A. Lustig, R. T. Fischer, J. Yoder, S. Marshall, and D. L. Longo
Autoreactive B Cells Escape Clonal Deletion by Expressing Multiple Antigen Receptors
J. Immunol., April 15, 2000; 164(8): 4111 - 4119.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
V. Barreto and A. Cumano
Frequency and Characterization of Phenotypic Ig Heavy Chain Allelically Included IgM-Expressing B Cells in Mice
J. Immunol., January 15, 2000; 164(2): 893 - 899.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
N. Watanabe, S. Nisitani, K. Ikuta, M. Suzuki, T. Chiba, and T. Honjo
Expression Levels of B Cell Surface Immunoglobulin Regulate Efficiency of Allelic Exclusion and Size of Autoreactive B-1 Cell Compartment
J. Exp. Med., August 16, 1999; 190(4): 461 - 470.
[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.