The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online 19 February 2001.
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© The Rockefeller University Press, 0022-1007/2001/2/435/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 4, February 19, 2001 435-446


Original Article

Loss of Precursor B Cell Expansion but Not Allelic Exclusion in VpreB1/VpreB2 Double-Deficient Mice

Cornelia Mundta, Steve Licencea, Takeyuki Shimizub, Fritz Melchersb, and Inga-Lill Mårtenssona

a Developmental Immunology, The Babraham Institute, Cambridge CB2 4AT, United Kingdom
b Basel Institute for Immunology, 4005 Basel, Switzerland
Developmental Immunology, The Babraham Institute, Cambridge CB2 4AT, UK.44-1223-49602244-1223-496469

lill.martensson{at}bbsrc.ac.uk

The pre-B cell receptor consists of immunoglobulin (Ig) µ heavy chains and surrogate light chain, i.e., the VpreB and {lambda}5 proteins. To analyze the role of the two VpreB proteins, mice lacking the VpreB1 and VpreB2 genes were generated. VpreB1/VpreB2/ mice were impaired in their B cell development at the transition from pre-BI to large pre-BII cells. Pre-BII cells did not expand by proliferation, consequently 40-fold less small pre-BII and immature B cells were found in bone marrow, and the generation of immature and mature conventional B cells in spleen appeared reduced. In addition, only low numbers of B-1a cells were detected in the peritoneum. Surprisingly, Ig heavy chain allelic exclusion was still active, apparently ruling out a signaling role of a VpreB1/VpreB2–containing receptor in this process.

Key Words: B cell development • surrogate light chain • pre-B cell receptor • B cell deficiency • B1-a B cells


Abbreviations used in this paper: BCR, B cell receptor; ES, embryonic stem; RAG, recombination activating gene; RT, reverse transcription; SL, surrogate light.

© 2001 The Rockefeller University Press


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