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

doi:10.1084/jem.193.4.435

Published online 12 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 Mundt^a, Steve Licence^a, Takeyuki Shimizu^b, Fritz Melchers^b, and Inga-Lill Mårtensson^a
^a Developmental Immunology, The Babraham Institute, Cambridge CB2 4AT, United Kingdom
^b Basel Institute for Immunology, 4005 Basel, Switzerland

Correspondence to: Inga-Lill Mårtensson, Developmental Immunology, The Babraham Institute, Cambridge CB2 4AT, UK. Tel:44-1223-496469 Fax:44-1223-496022 E-mail:lill.martensson{at}bbsrc.ac.uk.

The pre-B cell receptor consists of immunoglobulin (Ig) µheavy chains and surrogate light chain, i.e., the VpreB and ${lambda}$ 5 proteins. To analyze the role of the two VpreB proteins, micelacking the VpreB1 and VpreB2 genes were generated. VpreB1^-^/-VpreB2^-^/-mice were impaired in their B cell development at the transitionfrom pre-BI to large pre-BII cells. Pre-BII cells did not expandby proliferation, consequently 40-fold less small pre-BII andimmature B cells were found in bone marrow, and the generationof immature and mature conventional B cells in spleen appearedreduced. In addition, only low numbers of B-1a cells were detectedin the peritoneum. Surprisingly, Ig heavy chain allelic exclusionwas still active, apparently ruling out a signaling role ofa 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

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