Abstract:
:Mice deficient for the adapter protein SLP65 (BLNK) show a partial block in early B cell development, reduced numbers of mature B cells in the periphery, an absence of B1 cells and a reduction of IgM and IgG3 serum immunoglobulin levels. A strikingly similar phenotype is observed in Btk-deficient mice. To investigate the consequences of mutations in both SLP65 and Btk, we generated SLP65/ Btk double-mutant mice by crossing the single-mutant mice. Analysis of the double-mutant mice reveals a much more severe defect in B cell development. B cells in the SLP65/Btk double-mutant mice are arrested at the preB cell stage and, surprisingly, express the preB cell receptor. Normally, preB cell receptor expression in wild-type mice is restricted to a very small fraction of B cells making it difficult to identify these cells in the bone marrow. Together, the data demonstrate the synergistic role of SLP65 and Btk in B cell development and describe a situation where large numbers of preB cell receptor-positive cells accumulate in the bone marrow and spleen.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Jumaa H,Mitterer M,Reth M,Nielsen PJdoi
10.1002/1521-4141(200107)31:7<2164::aid-immu2164>3keywords:
subject
Has Abstractpub_date
2001-07-01 00:00:00pages
2164-9issue
7eissn
0014-2980issn
1521-4141pii
10.1002/1521-4141(200107)31:7<2164::AID-IMMU2164>3journal_volume
31pub_type
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