| First Author | Jumaa H | Year | 2001 |
| Journal | Eur J Immunol | Volume | 31 |
| Issue | 7 | Pages | 2164-9 |
| PubMed ID | 11449370 | Mgi Jnum | J:70406 |
| Mgi Id | MGI:2137166 | Doi | 10.1002/1521-4141(200107)31:7<2164::aid-immu2164>3.0.co;2-s |
| Citation | Jumaa H, et al. (2001) The absence of SLP65 and Btk blocks B cell development at the preB cell receptor-positive stage. Eur J Immunol 31(7):2164-9 |
| abstractText | 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. |
