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The absence of SLP65 and Btk blocks B cell development at the preB cell receptor‐positive stage

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 reductionof 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 numbersof preB cell receptor‐positive cells accumulate in the bone marrow and spleen.