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Department of Immunology, Erasmus Medical Center, Rotterdam, The Netherlands
Bruton’s tyrosine kinase (Btk) is a cytoplasmic signaling molecule
that is crucial for precursor (pre-B) cell differentiation in humans.
In this study, we show that during the transition of large cycling to
small resting pre-B cells in the mouse, Btk-deficient cells failed to
efficiently modulate the expression of CD43, surrogate L chain, CD2,
and CD25. In an analysis of the kinetics of pre-B cell differentiation
in vivo, Btk-deficient cells manifested a specific developmental delay
within the small pre-B cell compartment of 
3 h, when compared with
wild-type cells. Likewise, in in vitro bone marrow cultures,
Btk-deficient large cycling pre-B cells showed increased IL-7 mediated
expansion and reduced developmental progression into noncycling
CD2+CD25+ surrogate L chain-negative small
pre-B cells and subsequently into Ig-positive B cells. Furthermore, the
absence of Btk resulted in increased proliferative responses to IL-7 in
recombination-activating gene-1-deficient pro-B cells. These findings
identify a novel role for Btk in the regulation of the differentiation
stage-specific modulation of IL-7 responsiveness in pro-B and pre-B
cells. Moreover, our results show that Btk is critical for an efficient
transit through the small pre-B cell compartment, thereby regulating
cell surface phenotype changes during the developmental progression of
cytoplasmic µ H chain expressing pre-B cells into immature
IgM+ B cells.
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