Abstract
The gene encoding BILL‐cadherin/cadherin‐17, a nonclassical cadherin expressed on B lymphocytes in a stage‐and‐site‐specific manner, was inactivated by targeted disruption of its transmembrane/cytoplasmic portion‐encoding parts. BILL‐cadherin deficiency caused a threefold proB cell accumulation, as well as a reduction to half of the numbers of immature B cells in bone marrow. In spleen, CD21^hi^CD23^lo^ marginal zone B cells were found reduced and the structure of the marginal zone was impaired. In addition, the size and number of germinal center as well as the number of PNA^+^ cells were significantly reduced in BILL‐cadherin‐deficient mice. In the peritoneal cavity of mutant mice IgM^+^Mac‐1^+^CD5^+^ B1a cell, that express high BILL‐cadherin in wild‐type mice, was also reduced in number. The IgG1 and IgG3 antibody response to the T‐independent antigen, TNP‐Ficoll, was impaired in the mutant mice. These results indicate that BILL‐cadherin participates in B lymphocyte development at least at two stages, first at the transition of pro/preB‐I cells to preB‐II cells possibly in association with surrogate light chain in bone marrow, and later at the point of development, accumulation and reactiveness of immature B cells in spleen.