B cells need their flip-flops.

摘要

Detailed analysis on the Atpllc mutant mice by both groups revealed normal numbers of pre-pro-B cells but a progressive loss of pro-B and pre-B cells.1'2 This phenotype reported by Yabas et al. and Siggs et al. is suspiciously reminiscent of mice with defects in IL-7 signalling, that is a block in the pro-B cell to pre-B cell transition in bone marrow, while fetal B cell development is relatively intact.10 However, several inconsistencies remain. Although Siggs et al. demonstrated that the IL-7R signalling is intact in pro-B cells in vitro, Yabas et al. found that transgenic overexpression of IL-7 in Atpllc mutant mice was incapable of rescuing B-cell development. Inability to form a pre-BCR, through either defective VDJ recombination or pre-BCR signalling, was also a strong candidate for the defect in Atpllc mutant B cells.