Negative regulation of apoptotic death in immature B cells by CD45

Cross-linking of membrane IgM receptor on B cells induces tyroslne phosphorylation within 1 mln. This biochemical alteration triggers a cascade of signaling events which ultimately leads to activation in mature B cells but growth arrest and cell death by apoptosis in immature B cells. To study the mechanisms underlying the bifurcation of signals, we chose to examine the role of receptor-type protein tyroslne phosphatase (PTP) CD45 using CD45^- clones isolated from an immature B cell line WEHI-231. Here we report that in CD45^- clones, tyroslne phosphorylation was constltutlvely induced but not enhanced by antl-IgM stimulation and anti-lgM-lnduced Ca²⁺ flux was slightly delayed but evidently prolonged. Further, the degree of growth arrest and DNA fragmentation induced by antl-IgM antibody was more evident in CD45^- clones than the parental cells. These results indicate that initial alterations in signaling are effectively transduced into effector signals and that IgM receptor-mediated growth arrest and apoptosis in immature B cells are negatively regulated by CD45.