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Late events in B cell activation. Expression of membrane alkaline phosphatase activity.
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1989
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B Cell ActivationCell DeathPathologyAlkaline PhosphataseCellular PhysiologyB Cell MitogensB Cell ProliferationCell RegulationCellular Regulatory MechanismLate EventsCell SignalingCell PhysiologyBiochemistryMembrane BiologyCell BiologyProtein PhosphorylationSignal TransductionNatural SciencesPathogenesisCellular BiochemistryMedicineImmune Cell Activation
Alkaline phosphatase (APase) has been previously described as a membrane marker correlating with B cell proliferation after stimulation by selected B cell mitogens. We have found, however, that the appearance of B cell membrane APase correlates more closely with differentiation than with proliferation. This conclusion has been drawn from the following observations: 1) APase activity appears well after peak B cell thymidine uptake, 2) mitogens which stimulate only B cell proliferation (Salmonella typhimurium mitogen) fail to induce expression of the enzyme, and 3) when proliferation of mitogen-activated B cells is inhibited, APase activity is not suppressed and may even be augmented. In addition to membrane expression, APase is also spontaneously shed into the surrounding milieu, perhaps as a result of endogenous phospholipase activity. By using a group of well-characterized inhibitors, the APase activity was shown to belong to class I (similar to the bone/liver/kidney class). Because APase always appears in differentiating but not proliferating cells, we would propose that the enzyme appearance is a late marker of B cell activation, associated with cell progression to differentiation and consequent IgM synthesis.