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A monoclonal antibody to CD72, the 45-kDa human homolog of murine Lyb-2, was found to augment selective activation pathways in tonsillar B lymphocytes. By itself, CD72 antibody provided a weak direct stimulus to resting B cells as assessed by 3HdThd incorporation; this was modestly enhanced on the addition of interleukin 4 (IL4) or following ligation of surface CD40. CD72-delivered signals were more evident in co-stimulation assays with phorbol ester and with a synergistic combination of IL4 and CD40 antibody, but not with calcium ionophore or a CD23 antibody; rapidly cycling B cells were refractory to signaling via CD72 whether or not other co-stimuli were present. A unique feature of the CD72-delivered signal was its ability to enhance synergistically stimulations triggered with immobilized antibody to IgM, while failing to augment responses initiated by soluble anti-mu. On direct culture of resting B lymphocytes with CD72 antibody, an approximately twofold increase in the expression of major histocompatibility complex class II DQ antigen was observed, an augmentation similar to that achieved with IL 4; CD72 antibody also mimicked IL 4 in its ability to drive G0 cells into the early G1 phase of cell cycle. In contrast to IL 4-promoted stimulation, CD72 antibody failed to up-regulate the surface expression of either IgM or the CD23 antigen. CD72 expression itself was found to be weak on resting B lymphocytes and was modestly enhanced following culture with IL 4. The findings are discussed with reference to observations made on the triggering of murine B lymphocytes through Lyb-2 and within the context of previously defined human B cell activation pathways.
Kamal et al. (Sat,) studied this question.