| Abstract
| - Abstract. Mature B cells undergo programmed cell death when surface(s)IG is extensively multimerized. A signal that blocks death of B cells is thus required for activation of B cells in response to antigen stimulation.Here we show that only a few diversetransmembrane signals capable of Inducing activation and proliferation of B cell blocked sig-mediated death of normal mature B cells,from death.The results suggest that a specific signal is required for abrogating B cell death induced by sigcross-linking.Signaling via IL-4 receptor and CD40, both of which are derived from activated T cells, blocked sig-mediated death,as decribed previously.Signaling through a B cell antigen CD72,a counter-receptor of the pan-T antigen CD4,also blocked death of anti-Ig-treated mouse spleen B cells.CD72 signalmay play a role in survival of B cells at the initial step of T B interaction, where resting T cells recongnize antigens such as llpopolyasccharide and dextran sulfate,and spleen B cells from New Zealand mice, which are prone to autoantibody-dependent autoimmune diseases,were resistant to required in antibody response to freigin antigens regardless of T independence or T dependence and in autoantibody production.
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