Abstract
The data presented in this report demonstrate that antibodies directed against B-cell specific surface antigens can block different modes of B-cell activation. The anti-CD 19 antibody HD37 strongly blocks the stimulation of thymidine incorporation induced by anti-mu and MLR supernatant and also partially inhibits the growth of long-term EBV-transformed cell lines. The anti-CD20 antibody B1, on the other hand, has little effect on anti-mu activation but prevents the stimulation of thymidine incorporation and transformation by EBV. We conclude that different mechanisms operate during B-cell activation by anti-mu and EBV involving different B-cell surface molecules.
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