Golay J T, Crawford D H
Department of Virology, Royal Postgraduate Medical School, London, U.K.
Immunology. 1987 Oct;62(2):279-84.
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.
本报告中呈现的数据表明，针对B细胞特异性表面抗原的抗体可阻断B细胞活化的不同模式。抗CD19抗体HD37强烈阻断抗μ抗体和混合淋巴细胞反应（MLR）上清液诱导的胸苷掺入刺激，并且还部分抑制长期EB病毒转化细胞系的生长。另一方面，抗CD20抗体B1对抗μ抗体活化几乎没有影响，但可阻止EB病毒诱导的胸苷掺入刺激和转化。我们得出结论，在抗μ抗体和EB病毒介导的B细胞活化过程中，涉及不同B细胞表面分子的不同机制发挥作用。
