CD_(23)McAb抑制活化B细胞增殖机制的初步探讨

MECHANISMS OF INHIBITING B CELL PROLIFERATION OF CD 23 MCAB

本研究用CD_(23)单克隆抗体(CD_(23)McAb)交联活化的人扁桃体B细胞,证明CD_(23)McAb对B细胞呈双向调节效应,即:高浓度区抑制B细胞增殖,低浓度区促进B细胞增殖。继而,用对B细胞有抑制效应浓度的CD_(23)McAb交联B细胞膜CD_(23)分子,通过研究抑制效应恢复条件,探讨了CD_(23)McAb产生抑制效应的作用机制。结果显示;去除CD_(23)McAb后,抑制作用不能恢复,用SAC再次活化,使B细胞恢复增殖状态,用促B细胞增殖浓度的CD_(23)M-cAb却无此作用。提示:过量CD_(23)McAb过度交联B细胞膜CD_(23)分子后,所产生的抑制B细胞增殖现象,可能是由于促使B细胞从细胞增殖周期进入非增殖状态的G_0期所致。

Effects of CD 23 McAb on B cells activated with SAC were studied by MTT method. We found that CD 23 McAb could influence significantly the proliferation of CD23+ B cells at a figure of two-way phenomenon, that high concentration of ligands inhibited the proliferation of B cells, whereas a suitable concentration of CD 23 McAb improved the proliferation. Furth-erly, the mechanisms of proliferation inhibition by CD 23 McAb (2.0mg/ml) of B cells activated with SAC were also tested. The result indicated that proliferation of B cells could not be restored by simply removing CD 2 3 McAb or adding CD 23 McAb at stimulating concentra-tion(0.05μg/ml). However, SAC could eliminate the inhibition effect of high concentration of CD 23 McAb on B cells. We proposed that overdose CD 23 McAb could cross-link extensively the CD 23 molecules and produces negative signals that induce B cells into G8.