抗人血小板单克隆抗体APt＿4诱导血小板活化机制的研究  

MECHANlSM OF PLATELET AGGREGATlON INDUCED BYANTl-HUMAN PLATELET MONOCLONAL ANTlBODYAPT4

作　　者：于爱新[1] 李家增[1] 连俊一[1] 

机构地区：[1]中国医学科学院血液学研究所,美国迈阿密大学医学院

出　　处：《中华血液学杂志》1994年第3期115-118,共4页Chinese Journal of Hematology

摘　　要：抗人血小板单克隆抗体ＡＰｔ＿４可特异的诱导正常人及１例巨大血小板病（ＢＳＳ）患者的血小板聚集，而对２例Ⅰ型血小板无力症（ＧＴ）患者的血小板无致聚作用。ＡＰｔ＿４的Ｆ（ａｂ＇）＿２不能诱导血小板的活化，但能与血小板特异结合并抑制ＡＰｔ＿４的ＩｇＧ，ＡＤＰ，胶原和肾上腺素诱导的血小板聚集。多种血小板抑制物可阻断ＡＰｔ＿４诱导的血小板聚集。免疫试验结果表明Ａｔｐ＿４识别血小板膜表面分子量为１４万和９．７万的糖蛋白。综上所述，ＡＰｔ＿４诱导血小板活化的机制可能与钙离子的存在，能量代谢中ｃＡＭＰ的降低，ＡＤＰ的释放和抗体Ｆｃ段的存在有关。monoclonal antibody designated APT4 was pro-duced by fusion of mouse myeloma cells to spleen cellsfrom a BALB/C mouse immunized with normal humanplatelets. APT4 IgG caused the aggregation of bothPRP and washed platelets from normal subjects and apatient with Bernard Soulier's syndrome , but not thosefrom two patients with the type 1 Glanzmann's throm-basthemia. No aggregation was observed when APT4 F(ab') 2 was used. SDS-PAGE of the immunoprecipi-tates of ￣(125)I labeled platelet membrane lysates by APT4showed two protein bands corresponding to GPⅡb and Ⅰ-Ⅱa. In conclusion, APT4 binded to GPⅡb-Ⅲa complexand induced aggregation requiring energy metabolism,calcium , Fc fragment of Igu and ADP release , but inde-pendent of thromboxane AZ formation.

关 键 词：血小板 糖蛋白 复合物 单克隆抗体 

分 类 号：R331.143[医药卫生—人体生理学]