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。 APt_4, an anti-human platelet monoclonal antibody, can specifically induce platelet aggregation in normal individuals and in one patient with giant platelet disease (BSS), but not in two patients with type I platelet failure (GT). F (ab ’) _ 2 of APt_4 failed to induce platelet activation, but could specifically bind to platelets and inhibit APt_4-induced IgG, ADP, collagen and epinephrine-induced platelet aggregation. A variety of platelet inhibitors block APt_4-induced platelet aggregation. Immunoassay results showed that Atp_4 recognized glycoproteins with a molecular weight of 140,000 and 97,000 on the platelet membrane surface. In summary, the mechanism of APT_4-induced platelet activation may be related to the presence of calcium ion, cAMP in energy metabolism, release of ADP and the presence of Fc fragment.