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目的：探讨血小板和Ｔ细胞活化抗原１（ＰＴＡ１）诱导人血小板活化聚集和对血小板胞浆Ｃａ２＋水平影响的机制。方法：血小板聚集与ＡＴＰ释放试验及血小板胞浆Ｃａ２＋水平测定。结果：ＰＴＡ１单克隆抗体（ＭｃＡｂ）体外可诱导人血小板活化聚集，ＥＧＴＡ与ＰＧＩ２可以完全抑制ＰＴＡ１ＭｃＡｂ诱导的血小板活化聚集，ＰＴＡ１ＭｃＡｂＦ（ａｂ′）２对ＣＤ９或ＣＤ４１诱导的血小板活化聚集无明显影响。ＰＴＡ１ＭｃＡｂ促进血小板胞浆Ｃａ２＋水平升高。结论：ＰＴＡ１ＭｃＡｂ的刺激作用与血小板膜表面Ｆｃ受体和ＣＤ４１／ＣＤ６１（ⅡｂⅢａ）复合物有关，促进血小板胞浆Ｃａ２＋水平升高为胞外Ｃａ２＋内流与胞浆内Ｃａ２＋储存释放共同作用所致。
Objective: To investigate the mechanism of platelet and T cell activating antigen 1 (PTA1) inducing human platelet activation and aggregation and its effect on platelet cytoplasmic Ca2 + level. Methods: Platelet aggregation and ATP release assay and platelet cytoplasmic Ca2 + levels were measured. Results: PTA1 monoclonal antibody (McAb) induced the aggregation of human platelet in vitro. EGTA and PGI2 could completely inhibit PTA1McAb-induced platelet aggregation. PTA1McAbF (ab ’) 2 had no effect on CD9 or CD41-induced platelet aggregation. PTA1McAb promotes platelet cytoplasmic Ca2 + levels. CONCLUSION: The stimulatory effect of PTA1McAb is related to the Fc receptor and CD41 / CD61 (ⅡbⅢa) complex on platelet membrane surface and promotes the elevation of platelet cytoplasmic Ca2 + level resulting from the combined action of extracellular Ca2 + influx and cytoplasmic Ca2 + storage and release.