Altieri D C, Mannucci P M
J Exp Med. 1986 Nov 1;164(5):1815-20. doi: 10.1084/jem.164.5.1815.
Human monocytes potentiate the ADP-stimulated aggregation of autologous platelets through a fourfold increased binding of 125I-fibrinogen to the platelet surface. The enhancement of platelet function is rapid, relatively transient and is due to thromboxane (Tx) synthesized by monocytes under these conditions. Tx generation by monocytes is triggered by the interaction between fibrinogen and the specific monocyte membrane receptor. These data suggest that the monocyte enhancement of platelet function combined with the clot-promoting activity of these cells might unbalance normal hemostasis.
人类单核细胞通过使125I-纤维蛋白原与血小板表面的结合增加四倍,增强了自体血小板的ADP刺激聚集。血小板功能的增强迅速且相对短暂,这是由于在这些条件下单核细胞合成的血栓素(Tx)所致。单核细胞产生Tx是由纤维蛋白原与特定单核细胞膜受体之间的相互作用触发的。这些数据表明,单核细胞对血小板功能的增强作用,结合这些细胞的促凝活性,可能会破坏正常的止血平衡。