Polley M J, Nachman R L, Weksler B B
J Exp Med. 1981 Feb 1;153(2):257-68. doi: 10.1084/jem.153.2.257.
Arachidonate-mediated release of 14C serotonin and thromboxane B2 (TXB2) is significantly enhanced in the presence of complement. Only purified complement components C5, C6, C7, C8, and C9 are required for this reactivity. No known activating mechanism of the classical or alternative pathway is required, nor is C3. In the absence of exogenously added complement, platelet membrane-bound complement components play an essential role in modulating arachidonate-mediated serotonin release. Incubation of platelet membranes with arachidonate and C5--C9 led to the production of dimers of the membrane attack complex (C5b--9) on the platelet surface. These macromolecular complexes were eluted from the platelet membrane and were identified physicochemically and morphologically. The possibility arises that C3 in association with C5--C9 is required for mobilization of the arachidonic acid from the phospholipid of the platelet membrane. Once the arachidonic acid is mobilized, C3 is no longer required, C5--C9 being sufficient to modulate this pathway leading to enhanced production of TXB2.
在补体存在的情况下，花生四烯酸介导的14C血清素和血栓素B2（TXB2）释放显著增强。这种反应性仅需要纯化的补体成分C5、C6、C7、C8和C9。不需要经典途径或替代途径的已知激活机制，也不需要C3。在没有外源添加补体的情况下，血小板膜结合的补体成分在调节花生四烯酸介导的血清素释放中起重要作用。用花生四烯酸和C5 - C9孵育血小板膜导致血小板表面形成膜攻击复合物（C5b - 9）的二聚体。这些大分子复合物从血小板膜上洗脱下来，并通过物理化学和形态学方法进行鉴定。有可能C3与C5 - C9结合是从血小板膜磷脂中动员花生四烯酸所必需的。一旦花生四烯酸被动员，就不再需要C3，C5 - C9足以调节该途径，导致TXB2产生增加。
