Boucheix C, Soria C, Mirshahi M, Soria J, Perrot J Y, Fournier N, Billard M, Rosenfeld C
FEBS Lett. 1983 Sep 19;161(2):289-95. doi: 10.1016/0014-5793(83)81027-8.
The leukemia-associated cell surface antigen p 24 is found on normal platelets as well as on Bernard Soulier syndrome and thrombasthenia type I platelets. ALB6 IgG (a monoclonal antibody against p 24) induces the aggregation of platelets from normal donors but not from thrombasthenia. In contrast, ALB6 Fab inhibits platelet aggregation induced by collagen, ADP, thrombin, ionophore A 23187 and ALB6 IgG. The results suggest that ALB6 interferes with a mechanism common to all aggregation pathways; the possible mechanisms are discussed.
白血病相关细胞表面抗原p 24在正常血小板以及伯纳德·索利尔综合征和Ⅰ型血小板无力症的血小板上均有发现。ALB6 IgG(一种抗p 24的单克隆抗体)可诱导正常供体的血小板聚集,但不能诱导血小板无力症患者的血小板聚集。相反,ALB6 Fab可抑制由胶原、ADP、凝血酶、离子载体A 23187和ALB6 IgG诱导的血小板聚集。结果表明,ALB6干扰了所有聚集途径共有的一种机制;并对可能的机制进行了讨论。