Newman P J
Thromb Haemost. 1991 Jul 12;66(1):111-8.
Recent advances in molecular and cellular biology have made it possible to build upon previous serologic and biochemical studies of glycoproteins IIb and IIIa in important and exciting ways. In addition to providing a detailed basic understanding of the polymorphisms that are responsible for Glanzmann's thrombasthenia, and in other cases for eliciting an alloimmune response, the molecular characterization of platelet membrane glycoprotein polymorphisms is expected to have an increasingly large clinical impact. As the molecular basis of the remaining platelet antigen systems becomes known, our ability to design novel diagnostic and therapeutic approaches for the care and management of patients with PTP and NATP should improve. For Glanzmann's disease, the future holds the promise of gene therapy to correct the platelet abnormality. Establishment of animal models for GT will be an important first step in this direction.
分子和细胞生物学的最新进展使得在以往对糖蛋白IIb和IIIa的血清学和生物化学研究基础上，以重要且令人兴奋的方式取得进展成为可能。除了对导致Glanzmann血小板无力症的多态性以及在其他情况下引发同种免疫反应的多态性提供详细的基础理解之外，血小板膜糖蛋白多态性的分子特征预计将产生越来越大的临床影响。随着其余血小板抗原系统的分子基础为人所知，我们为血小板输注后紫癜（PTP）和新生儿同种免疫血小板减少症（NATP）患者设计新型诊断和治疗方法以进行护理和管理的能力应该会得到提高。对于Glanzmann病，未来有望通过基因疗法纠正血小板异常。建立Glanzmann血小板无力症的动物模型将是朝这个方向迈出的重要第一步。
