Mehta Y S, Badakere S S
Institute of Immunohematology (ICMR), KEM Hospital, Parel, Mumbai.
J Postgrad Med. 1996 Apr-Jun;42(2):46-9.
Autoimmune thrombocytopenia (AITP) is caused by autoantibodies to platelet glycoprotein antigens. Intravenous immunoglobulin (i.v.IgG) and Rh immunoglobulin infusions have found great significance in the treatment of AITP patients not responding to corticosteroids and other modes of therapy. In our study, it was observed that immunoglobulins (i.v.IgG & Rh), and their Fab fragments inhibited the binding of antiplatelet autoantibodies to normal platelets, from 15.8 to 90.7% and 25.6 to 90.08% respectively; whereas, their Fc portion did not show any inhibition. The presence of specific anti-idiotypic antibodies to antiplatelet autoantibodies was established by using monoclonal antibodies to Glycoprotein IIb/IIa and Glycoprotein Ib/IX, as the specific idiotype source. The i.v.IgG and Rh immunoglobulin products reacted with the monoclonal antibodies, only through their Fab and not through the Fc portions, thereby confirming its specific anti-idiotype activity.
自身免疫性血小板减少症（AITP）由针对血小板糖蛋白抗原的自身抗体引起。静脉注射免疫球蛋白（i.v.IgG）和Rh免疫球蛋白输注在治疗对皮质类固醇及其他治疗方式无反应的AITP患者中具有重要意义。在我们的研究中，观察到免疫球蛋白（i.v.IgG和Rh）及其Fab片段分别将抗血小板自身抗体与正常血小板的结合抑制了15.8%至90.7%和25.6%至90.08%；而它们的Fc部分未显示出任何抑制作用。通过使用针对糖蛋白IIb/IIa和糖蛋白Ib/IX的单克隆抗体作为特异性独特型来源，证实了存在针对抗血小板自身抗体的特异性抗独特型抗体。i.v.IgG和Rh免疫球蛋白产品仅通过其Fab而非Fc部分与单克隆抗体发生反应，从而证实了其特异性抗独特型活性。
