Platelet-associated antibody to glycoprotein IIb/IIIa from chronic immune thrombocytopenic purpura patients often binds to divalent cation-dependent antigens.
Platelet-associated antibody to glycoprotein IIb/IIIa from chronic immune thrombocytopenic purpura patients often binds to divalent cation-dependent antigens.
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DOI：
10.1182/blood.v81.5.1284.1284
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发表时间：
1993-03
期刊：
影响因子：
20.3
通讯作者：
K. Fujisawa;P. Tani;R. Mcmillan
中科院分区：
文献类型：
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作者：
K. Fujisawa;P. Tani;R. Mcmillan
慢性免疫性血小板减少性紫癜(ITP)是一种由于抗血小板相关抗原自身抗体引起的破坏性血小板减少综合征。这些抗原通常位于血小板膜糖蛋白(GP)IIb/IIIa复合体上。在目前的研究中，我们发现许多来自慢性ITP患者的血小板相关抗GPIIb/IIIa自身抗体依赖于构象完整的GPIIb/IIIa来最大限度地结合。我们研究了19例ITP患者(15例与血小板相关，8例血浆)的抗GPIIb/IIIa自身抗体和3例输血后紫癜患者的同种异体抗体(抗PIA1)。抗体与纯化的完整的GPIIb/IIIa、EDTA解离的GPIIb/IIIa、GPIIIa或GPIIb预先孵育2小时，然后在抗原捕获试验中检测残留抗体。结合结果与在缓冲液中预先孵育的抗体的结合结果进行比较。在所研究的15个与血小板相关的自身抗体中，完整的GPIIb/IIIa复合体比EDTA解离的复合体对抗体结合的抑制作用更大，平均抑制率(完整/解离)为7.9(范围从1.4到30.3)。无论使用GPIIb还是使用GPIIIa，抑制作用都很小。相反，分离的复合体或纯化的GPIIIa能更有效地抑制ITP患者抗PIA1同种异体抗体或抗GPIIIa C末端的自身抗体。我们认为，慢性ITP患者的血小板相关抗GPIIb/IIIa自身抗体主要针对阳离子依赖构象抗原。
Chronic immune thrombocytopenic purpura (ITP) is a syndrome of destructive thrombocytopenia due to autoantibodies against platelet-associated antigens. These antigens are most commonly located on the platelet glycoprotein (GP) IIb/IIIa complex. In the present studies, we show that many platelet-associated anti-GPIIb/IIIa autoantibodies from chronic ITP patients depend on conformationally intact GPIIb/IIIa for maximal binding. We studied anti-GPIIb/IIIa autoantibodies from 19 ITP patients (15 platelet-associated, 8 plasma) and alloantibodies from three patients with posttransfusion purpura (anti-PIA1). Antibodies were preincubated with purified intact GPIIb/IIIa, EDTA-dissociated GPIIb/IIIa, GPIIIa, or GPIIb for 2 hours and then residual antibody was measured in an antigen capture assay. The binding results were compared with those obtained using antibody preincubated in buffer. Of the 15 platelet-associated autoantibodies studied, the intact GPIIb/IIIa complex resulted in greater inhibition of antibody binding than the EDTA-dissociated complex, with a mean inhibition ratio (intact/dissociated) of 7.9 (range, 1.4 to 30.3). Little inhibition was noted using either GPIIb or GPIIIa. Conversely, plasma anti-PIA1 alloantibodies or plasma autoantibodies from ITP patients against the c-terminal region of GPIIIa were more efficiently inhibited by the dissociated complex or purified GPIIIa. We conclude that platelet-associated anti-GPIIb/IIIa autoantibodies in chronic ITP are frequently directed to cation-dependent conformational antigens.