Nomura S, Miyazaki Y, Miyake T, Yamaguchi K, Kido H, Kawakatsu T, Fukuroi T, Kagawa H, Suzuki M, Yanabu M
First Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
Clin Exp Immunol. 1993 Sep;93(3):452-5. doi: 10.1111/j.1365-2249.1993.tb08200.x.
We investigated the increase of platelet-associated IgG and complement component 3 (C3) caused by the in vitro action of anti-platelet MoAbs, and the effect of mouse and human IgG on these events. Anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib MoAbs caused a slight increase of C3, but not of platelet-associated IgG. In contrast, anti-CD9 and anti-Fc gamma II receptor MoAbs caused an increase of both platelet-associated C3 and IgG. In particular, three MoAbs which activated the complement system caused a marked increase of C3. When platelet-rich plasma was treated with aspirin and prostaglandin E1 before incubation with antibodies, the increase of platelet-associated IgG was inhibited in all cases. In contrast, the increase of platelet-associated C3 was scarcely influenced. These results suggest that the binding to platelets of platelet-activating antibodies caused the increased expression of IgG molecules on the platelet surface and a possible increase of platelet-associated IgG. However, the increase of platelet-associated C3 appeared to depend on specific characteristics of the antibodies tested, such as a complement-activating effect. In addition, intact mouse or human IgG inhibited the increase of platelet-associated C3 caused by complement-activating antibodies, while F(ab')2 mouse or human IgG had no such effect. This suggested that the Fc portion of IgG may block the increase of C3 mediated by anti-platelet antibodies.
我们研究了抗血小板单克隆抗体的体外作用所引起的血小板相关IgG和补体成分3（C3）的增加，以及小鼠和人IgG对这些事件的影响。抗糖蛋白IIb/IIIa和抗糖蛋白Ib单克隆抗体导致C3略有增加，但未引起血小板相关IgG的增加。相反，抗CD9和抗FcγII受体单克隆抗体导致血小板相关C3和IgG均增加。特别是，三种激活补体系统的单克隆抗体导致C3显著增加。当富含血小板的血浆在与抗体孵育前用阿司匹林和前列腺素E1处理时，在所有情况下血小板相关IgG的增加均受到抑制。相反，血小板相关C3的增加几乎未受影响。这些结果表明，血小板活化抗体与血小板的结合导致血小板表面IgG分子表达增加以及血小板相关IgG可能增加。然而，血小板相关C3的增加似乎取决于所测试抗体的特定特性，例如补体激活作用。此外，完整的小鼠或人IgG抑制了补体激活抗体引起的血小板相关C3的增加，而F(ab')2小鼠或人IgG则没有这种作用。这表明IgG的Fc部分可能会阻断抗血小板抗体介导的C3增加。
