Detection of antitrophoblast antibodies in the sera of patients with anticardiolipin antibodies and fetal loss.

Detection of antitrophoblast antibodies in the sera of patients with anticardiolipin antibodies and fetal loss.
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DOI:
10.1182/blood.v82.9.2730.2730
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发表时间:
1993-11
期刊:
影响因子:
20.3
通讯作者:
K. McCrae;A. DeMichele;Prem Pandhi;Micheal J. Balsai;P. Samuels;C. Graham;P. Lala;D. Cines
K. McCrae;A. DeMichele;Prem Pandhi;Micheal J. Balsai;P. Samuels;C. Graham;P. Lala;D. Cines
中科院分区:
医学1区
文献类型:
--
作者:
K. McCrae;A. DeMichele;Prem Pandhi;Micheal J. Balsai;P. Samuels;C. Graham;P. Lala;D. Cines

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具有抗心磷脂抗体(ACLA)的妇女胎儿丢失的风险增加。这种结果的一个潜在解释是,这些个体的血清含有与滋养层细胞反应的抗体,滋养层细胞参与子宫胎盘血管系统的建立和胎盘血液流动性的维持。为了验证这一假设,我们比较了27例有流产史的ACLA患者与29例正常孕妇的滋养层反应性抗体的发生率。20名患者的血清中含有滋养层反应性抗体,而对照组中只有1名患者的血清中含有滋养层反应性抗体(P <0.001)。这些抗体不针对主要组织相容性I类抗原,并与长期和妊娠早期滋养层细胞反应。在大多数情况下,ACLA被含心磷脂的脂质体吸附的血清保持对细胞的反应性。此外,患者IG组分免疫沉淀滋养层细胞表面约62 kD的蛋白质,刺激滋养层细胞释放花生四烯酸和血栓素A2,并抑制滋养层细胞尿激酶受体结合尿激酶原。这些观察结果表明,ACLA和胎儿丢失史的妇女血清中含有抗滋养层抗体。这些抗体在血清学上可能与ACLA不同,并可能导致胎儿死亡的发病机制。
Women with anticardiolipin antibodies (ACLA) are at increased risk for fetal loss. One potential explanation for this outcome is that sera from these individuals contain antibodies reactive with trophoblast cells, which are involved in the establishment of the uteroplacental vasculature and maintenance of placental blood fluidity. To examine this hypothesis, we compared the incidence of trophoblast-reactive antibodies in 27 patients with ACLA and a history of fetal loss with that in 29 normal pregnant women. Sera from 20 patients, but only one control, contained trophoblast-reactive antibodies (P < .001). These antibodies were not directed against major histocompatibility class I antigens, and reacted with both term and first-trimester trophoblast cells. In most cases, sera from which ACLA were adsorbed by cardiolipin-containing liposomes maintained reactivity against cells. In addition, patient Ig fractions immunoprecipitated an approximately 62-kD protein from the trophoblast cell surface, stimulated the release of arachidonic acid and thromboxane A2 by trophoblasts, and inhibited the binding of prourokinase to trophoblast urokinase receptors. These observations show that sera from women with ACLA and a history of fetal loss contain antitrophoblast antibodies. These antibodies may be serologically distinct from ACLA, and may contribute to the pathogenesis of fetal demise.