The expression of human endogenous retrovirus-3 in fetal cardiac tissue and antibodies in congenital heart block.

The expression of human endogenous retrovirus-3 in fetal cardiac tissue and antibodies in congenital heart block.
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人内源性逆转录病毒3在胎儿心脏组织中的表达及先天性心脏传导阻滞中的抗体。

DOI:
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发表时间:
1996
影响因子:
4.6
通讯作者:
P. J. Venables
P. J. Venables
中科院分区:
医学3区
文献类型:
--
作者:
Jian;W. Fan;A. Horsfall;A. C. Anderson;S. Rigby;Erik Larsson;P. J. Venables

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内源性逆转录病毒-3(ERV-3)是一种内源性逆转录病毒,编码胎盘中表达的包膜蛋白的开放阅读框架。在这项研究中,我们还发现了胎儿心脏中的高水平表达,峰值表达发生在妊娠11至17周之间。用ELISA法检测了32名健康妇女、47名妊娠妇女、19名产后妇女、34名干燥综合征(SS)患者、28名系统性红斑狼疮(SLE)患者和48名先天性心脏传导阻滞(CHB)婴儿母亲血清中ERV-3抗原表位肽抗体。在正常妊娠和SS或SLE患者中发现ERV-3抗体水平升高。与正常对照组比较,CHB患儿母亲血清中的HBV-DNA水平最高(P < 0.001)。来自三位CHB母亲的血清的抗体在免疫印迹上结合ERV-3的重组跨膜蛋白,并结合胎儿心脏组织和胎盘的切片。这项研究显示了妊娠期间ERV-3自身免疫的证据,CHB婴儿的母亲中抗体水平特别高。ERV-3在胎儿心脏中的表达和母亲血清中抗体的存在表明在CHB的发病机制中可能起作用。
Endogenous retrovirus-3 (ERV-3) is an endogenous retrovirus encoding an open reading frame for an envelope protein expressed in placenta. In this study we also found high levels of expression in fetal heart, with peak expression occurring between 11 and 17 weeks of gestation. Antibodies to a peptide corresponding to a predicted epitope of ERV-3 were studied by ELISA in sera from 32 healthy women, 47 women during pregnancy, 19 post-partum, 34 with Sjogren's syndrome (SS), 28 with systemic lupus erythematosus (SLE) and 48 mothers of babies with congenital heart block (CHB). Elevated levels of antibodies to ERV-3 were found in normal pregnancy and in patients with SS or SLE. Compared with normal sera the highest levels occurred in mothers of CHB babies (P < 0.001). Antibodies from sera from three CHB mothers bound to recombinant transmembrane protein of ERV-3 on immunoblots, and to sections of fetal cardiac tissue and placenta. This study has shown evidence of autoimmunization to ERV-3 during pregnancy, with particularly high levels of antibodies in mothers of CHB babies. The expression of ERV-3 in fetal heart and the presence of antibodies in maternal sera suggest a possible role in the pathogenesis of CHB.