Inadequate tolerance induction may induce pre-eclampsia
Inadequate tolerance induction may induce pre-eclampsia
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DOI：
10.1016/j.jri.2007.08.002
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发表时间：
2007-12-01
影响因子：
3.4
通讯作者：
Shiozaki, Arihiro
中科院分区：
文献类型：
--
作者：
Saito, Shigeru;Sakai, Masatoshi;Shiozaki, Arihiro
胎儿是母体的半同种异体移植物，因此，妊娠期间必须存在耐受系统。流行病学研究结果支持先兆子痫和耐受诱导失败之间的关系。为了诱导主要组织相容性复合体（MHC）I类特异性耐受，长期暴露于含有父系可溶性MHC I类抗原的精液中可能诱导父系MHC I类特异性耐受。此外，可溶性HLA-G1诱导CD 8（+）T细胞的缺失，以及NK细胞上的母体免疫球蛋白样受体（KIR）和胎儿HLA-C的结合，影响NK细胞、调节性CD 8（+）T细胞和调节性NK细胞的抑制和激活信号之间的平衡，可能在诱导MHC I类特异性耐受中起非常重要的作用。另一方面，暴露于表达父亲HLA-DR的精子和含有细胞内胎儿HLA-DR的滋养层碎片可能诱导父亲MHC II类特异性耐受。在这个过程中，CD 4（+）CD 25（+）调节性T（Treg）细胞起着核心作用。在这篇综述中，我们讨论了先兆子痫的风险和耐受诱导之间的关系。(C)2007爱思唯尔爱尔兰有限公司保留所有权利。
The fetus is semi-allograft to the matemal host; therefore, a system of tolerance must be present during pregnancy. Epidemiological findings support a relationship between pre-eclampsia and the failure of tolerance induction. For induction of major histocompatibility complex (MHC) class I-specific tolerance, long-term exposure to seminal fluid, which contains paternal soluble MHC class I antigens, may induce paternal MHC class I-specific tolerance. Furthermore, soluble HLA-G1, which induces the deletion of CD8(+) T-cells, and the combination of maternal killer-immunoglobulin-like receptors (KIR) on NK cells and fetal HLA-C, which affects the balance between inhibition and activation signals of NK cells, regulatory CD8(+) T cells, and regulatory NK cells, may play very important roles in the induction of MHC class I-specific tolerance. On the other hand, exposure to sperm, which express paternal HLA-DR, and trophoblastic debris, which contain intracellular fetal HLA-DR, may induce paternal MHC class II-specific tolerance. In this process, CD4(+)CD25(+) regulatory T (Treg)-cells play central roles. In this review, we discuss the relationship between the risk of pre-eclampsia and tolerance induction. (C) 2007 Elsevier Ireland Ltd. All rights reserved.