Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6
Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6
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DOI：
10.1073/pnas.0607514104
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发表时间：
2007-02-13
影响因子：
11.1
通讯作者：
Mantovani, Alberto
中科院分区：
文献类型：
--
作者：
de la Torre, Yeny Martinez;Buracchi, Chiara;Mantovani, Alberto
动物和人类的胎儿丢失通常与炎症有关。D 6是一种具有诱饵功能的混杂趋化因子受体，表达于淋巴内皮中，其识别并靶向降解大多数炎性CC趋化因子。在这里，我们报告说，D 6在胎盘中表达的绒毛外滋养层细胞和合体滋养层细胞的顶端，在母体血液和胎儿之间的界面。D 6（-/-）妊娠小鼠暴露于LIPS或抗磷脂自身抗体导致炎性CC趋化因子水平升高和胎盘中白细胞浸润增加，导致胎儿丢失率增加，这可通过阻断炎性趋化因子来预防。因此，炎性CC趋化因子D 6的混杂诱饵受体在防止由全身性炎症和抗磷脂抗体引起的胎儿丢失中起着非冗余的作用。
Fetal loss in animals and humans is frequently associated with inflammatory conditions. D6 is a promiscuous chemokine receptor with decoy function, expressed in lymphatic endothelium, that recognizes and targets to degradation most inflammatory CC chemokines. Here, we report that D6 is expressed in placenta on invading extravillous trophoblasts and on the apical side of syncytiotrophoblast cells, at the very interface between maternal blood and fetus. Exposure of D6(-/-) pregnant mice to LIPS or antiphospholipid autoantibodies results in higher levels of inflammatory CC chemokines and increased leukocyte infiltrate in placenta, causing an increased rate of fetal loss, which is prevented by blocking inflammatory chemokines. Thus, the promiscuous decoy receptor for inflammatory CC chemokines D6 plays a nonredundant role in the protection against fetal loss caused by systemic inflammation and antiphospholipid antibodies.