Ovarian insufficiency and early pregnancy loss induced by activation of the innate immune system.
Ovarian insufficiency and early pregnancy loss induced by activation of the innate immune system.
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先天免疫系统激活引起的卵巢功能不全和早孕流产。
DOI：
10.1172/jci20645
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Glimcher,LaurieH
中科院分区：
文献类型：
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作者：
Erlebacher,Adrian;Zhang,Dorothy;Parlow,AlbertF;Glimcher,LaurieH
我们描述了一种由CD 40免疫共刺激通路系统激活诱导的早期妊娠失败的小鼠模型。虽然胎儿丢失涉及NK细胞中间体，但不是由于淋巴细胞介导的胎儿和胎盘破坏。相反，妊娠失败是由于卵巢黄体合成孕酮受损，这是一种内分泌缺陷，反过来又与卵巢对催乳素促性腺作用的抵抗有关。妊娠失败也需要促炎细胞因子TNF-α，并与催乳素受体信号抑制剂细胞因子信号抑制因子1（Socs 1）和Socs 3的黄体诱导相关。免疫激活和生殖内分泌功能障碍之间的这种联系可能与妊娠丢失和其他临床生殖疾病有关。
We describe a murine model of early pregnancy failure induced by systemic activation of the CD40 immune costimulatory pathway. Although fetal loss involved an NK cell intermediate, it was not due to lymphocyte-mediated destruction of the fetus and placenta. Rather, pregnancy failure resulted from impaired progesterone synthesis by the corpus luteum of the ovary, an endocrine defect in turn associated with ovarian resistance to the gonadotropic effects of prolactin. Pregnancy failure also required the proinflammatory cytokine TNF-α and correlated with the luteal induction of the prolactin receptor signaling inhibitors suppressor of cytokine signaling 1 (Socs1) and Socs3. Such links between immune activation and reproductive endocrine dysfunction may be relevant to pregnancy loss and other clinical disorders of reproduction.