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Regulatory T Cells Play a Role in a Subset of Idiopathic Preterm Labor/Birth and Adverse Neonatal Outcomes.
Cell Reports ( IF 8.8 ) Pub Date : 2020-07-07 , DOI: 10.1016/j.celrep.2020.107874
Nardhy Gomez-Lopez 1 , Marcia Arenas-Hernandez 2 , Roberto Romero 3 , Derek Miller 4 , Valeria Garcia-Flores 4 , Yaozhu Leng 4 , Yi Xu 4 , Jose Galaz 4 , Sonia S Hassan 5 , Chaur-Dong Hsu 5 , Harley Tse 6 , Carmen Sanchez-Torres 7 , Bogdan Done 4 , Adi L Tarca 8
Affiliation  

Regulatory T cells (Tregs) have been exhaustively investigated during early pregnancy; however, their role later in gestation is poorly understood. Herein, we report that functional Tregs are reduced at the maternal-fetal interface in a subset of women with idiopathic preterm labor/birth, which is accompanied by a concomitant increase in Tc17 cells. In mice, depletion of functional Tregs during late gestation induces preterm birth and adverse neonatal outcomes, which are rescued by the adoptive transfer of such cells. Treg depletion does not alter obstetrical parameters in the mother, yet it increases susceptibility to endotoxin-induced preterm birth. The mechanisms whereby depletion of Tregs induces adverse perinatal outcomes involve tissue-specific immune responses and mild systemic maternal inflammation, together with dysregulation of developmental and cellular processes in the placenta, in the absence of intra-amniotic inflammation. These findings provide mechanistic evidence supporting a role for Tregs in the pathophysiology of idiopathic preterm labor/birth and adverse neonatal outcomes.



中文翻译:

调节性T细胞在特发性早产/出生和不良新生儿结局中发挥作用。

妊娠早期对调节性T细胞(Tregs)进行了详尽的研究。然而,人们对它们在妊娠后期的作用知之甚少。在本文中,我们报告说,在特发性早产/分娩的女性子集中,母体-胎儿界面的功能性Treg降低,同时伴随着Tc17细胞的增加。在小鼠中,妊娠后期功能性Treg的耗竭会诱发早产和不利的新生儿结局,这些后果可通过此类细胞的过继转移得以挽救。Treg的消耗不会改变母亲的产科参数,但会增加内毒素诱发的早产的易感性。耗竭Treg导致不良围生期结局的机制包括组织特异性免疫反应和轻度全身性产妇炎症,在没有羊水内炎症的情况下,胎盘发育和细胞过程失调。这些发现提供了机械证据支持Tregs在特发性早产/出生和不良新生儿结局的病理生理中的作用。

更新日期:2020-07-07
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