先天免疫系统
黄体溶解
生物
子宫
免疫
先天性淋巴细胞
细胞生物学
免疫学
内分泌学
激素
免疫系统
排卵
作者
Johan Siewiera,Tara I. McIntyre,Kelly M. Cautivo,Karim Mahiddine,Damon Rideaux,Ari B. Molofsky,Adrian Erlebacher
出处
期刊:Immunity
[Elsevier]
日期:2023-03-01
卷期号:56 (3): 606-619.e7
被引量:2
标识
DOI:10.1016/j.immuni.2023.01.005
摘要
Although mice normally enter labor when their ovaries stop producing progesterone (luteolysis), parturition can also be triggered in this species through uterus-intrinsic pathways potentially analogous to the ones that trigger parturition in humans. Such pathways, however, remain largely undefined in both species. Here, we report that mice deficient in innate type 2 immunity experienced profound parturition delays when manipulated endocrinologically to circumvent luteolysis, thus obliging them to enter labor through uterus-intrinsic pathways. We found that these pathways were in part driven by the alarmin IL-33 produced by uterine interstitial fibroblasts. We also implicated important roles for uterine group 2 innate lymphoid cells, which demonstrated IL-33-dependent activation prior to labor onset, and eosinophils, which displayed evidence of elevated turnover in the prepartum uterus. These findings reveal a role for innate type 2 immunity in controlling the timing of labor onset through a cascade potentially relevant to human parturition.
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