小柯机器人

美国加州大学Adrian Erlebacher团队近期取得重要工作进展，他们通过研究避开黄体溶解揭示出依赖于先天性2型免疫的小鼠分娩途径。相关研究论文2023年2月6日在线发表于《免疫》杂志上。

据介绍，尽管小鼠通常在卵巢停止产生黄体酮（黄体溶解）时进入分娩，但该物种的分娩也可以通过子宫内在途径触发，可能类似于人类的分娩途径。然而，在这两个物种中，这样的途径在很大程度上仍然没有定义。

研究人员报告了先天性2型免疫缺陷小鼠在内分泌操作以避免黄体溶解时经历了严重的分娩延迟，从而迫使它们通过子宫内在途径进入分娩。研究人员发现，这些途径部分由子宫间质成纤维细胞产生的警报素IL-33驱动。研究人员还发现子宫2组先天性淋巴细胞和嗜酸性粒细胞的重要作用，前者在分娩开始前表现出IL-33依赖性激活，后者表现出产前子宫周转率升高的证据。

总之，这些发现揭示了先天性2型免疫在通过与人类分娩潜在相关的级联控制分娩开始时间中的作用。

附：英文原文

Title: Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity

Author: Johan Siewiera, Tara I. McIntyre, Kelly M. Cautivo, Karim Mahiddine, Damon Rideaux, Ari B. Molofsky, Adrian Erlebacher

Issue&Volume: 2023-02-06

Abstract: Although mice normally enter labor when their ovaries stop producing progesterone(luteolysis), parturition can also be triggered in this species through uterus-intrinsicpathways potentially analogous to the ones that trigger parturition in humans. Suchpathways, however, remain largely undefined in both species. Here, we report thatmice deficient in innate type 2 immunity experienced profound parturition delays whenmanipulated endocrinologically to circumvent luteolysis, thus obliging them to enterlabor through uterus-intrinsic pathways. We found that these pathways were in partdriven by the alarmin IL-33 produced by uterine interstitial fibroblasts. We alsoimplicated important roles for uterine group 2 innate lymphoid cells, which demonstratedIL-33-dependent activation prior to labor onset, and eosinophils, which displayedevidence of elevated turnover in the prepartum uterus. These findings reveal a rolefor innate type 2 immunity in controlling the timing of labor onset through a cascadepotentially relevant to human parturition.

DOI: 10.1016/j.immuni.2023.01.005

Source: https://www.cell.com/immunity/fulltext/S1074-7613(23)00015-8

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