Key Laboratory of Organ Regeneration & Transplantation of Ministry of Education, Department of Obstetrics, Obstetrics and Gynaecology Center, The First Hospital of Jilin University, Changchun, China.
National-Local Joint Engineering Laboratory of Animal Models for Human Diseases, Changchun, China.
JCI Insight. 2024 Oct 22;9(20):e176527. doi: 10.1172/jci.insight.176527.
Materno-fetal immunity possesses specialized characteristics to ensure pathogen clearance while maintaining tolerance to the semiallogeneic fetus. Most of our understanding on human materno-fetal immunity is based on conventional rodent models that may not precisely represent human immunological processes owing to the huge evolutionary divergence. Herein, we developed a pregnant human immune system (HIS) mouse model through busulfan preconditioning, which hosts multilineage human immune subset reconstitution at the materno-fetal interface. Human materno-fetal immunity exhibits a tolerogenic feature at the midgestation stage (embryonic day [E] 14.5), and human immune regulatory subsets were detected in the decidua. However, the immune system switches to an inflammatory profile at the late gestation stage (E19). A cell-cell interaction network contributing to the alternations in the human materno-fetal immune atmosphere was revealed based on single-cell RNA-Seq analysis, wherein human macrophages played crucial roles by secreting several immune regulatory mediators. Furthermore, depletion of Treg cells at E2.5 and E5.5 resulted in severe inflammation and fetus rejection. Collectively, these results demonstrate that the pregnant HIS mouse model permits the development of functional human materno-fetal immunity and offers a tool for human materno-fetal immunity investigation to facilitate drug discovery for reproductive disorders.
母体-胎儿免疫具有特殊的特征,可确保清除病原体,同时对半同种异体胎儿保持耐受。我们对人类母体-胎儿免疫的大部分了解都是基于传统的啮齿动物模型,由于巨大的进化差异,这些模型可能无法准确地代表人类的免疫过程。在此,我们通过白消安预处理开发了一种怀孕人类免疫系统(HIS)小鼠模型,该模型在母体-胎儿界面上具有多谱系人类免疫亚群的重建。人类母体-胎儿免疫在妊娠中期(胚胎日[E]14.5)表现出耐受特征,在蜕膜中检测到人类免疫调节亚群。然而,免疫系统在妊娠晚期(E19)转变为炎症状态。通过单细胞 RNA-Seq 分析揭示了一个有助于改变人类母体-胎儿免疫氛围的细胞-细胞相互作用网络,其中人类巨噬细胞通过分泌几种免疫调节介质发挥关键作用。此外,在 E2.5 和 E5.5 时耗尽 Treg 细胞会导致严重的炎症和胎儿排斥。总之,这些结果表明,怀孕 HIS 小鼠模型允许功能性人类母体-胎儿免疫的发展,并为人类母体-胎儿免疫研究提供了一种工具,以促进生殖障碍的药物发现。