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蜕膜巨噬细胞功能障碍是子痫前期发生的一个潜在危险因素。

Dysfunction of Decidual Macrophages Is a Potential Risk Factor in the Occurrence of Preeclampsia.

作者信息

Rong Miaomiao, Yan Xingyu, Zhang Hongya, Zhou Chan, Zhang Cong

机构信息

Shandong Provincial Key Laboratory of Animal Resistance Biology, College of Life Sciences, Shandong Normal University, Ji'nan, China.

School of Medicine, Xiamen University, Xiamen, China.

出版信息

Front Immunol. 2021 May 12;12:655655. doi: 10.3389/fimmu.2021.655655. eCollection 2021.

DOI:10.3389/fimmu.2021.655655
PMID:34054819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8152936/
Abstract

Preeclampsia is a multi-factorial and multi-genetic disorder that affects more than eight million mother and baby pairs each year. Currently, most of the attention to the pathogenesis of preeclampsia has been focused on placenta, but recent progresses suggest that excellent decidualization lays foundation for placentation and growth. Moreover, preeclampsia is associated with an imbalance in immunoregulatory mechanisms, however, how the immune regulatory system in the decidua affects preeclampsia is still unclear. In our study, after intersecting the genes of differentially expressed between preeclampsia and the control gotten by conventional expression profile analysis and the genes contained in the ligand receptor network, we found eight differentially expressed genes in a ligand-receptor relationship, and the eight genes have a characteristic: most of them participate in the interaction between decidual macrophages and other decidual immune cells. The results of single-cell sequencing of decidual cells further demonstrated that decidual macrophages affect the functions of other immune cells through export. As a result, abnormal gene expression affects the export function of decidual macrophages, which in turn affects the interaction of decidual macrophages with other immune cells, thereby destroying the original immune regulation mechanism, and ultimately leading to the occurrence of preeclampsia.

摘要

子痫前期是一种多因素、多基因的疾病,每年影响超过800万母婴。目前,对子痫前期发病机制的研究大多集中在胎盘,但最近的研究进展表明,良好的蜕膜化是胎盘形成和生长的基础。此外,子痫前期与免疫调节机制失衡有关,然而,蜕膜中的免疫调节系统如何影响子痫前期仍不清楚。在我们的研究中,通过常规表达谱分析得到子痫前期与对照组之间差异表达的基因,并与配体-受体网络中包含的基因进行交叉分析后,我们发现了8个具有配体-受体关系的差异表达基因,这8个基因具有一个特点:它们大多参与蜕膜巨噬细胞与其他蜕膜免疫细胞之间的相互作用。蜕膜细胞单细胞测序结果进一步表明,蜕膜巨噬细胞通过输出影响其他免疫细胞的功能。因此,基因表达异常影响蜕膜巨噬细胞的输出功能,进而影响蜕膜巨噬细胞与其他免疫细胞的相互作用,从而破坏原有的免疫调节机制,最终导致子痫前期的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f142/8152936/223d19e93b61/fimmu-12-655655-g007.jpg
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