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母源性微嵌合细胞的转运及其生物学后果取决于母胎界面炎症的发生。

Maternal microchimeric cell trafficking and its biological consequences depend on the onset of inflammation at the feto-maternal interface.

作者信息

Slaats Emiel, Bramreiter Bernadette, Chua Kristine J, Quilang Rachel C, Sallinger Katja, Eikmans Michael, Kroneis Thomas

机构信息

Gottfried Schatz Research Center, Division of Cell Biology, Histology and Embryology, Medical University of Graz, Graz, Austria.

Department of Anthropology, University of California Santa Barbara, Santa Barbara, CA, USA.

出版信息

Semin Immunopathol. 2025 Jan 17;47(1):8. doi: 10.1007/s00281-025-01037-w.

DOI:10.1007/s00281-025-01037-w
PMID:39820729
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11742462/
Abstract

Microchimerism is defined as the presence of a small population of genetically distinct cells within a host that is derived from another individual. Throughout pregnancy, maternal and fetal cells are known to traffic across the feto-maternal interface and result in maternal and fetal microchimerism, respectively. However, the routes of cell transfer, the molecular signaling as well as the timing in which trafficking takes place are still not completely understood. Recently, the presence of inflammation at the feto-maternal interface has been linked with maternal microchimeric cells modulating organ development in the fetus. Here, we review the current literature and suggest that inflammatory processes at the feto-maternal interface tissues are a physiological prerequisite for the establishment of microchimerism. We further propose a spatio-temporal corridor of microchimeric cell migration to potentially explain some biological effects of microchimerism. Additionally, we elaborate on the possible consequences of a shift in this spatio-temporal corridor, potentially responsible for the development of pathologies in the neonate.

摘要

微嵌合体的定义是宿主内存在一小群源自另一个体的基因不同的细胞。在整个孕期,已知母胎细胞会穿过母胎界面,分别导致母体和胎儿微嵌合体的形成。然而,细胞转移的途径、分子信号传导以及转移发生的时间仍未完全明确。最近,母胎界面处的炎症与母体微嵌合细胞调节胎儿器官发育有关。在此,我们回顾当前文献,并提出母胎界面组织处的炎症过程是微嵌合体形成的生理前提。我们进一步提出微嵌合细胞迁移的时空通道,以潜在解释微嵌合体的一些生物学效应。此外,我们详细阐述了这一时空通道发生改变可能产生的后果,这可能是新生儿发病的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b26e/11742462/ab3c092facb3/281_2025_1037_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b26e/11742462/6218250618da/281_2025_1037_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b26e/11742462/ab3c092facb3/281_2025_1037_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b26e/11742462/6218250618da/281_2025_1037_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b26e/11742462/ab3c092facb3/281_2025_1037_Fig2_HTML.jpg

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本文引用的文献

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Transplacental migration of maternal natural killer and T cells assessed by ex vivo human placenta perfusion.通过体外人胎盘灌注评估母源性自然杀伤细胞和 T 细胞的胎盘转移。
Placenta. 2024 Feb;146:42-49. doi: 10.1016/j.placenta.2023.12.005. Epub 2023 Dec 20.
2
Inflammatory placental lesions are specifically observed in healthy oocyte donation pregnancies with extreme fetal-maternal incompatibility.炎症性胎盘病变在胎儿与母体极度不相容的健康卵母细胞捐赠妊娠中尤为常见。
Placenta. 2023 Nov;143:100-109. doi: 10.1016/j.placenta.2023.10.005. Epub 2023 Oct 10.
3
Pregnancy-induced transfer of pathogen-specific T cells from mother to fetus in mice.
小鼠中孕期诱导的病原体特异性T细胞从母体向胎儿的转移。
EMBO Rep. 2023 Oct 9;24(10):e56829. doi: 10.15252/embr.202356829. Epub 2023 Aug 23.
4
Placental cell type deconvolution reveals that cell proportions drive preeclampsia gene expression differences.胎盘细胞类型解析揭示了细胞比例驱动子痫前期基因表达差异。
Commun Biol. 2023 Mar 13;6(1):264. doi: 10.1038/s42003-023-04623-6.
5
Placental Inflammation Leads to Abnormal Embryonic Heart Development.胎盘炎症导致胚胎心脏发育异常。
Circulation. 2023 Mar 21;147(12):956-972. doi: 10.1161/CIRCULATIONAHA.122.061934. Epub 2022 Dec 9.
6
Postnatal depletion of maternal cells biases T lymphocytes and natural killer cells' profiles toward early activation in the spleen.产后母体细胞耗竭使脾脏中 T 淋巴细胞和自然杀伤细胞的特征向早期激活偏移。
Biol Open. 2022 Nov 1;11(11). doi: 10.1242/bio.059334. Epub 2022 Nov 9.
7
Matrix metalloproteinases in preterm prelabor rupture of membranes in the setting of chorioamnionitis: A scoping review.绒毛膜羊膜炎背景下胎膜早破中的基质金属蛋白酶:一项范围综述
Am J Reprod Immunol. 2023 Jan;89(1):e13642. doi: 10.1111/aji.13642. Epub 2022 Nov 9.
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Neurobiol Dis. 2022 Nov;174:105892. doi: 10.1016/j.nbd.2022.105892. Epub 2022 Oct 12.
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Nat Commun. 2022 Aug 5;13(1):4571. doi: 10.1038/s41467-022-32230-2.
10
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Dev Cell. 2022 Jun 20;57(12):1442-1452. doi: 10.1016/j.devcel.2022.05.018. Epub 2022 Jun 13.