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人类胎盘塑造了蜕膜巨噬细胞的表型。

The human placenta shapes the phenotype of decidual macrophages.

机构信息

Department of Obstetrics and Gynecology, Reproductive Biology Unit, Maternal-fetal Immunology Group, Medical University of Vienna, Vienna, Austria.

Division of Inflammation and Infection (II), Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden.

出版信息

Cell Rep. 2023 Jan 31;42(1):111977. doi: 10.1016/j.celrep.2022.111977. Epub 2023 Jan 10.

DOI:10.1016/j.celrep.2022.111977
PMID:36640334
Abstract

During human pregnancy, placenta-derived extravillous trophoblasts (EVTs) invade the decidua and communicate with maternal immune cells. The decidua distinguishes into basalis (decB) and parietalis (decP). The latter remains unaffected by EVT invasion. By defining a specific gating strategy, we report the accumulation of macrophages in decB. We describe a decidua basalis-associated macrophage (decBAM) population with a differential transcriptome and secretome compared with decidua parietalis-associated macrophages (decPAMs). decBAMs are CD11c and efficient inducers of Tregs, proliferate in situ, and secrete high levels of CXCL1, CXCL5, M-CSF, and IL-10. In contrast, decPAMs exert a dendritic cell-like, motile phenotype characterized by induced expression of HLA class II molecules, enhanced phagocytosis, and the ability to activate T cells. Strikingly, EVT-conditioned media convert decPAMs into a decBAM phenotype. These findings assign distinct macrophage phenotypes to decidual areas depending on placentation and further highlight a critical role for EVTs in the induction of decB-associated macrophage polarization.

摘要

在人类妊娠期间,胎盘来源的绒毛外滋养层细胞(EVT)浸润蜕膜并与母体免疫细胞进行通讯。蜕膜分为基底层(decB)和壁层(decP)。后者不受 EVT 浸润的影响。通过定义特定的门控策略,我们报告了巨噬细胞在 decB 中的积累。与壁层蜕膜相关巨噬细胞(decPAMs)相比,我们描述了一种具有差异转录组和分泌组的蜕膜基底层相关巨噬细胞(decBAMs)。decBAMs 表达 CD11c,是 Treg 的有效诱导物,在原位增殖,并分泌高水平的 CXCL1、CXCL5、M-CSF 和 IL-10。相比之下,decPAMs 表现出树突状细胞样的、运动的表型,其特征是 HLA Ⅱ类分子的诱导表达、增强的吞噬作用以及激活 T 细胞的能力。引人注目的是,EVT 条件培养基将 decPAMs 转化为 decBAM 表型。这些发现根据胎盘形成将不同的巨噬细胞表型分配给蜕膜区域,并进一步强调了 EVT 在诱导 decB 相关巨噬细胞极化中的关键作用。

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