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简介：AbstractThe maternal-fetal interface is a key barrier to protect the fetus from infection. Toll-like receptors (TLRs) at the maternal-fetal interface are involved in antiviral responses. TLRs are expressed in both maternal decidua and fetal trophoblasts. Virus-induced activation of TLR signaling pathways triggers the release of interferon-related antiviral molecules and other inflammatory cytokines and/or chemokines by the host innate immune system, which may disrupt immune tolerance at the maternal-fetal interface and lead to pregnancy complications. In this review, we summarize the state of knowledge on the most common viral infections during pregnancy, antiviral TLR responses at the maternal-fetal interface, and TLR-associated pregnancy complications.

简介：Abstract2019 novel coronavirus disease has resulted in thousands of critically ill patients in China, which is a serious threat to people’s life and health. Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) was reported to share the same receptor, angiotensin-converting enzyme 2 (ACE2), with SARS-CoV. Here, based on the public single-cell RNA-sequencing database, we analyzed the mRNA expression profile of putative receptor ACE2 and AXL receptor tyrosine kinase (AXL) in the early maternal-fetal interface. The result indicates that the ACE2 has very low expression in the different cell types of early maternal-fetal interface, except slightly high in decidual perivascular cells cluster 1 (PV1). Interestingly, we found that the Zika virus (ZIKV) receptor AXL expression is concentrated in perivascular cells and stromal cells, indicating that there are relatively more AXL-expressing cells in the early maternal-fetal interface. This study provides a possible infection route and mechanism for the SARS-CoV-2- or ZIKV-infected mother-to-fetus transmission disease, which could be informative for future therapeutic strategy development.

简介：在母亲/胎儿的接口的Th2偏爱的规章的机制仍然保持不清楚。在这研究，我们在蜕膜的stromal描绘了cytokine生产房间(DSC)，蜕膜的有免疫力的房间(DIC)和导出胚胎的trophoblast房间，并且在早人的怀孕在母亲/胎儿的接口在Th2偏爱上调查了CXCL12/CXCR4相互作用的规定。我们由trophoblasts，DSC和DIC发现了Th1类型和Th2类型cytokines的微分生产。这些cytokines的分泌物在不同房间cocultures变化了，导致了到Th2偏爱。流动cytometry与DSC显示出trophoblasts的那coculture，DIC显著地在DSC在trophoblasts，和IL-10生产增加了IL-4和IL-10生产。然而，有DSC和DIC的trophoblasts的coculture显著地增加了干扰素(IFN)-γ；在DSC，和肿瘤坏死因素(TNF)-α的表示；在DIC的表示。没有变化在所有cocultures在DIC在trophoblasts，并且在Th2类型cytokine生产在Th1类型cytokine生产被看见。而且，有抵销抗体upregulated的anti-CXCR4的预告的处理Th1类型cytokinesIFN-γ的生产；并且TNF-α；，并且downregulatedTh2类型cytokinesIL-4和IL-10的生产在trophoblasts，DSC，DIC或他们的cocultures。有趣地，rhCXCL12禁止了Th1类型cytokineTNF-α的生产；并且在DIC提高了象IL-4和IL-10那样的Th2类型cytokines的表示；这效果被anti-CXCR4抗体废除。我们的现在的学习阐明了到塑造Th2的部件房间的单个贡献偏导，并且揭开经由在在早人的怀孕的母亲/胎儿的接口的CXCL12/CXCR4信号的复杂串音。