Chen Chie-Pein, Piao Longzhu, Chen Xilin, Yu Jianhua, Masch Rachel, Schatz Frederick, Lockwood Charles J, Huang S Joseph
Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan.
Department of Obstetrics and Gynecology, The Ohio State University College of Medicine, Columbus, OH, USA.
Reprod Sci. 2015 Nov;22(11):1461-7. doi: 10.1177/1933719115585148. Epub 2015 May 11.
Human first-trimester decidual cells (FTDCs) chemoattract CXCR3-expressing circulating CD56(bright)CD16(-) natural killer (NK) cells, which increase uteroplacental blood flow by remodeling spiral arteries and arterioles. This recruitment reflects elevated FTDC expression of NK cell-recruiting induced protein 10 and interferon (IFN)-inducible T-cell-α chemoattractant produced in response to the synergistic effects of tumor necrosis factor α (TNF-α) and IFN-γ stimulation. Decidual macrophages express TNF-α, whereas the cellular origin of IFN-γ is unclear. Therefore, this study aims to identify the cell source(s) of IFN-γ in human first trimester decidua. Immunostaining of decidual sections revealed that both FTDCs and decidual NK (dNK) cells express IFN-γ. Although individual dNK cells express higher IFN-γ levels, the more numerous FTDCs account for greater proportion of total IFN-γ immunostaining. Freshly isolated FTDCs express greater IFN-γ staining than dNK cells as measured by flow cytometry, whereas incubation of dNK cells with documented NK cell activators significantly increases IFN-γ above FTDC levels. Confluent FTDCs intrinsically produce, but paradoxically respond to, exogenous IFN-γ.
人孕早期蜕膜细胞(FTDCs)对表达CXCR3的循环CD56(bright)CD16(-)自然杀伤(NK)细胞具有化学趋化作用,这些NK细胞通过重塑螺旋动脉和小动脉来增加子宫胎盘血流量。这种募集反映了FTDCs中NK细胞募集诱导蛋白10和干扰素(IFN)诱导的T细胞α化学趋化因子的表达升高,这些因子是在肿瘤坏死因子α(TNF-α)和IFN-γ刺激的协同作用下产生的。蜕膜巨噬细胞表达TNF-α,而IFN-γ的细胞来源尚不清楚。因此,本研究旨在确定人孕早期蜕膜中IFN-γ的细胞来源。蜕膜切片的免疫染色显示,FTDCs和蜕膜NK(dNK)细胞均表达IFN-γ。虽然单个dNK细胞表达的IFN-γ水平较高,但数量更多的FTDCs在总的IFN-γ免疫染色中占更大比例。通过流式细胞术检测,新鲜分离的FTDCs比dNK细胞表达更强的IFN-γ染色,而用已证实的NK细胞激活剂孵育dNK细胞可使其IFN-γ表达显著高于FTDC水平。汇合的FTDCs固有地产生外源性IFN-γ,但却对其产生矛盾反应。