The decidual stromal cells-secreted CCL2 induces and maintains decidual leukocytes into Th2 bias in human early pregnancy
The decidual stromal cells-secreted CCL2 induces and maintains decidual leukocytes into Th2 bias in human early pregnancy
复制标题
在人类妊娠早期，蜕膜基质细胞分泌的 CCL2 诱导并维持蜕膜白细胞偏向 Th2。
DOI：
10.1016/j.clim.2012.07.017
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发表时间：
2012-11-01
影响因子：
8.6
通讯作者：
Li, Da-Jin
中科院分区：
文献类型：
--
作者：
He, Yin-Yan;He, Xiao-Ju;Li, Da-Jin
母胎界面特征Th2占优势的确切机制仍未解决。在本研究中，我们研究了蜕膜来源的CCL2在母胎界面Th2优势中的作用。流式细胞仪检测显示，55%的CD56(+)、CD16(-)、CD3(-)的蜕膜NK细胞、52%的CD4(+)T细胞和75%的CD14(+)单核细胞表达CCR2。重组人CCL2(RhCCL2)和蜕膜基质细胞(DSCs)的培养上清可促进这些蜕膜白细胞(DLC)的增殖和抑制其凋亡，并促进Th2细胞因子IL-4和IL-10的产生，同时增加GATA-3的转录。蜕膜基质细胞分泌的CCL2增加蜕膜白细胞GATA-3的转录，降低T-bet的转录，从而导致母胎界面Th2极化。此外，Th2细胞因子IL-4和IL-10，而不是Th1细胞因子，可促进DSC分泌CCL2。
The precise mechanism of characteristic Th2 predominance at maternal-fetal interface remains unresolved. In the present study, we investigated roles of the decidua-derived CCL2 in Th2 predominance at maternal-fetal interface. FCM shows that 55% CD56(+)CD16(-)CD3(-) decidual NK, 52% CD4(+) T cells and 75% CD14(+) monocytes express CCR2. Recombinant human CCL2 (rhCCL2) and the decidual stromal cells (DSCs)-derived supernatant can enhance proliferation and inhibit apoptosis of these decidual leukocytes (DLCs), and promote Th2 cytokines production, IL-4 and IL-10, with an increase in GATA-3 transcription. They also inhibit the secretion of Th1 cytokines, TNF-alpha and IFN-gamma, with a decrease in T-bet transcription It is concluded that the secreted CCL2 by decidual stromal cells increases GATA-3 transcription and decreases T-bet transcription in the decidual leukocytes, which contributes to Th2 polarization at maternal-fetal interface. Furthermore, the Th2 cytokines, IL-4 and IL-10, rather than Th1 cytokines, was shown to increase CCL2 secretion of DSC.