cyclosporine a enhances th2 bias at the maternal-fetal interface in early human pregnancy with aid of the interaction between maternal and fetal cells环孢霉素增强th2偏见在早期人类怀孕的母胎界面之间的相互作用与援助孕产妇和胎儿细胞.pdf

Cyclosporine A Enhances Th2 Bias at the Maternal-Fetal Interface in Early Human Pregnancy with Aid of the Interaction between Maternal and Fetal Cells 1. 1. 1 1 1 1 1 1,2 Hai-Lan Piao , Song-Cun Wang , Yu Tao , Rui Zhu , Chan Sun , Qiang Fu , Mei-Rong Du *, Da-Jin Li * 1 Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, China, 2 Department of Obstetrics and Gynecology, Hainan Medical College Affiliated Hospital, Haikou, China Abstract Our previous study has demonstrated that cyclosporine A (CsA) administration in vivo induces Th2 bias at the maternal-fetal interface, leading to improved murine pregnancy outcomes. Here, we investigated how CsA treatment in vitro induced Th2 bias at the human maternal-fetal interface in early pregnancy. The cell co-culture in vitro in different combination of component cells at the maternal-fetal interface was established to investigate the regulation of CsA on cytokine production from the interaction of these cells. It was found that interferon (IFN)-c was produced only by decidual immune cells (DICs), and not by trophoblasts or decidual stromal cells (DSCs); all these cells secreted interleukin (IL)-4, IL-10, and tumor necrosis factor (TNF)-a. Treatment with CsA completely blocked IFN-c production in DICs and inhibited TNF-a production in all examined cells. CsA increased IL-10 and IL-4 production in trophoblasts co-cultured with DSCs and DICs although CsA treatment did not affect IL-10 or IL-4 production in any of the cells when cultured alone. These results suggest that CsA promotes Th2 bias at the materna