人早孕期蜕膜γδT细胞的数量明显增加，以Vδ1型为主，而复发性流产患者中Vδ2型γδT细胞比例升高。我们新近研究发现，滋养细胞可分泌大量的趋化因子CCL24，且90%的γδT细胞其受体CCR3为阳性。然而，滋养细胞来源的CCL24对蜕膜γδT细胞的数量和分泌功能是否有调节作用尚不明确。本课题将首先从细胞趋化、粘附、增殖和凋亡等方面分析CCL24对蜕膜γδT细胞的数量是否有选择性调节作用；其次，通过检测细胞因子分泌谱来判断CCL24对蜕膜γδT细胞功能的影响；随后；通过研究细胞内信号传导来解析CCL24发挥上述作用的信号通路；最后，我们将探讨CCL24/CCR3对γδT细胞调节的失衡是否与复发性流产相关。本课题的研究不但有助于我们加深对正常妊娠过程和复发性流产发病机制的了解，还有望对临床上防治复发性流产提一定的供理论依据。

In first-trimester pregnant women, the number of γδ T cells at decidua is significantly increased; in contrast to a V δ2 chain preference of decidual γδ T cells in recurrent spontaneous abortion (RSA) patients, the cells dominantly use V δ1 chain in normal pregnancy. Our recent work found that trophoblasts are an important source of CCL24 at the maternal-fetal interface. Meanwhile, decidual γδ T cells express the highest level of CCR3 compared to other immune cells. We now inferred that trophoblast-derived chemokine CCL24 could regulate the number and functions of decidual γδ T cells, and therefore contributing to an immune tolerance environment at the maternal-fetal interface. In the present study, we will first analyze whether trophoblast-derived chemokine CCL24 regulates the processes of selective chemotaxis, adhesion, cell proliferation and apoptosis of γδ T cells. Next, we will analyze the impact of CCL24 on the secreting function of decidual γδ T cells by using cytometric bead array. Following that, we will treat cells with inhibitors of intracellular CCL24 pathways, such as MAPK/ERK pathway and PI3K/Akt pathway, and then investigate the down-stream pathways of CCL24. Finally, we will evaluate whether the improper regulation of CCL24/CCR3 to γδ T cells is related to RSA. Our study would be helpful for understanding the mechanism of normal pregnancy and might offer clinical trails for treating RSA.