反复自然流产（RSA）是严重危害女性生殖健康的疾病。尽管目前已发现母胎界面的促/抑炎失衡是导致RSA的重要原因，但维持上述平衡的分子机制并不明确。申请人前期研究发现IL-33在RSA患者蜕膜中表达下降，进而导致蜕膜巨噬细胞（dMφ）向M1型转化，炎性因子释放增加，同时IL-33的可溶性受体可促进dMφ对凋亡细胞的清除（efferocytosis），而IL-33对dMφ的调控机制尚不明确。根据文献报道Mφ对凋亡细胞的清除增强有助于Mφ向M2型转化，抑炎因子增多，而IL-33也有促进Mφ向M2型转化的特点。因此，我们推测IL-33可能是通过促进dMφ清除凋亡细胞的能力而发挥其维持促/抑炎平衡和免疫稳态的作用。为证实这一假说，我们将在体内/体外两个水平，借助自然流产动物模型，采用分子生物学、流式细胞仪等技术，揭示IL-33对dMφ的调控途径，阐明IL-33在维持母胎界面促/抑炎平衡中的分子机制。

Recurrent spontaneous abortion (RSA) is a disease that constitutes a serious threat to women's reproductive health. Although it is found that the immunity imbalance of pro/anti inflammatory was an important reason of RSA, the molecular mechanism of maintaining the aforementioned balance remain unknown. We have demonstrated the expression of IL-33 decreased in patient with RSA, therefore induced decidual macrophage (dMφ) to differentiate into M1 phenotype with high level expression of inflammatory factors. Meanwhile, the ability of dMφ to eliminate apoptotic cell (efferocytosis) could be promoted by the soluble receptor of IL-33, but the mechanism of IL-33 regulating dMφ is incompletely understood. Current findings have revealed that efferocytosis could contribute to the polariztion of dMφ to anti-inflammatory M2 macrophage, and IL-33 could also shift the balance from Mφ to M2 macrophage differentiation. Hence, we speculate that IL-33/ST2 works in maintaining pro/anti inflammatory balance at maternal-fetal interface by regulating dMφ efferocytosis and promoting anti-inflammatory cytokine secretion. To confirm the hypothesis, we take advantage of RSA animal model, intend to study the molecular mechanism by which IL-33 modulates dMφ efferocytosis in vivo and in vitro with molecular biology technology, flow cytometer and so on.