正常妊娠需要适度的免疫反应，干扰素、杀伤性NK细胞和T细胞参与母胎界面的抗感染机制，适度炎性因子也促进胚胎发育。但是，微生物感染性炎症、自身免疫性炎症和代谢紊乱性炎症等，产生大量微生物致炎因子和内源细胞焦亡/坏死产物，会诱导生殖免疫微环境发生剧烈免疫应答，导致胚胎着床失败、发育异常或反复流产。我们曾经发现母胎界面生长因子PTN和OGN等促进胚胎发育，但是炎性因子IL-1b、IL-6促进Th17炎症反应，介导原因不明反复流产；IGF1促进NK细胞杀伤功能，增加胚胎免疫排斥风险。在本课题中，我们将试图分析诱发生殖免疫微环境炎症反应的各种因素、参与的效应细胞和介导炎症发生的直接因子，从中鉴别胚胎“保护性细胞因子”和“炎症性细胞因子”，尤其是鉴别干扰素刺激基因（ISGs）中的“保护性ISGs”和“致病性ISGs”，并对后者进行干预研究，为临床干预或治疗提供可能的靶点。

Normal pregnancy requires a moderate immune response. Interferon, cytotoxic Natural killer cells and T cells are involved in the anti-infection mechanism at the maternal-fetal interface. Moderate inflammatory factors also promote embryonic development. However, microbial infectious inflammation, autoimmune inflammation and metabolic disorder inflammation etc. produce a large number of microbial inflammatory factors and endogenous cell pyroptosis/necrocytosis products, which will induce a dramatic Immune response in reproductive immune microenvironment, leading to embryo implantation failure, abnormal development or repeated abortion. We have found that PTN and OGN, the growth promoting factors at the maternal and fetal interface, promote embryonic development, whereas inflammatory factors Il-1b and Il-6 promote Th17 inflammatory response and mediate unexplained repeated abortion. We also have found that IGF1 promotes the cytotoxic function of NK cells and increases the risk of embryo immune rejection. In this topic, we will try to analyze factors which induce the reproductive inflammatory response, the effective cells that have participated in the immune microenvironment, as well as the factor which directly mediate inflammation. We will also identify embryonic "protective cytokine" and "inflammatory cytokines", especially the identification of the “protective interferon stimulated gene (ISGs)" and "pathogenic ISGs" in the ISGs, and have research of the intervention study about the pathogenic ISGs, and provide possible targets for clinical intervention or treatment.