免疫学异常是导致原因不明复发性流产（URSA）的重要原因。本课题组前期工作已证实Th17细胞参与了USRA的发生，但对于URSA过程Th17细胞和Treg细胞如何生成,调节的机制尚不明确。最新研究证实BATF与IRF-4是调控Th17细胞和Treg细胞转录因子的重要蛋白。申请者拟采用染色质免疫共沉淀技术、凝胶电泳漂移、靶基因验证等技术，利用体内动物模型及体外模型，并以BATF/IRF-4为靶点，构建shRNA慢病毒载体，探讨从不同层面阻断及过表达BATF、IRF-4、BATF/IRF-4对调节Th17细胞和Treg细胞分化参与妊娠母-胎耐受的机制。揭示这些蛋白与母-胎免疫识别和耐受的关系，阐明BATF与IRF-4相互作用的模式，解析这些蛋白所参与的信息转导通路中上、下游关键基因的相互关系，丰富和发展母-胎免疫识别和免疫豁免理论，为提高妊娠相关疾病预防和诊治水平，提供科学依据。

Immulogical abnormance is the important reason for URSA,our previous study has proved that Th17 cells inparticapated in orrurence of URSA.But the mechanism of the regulation of Th 17 cells and Treg cell is not that unclear. It's recently proced that BATF and IRF-4 is invovled in regulation of Th17 cell and Treg transcription signals. We are supposed to unstablish in-vivo and in-vitro model, targeted at BATF and IRF-4, to explore BATF, IRF-4, in fetal-maternal cross-talk and tolerance mechanism . Thus, we can reveal the relationshipns of protein on fetal-maternal cross-talk and tolerance and explain action model of BATF and IRF-4,enrich and develop theory fo rfetal-maternal cross-talk and tolerance mechanism so as to provide evidence and improve prevention and diagnosis level.