Qing-Hui Li,1,2 Qiu-Yan Zhao,1 Wei-Jing Yang,1 Ai-Fang Jiang,2 Chun-E Ren,2 Yu-Han Meng2 

1School of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, 261021, People’s Republic of China; 2Center of Reproductive Medicine, Affiliated Hospital of Shandong Second Medical University, Weifang, Shandong, 261000, People’s Republic of China

Correspondence: Yu-Han Meng, Center of Reproductive Medicine, Affiliated Hospital of Shandong Second Medical University, No. 2428.Yuhe Road, Kuiwen District, Weifang, Shandong, 261031, People’s Republic of China, Tel/Fax +86 536-3081389, Email yhmeng6@163.com

Abstract: Recurrent spontaneous abortion (RSA) is defined as two or more consecutive pregnancy failures, which brings tremendous stress to women of childbearing age and seriously affects family well-being. However, the reason in about 50% of cases remains unknown and is defined as unexplained recurrent spontaneous abortion (URSA). The immunological perspective in URSA has attracted widespread attention in recent years. The embryo is regarded as a semi-allogeneic graft to the mother. A successful pregnancy requires transition to an immune environment conducive to embryo survival at the maternal–fetal interface. As an important member of regulatory immunity, regulatory T (Treg) cells play a key role in regulating immune tolerance at the maternal–fetal interface. This review will focus on the phenotypic plasticity and lineage stability of Treg cells to illustrate its relationship with URSA.

Keywords: immune homeostasis, Treg cells, phenotype, maternal–fetal tolerance