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Once maternal-fetal immune tolerance is broken, pregnancy complications such as preeclampsia (PE) will occur. Regulatory T cells (Tregs) as unique immunosuppressive cells, play an important role in this whole process. Programmed cell death 1 ligand 1 (PD-L1) is widely expressed in human placental trophoblasts, through binding with programmed cell death protein 1 (PD-1) to maternal-fetal immunomodulation. Exosomes belong to extracellular membrane-bound microvesicles (EMV) that get more and more attention in signaling pathways and disease regulation. The role of Tregs in the development of PE and the role of PD-1/PD-L1 in regulating the function of Tregs have been studied, but the mechanism of trophoblast-derived exosomes containing PD-L1 influences PE by mediating maternal-fetal interface immunity is still unclear. In this article, our specific hypothesis is that trophoblast-derived exosomes containing PD-L1 which may decrease in PE could regulate the proportion and differentiation of Tregs in the decidua. This mechanism of suppression must be further investigated as it may provide valuable clues to novel therapeutic design in the realm of PE research.

Trophoblast-derived exosomes containing PD-L1 may have protective effects on preeclampsia by regulating Tregs