The landscape of decidual immune cells at the maternal-fetal interface in parturition and preterm birth.

Abstract

Background: Parturition is similar to an inflammatory response in which resident and infiltrating immune cells release cytokines and chemokines into the maternal-fetal interface, promoting expulsion of the fetus from the mother. The untimely activation of these inflammatory pathways can result in preterm labor. The maternal-fetal interface is composed mainly of decidual tissue and placental villous space.

Objective: The objective of this review is to examine the role and mechanisms of decidual immune cells during parturition and preterm birth. A deeper understanding of decidual immune cells at the maternal-fetal interface could provide significant insight into parturition and preterm birth pathogenesis.

Methods: We searched major databases (including PubMed, Web of Science, and Google Scholar etc.) for literature encompassing decidual immune cells, parturition and preterm birth up to July 2024 and combined with studies found in the reference lists of the included studies.

Results: Decidual neutrophils release inflammatory mediators that facilitate parturition. The M1/M2 ratio of decidual macrophages increases among preterm birth population. Mast cells may cause uterine contractions. In parturition and preterm birth, there is an increase in CD56^dimCD16⁺ natural killer cells and immature dendritic cells. The increase of Th1/Th2 and Th17/Treg cells leads to preterm birth. Women with preterm birth had a higher proportion of decidual B cells. ILC2 can help protect the steady-state environment at the maternal-fetal interface. The activation of invariant NKT cells plays an important role in inflammation-induced preterm birth. These decidual immune cells communicate with each other. The development of sequencing technology enables a more in-depth study of decidual immune cells.

Conclusion: The dynamic balance of the maternal-fetal immune microenvironment plays a crucial role in maintaining human pregnancy and in the initiation of delivery. A deep understanding of the mechanism of decidual immune dysfunction is crucial for understanding the pathogenesis of preterm birth.