The role of maternal T cell and macrophage activation in preterm birth: Cause or consequence?

The role of the immune system in term (TL) and preterm labor (PTL) is unknown. Despite the fact that globally, PTL remains the most important cause of childhood mortality. Infection, typically of the fetal membranes, termed chorioamnionitis, is the best-understood driver of PTL, but the mechanisms underpinning other causes, including idiopathic and stretch-induced PTL, are unclear, but may well involve activation of the maternal immune system. The final common pathway of placental dysfunction, fetal membrane rupture, cervical dilation and uterine contractions are highly complex processes. At term, choriodecidual rather than myometrial inflammation is thought to drive the onset of labor and similar findings are present in different types of PTL including idiopathic PTL. Although accumulated data has confirmed an association between the immune response and preterm birth, there is yet a need to understand if this response is an initiator or a consequence of tissue-level dysregulation. This review focuses on the potential role of macrophages and T cells in innate and adaptive immunity relevant to preterm birth in humans and animal models.