Preterm birth (PTB) complicates 5–18% of pregnancies globally and is a leading cause of maternal and fetal morbidity and mortality. Most PTB is spontaneous and idiopathic, with largely undefined causes. To increase understanding of PTB, much research in recent years has focused on using animal models to recapitulate the pathophysiology of PTB. Dysfunctions of maternal immune adaptations have been implicated in a range of pregnancy pathologies, including PTB. A wealth of evidence arising from mouse models as well as human studies is now available to support that PTB results from a breakdown in fetal-maternal tolerance, along with excessive, premature inflammation. In this review, we examine the current knowledge of the bidirectional communication between fetal and maternal systems and its role in the immunopathogenesis of PTB. These recent insights significantly advance our understanding of the pathogenesis of PTB, which is essential to ultimately designing more effective strategies for early prediction and subsequent prevention of PTB.

早产（PTB）使全球怀孕的5-18％复杂化，是孕产妇和胎儿发病率和死亡率的主要原因。大多数PTB是自发性和特发性的，其病因很多。为了增加对PTB的了解，近年来许多研究都集中在使用动物模型来概括PTB的病理生理上。孕产妇的免疫适应功能异常已牵涉到包括PTB在内的一系列妊娠病理学中。现已从小鼠模型以及人体研究中获得了大量证据来支持PTB是由于胎儿-母亲耐受性下降以及过度，过早的炎症所致。在这篇综述中，我们检查了胎儿和母体系统之间双向通讯的当前知识及其在PTB免疫发病机制中的作用。