期刊
SEMINARS IN IMMUNOPATHOLOGY
卷 42, 期 4, 页码 413-429出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-020-00807-y
关键词
Preterm birth; Labor; Mouse models; Regulatory T cells; Inflammatory signaling pathways; Microbiome; Fetal signals
资金
- Projekt DEAL
- German Research Foundation [KFO296, AR232/25-2]
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.
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