Yue Shuang, Meng Jinlai
Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Department of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Am J Reprod Immunol. 2025 Jan;93(1):e70033. doi: 10.1111/aji.70033.
Preeclampsia is one of the most severe obstetric complications, yet its pathogenesis remains unclear. Decidual natural killer (dNK) cells, the most abundant immune cells at the maternal-fetal interface, are closely associated with preeclampsia due to abnormalities in their quantity, phenotype, and function. This review summarizes the molecular mechanisms by which dNK cells regulate extravillous trophoblast (EVT) invasion, promote uterine spiral artery remodeling, and maintain immune tolerance. Furthermore, it explores how disruptions in these mechanisms and changes in the decidual microenvironment alter dNK cell properties, driving the progression of preeclampsia. Understanding the mechanisms of dNK cells and identifying potential therapeutic targets may provide new insights for clinical intervention.
子痫前期是最严重的产科并发症之一，但其发病机制仍不清楚。蜕膜自然杀伤（dNK）细胞是母胎界面最丰富的免疫细胞，由于其数量、表型和功能异常，与子痫前期密切相关。本文综述了dNK细胞调节绒毛外滋养层（EVT）侵袭、促进子宫螺旋动脉重塑和维持免疫耐受的分子机制。此外，还探讨了这些机制的破坏和蜕膜微环境的变化如何改变dNK细胞特性，从而推动子痫前期的进展。了解dNK细胞的机制并确定潜在的治疗靶点可能为临床干预提供新的思路。
