Saito Shigeru, Shiozaki Arihiro, Nakashima Akitoshi, Sakai Masatoshi, Sasaki Yasushi
Department of Obstetrics and Gynecology, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Mol Aspects Med. 2007 Apr;28(2):192-209. doi: 10.1016/j.mam.2007.02.006. Epub 2007 Mar 4.
Recent data demonstrate that an altered immune response may play a key role in the development of preeclampsia. Some epidemiological findings and animal models support this idea. In this article, we review the innate immune system and adaptive immune system in preeclampsia and discuss the pathophysiology of preeclampsia from an immunological viewpoint. The most characteristic immunological finding in preeclampsia is the activation of both the innate and adaptive immune system. Activated neutrophils, monocytes, and NK cells initiate inflammation which induce endothelial dysfunction, and activated T cells may support inadequate tolerance during pregnancy. The cytokine profile in preeclampsia shows that the production of type 1 cytokines, which induce inflammation, is dominant while the production of type 2 cytokines, which regulates inflammation, is suppressed. Furthermore, the immunoregulatory system is down-regulated in preeclampsia and persistent inflammation reduces regulatory T cell function. Therefore, systematical immunoactivation may be one cause of preeclampsia.
近期数据表明，免疫反应改变可能在子痫前期的发生发展中起关键作用。一些流行病学研究结果和动物模型支持这一观点。在本文中，我们回顾了子痫前期中的固有免疫系统和适应性免疫系统，并从免疫学角度讨论子痫前期的病理生理学。子痫前期最具特征性的免疫学发现是固有免疫系统和适应性免疫系统均被激活。活化的中性粒细胞、单核细胞和自然杀伤细胞引发炎症，进而导致内皮功能障碍，而活化的T细胞可能会导致孕期耐受性不足。子痫前期的细胞因子谱显示，诱导炎症的1型细胞因子产生占主导，而调节炎症的2型细胞因子产生受到抑制。此外，子痫前期的免疫调节系统下调，持续的炎症会降低调节性T细胞功能。因此，系统性免疫激活可能是子痫前期的一个病因。
