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免疫细胞在子宫内膜异位症发病机制中的作用。

Involvement of immune cells in the pathogenesis of endometriosis.

作者信息

Izumi Gentaro, Koga Kaori, Takamura Masashi, Makabe Tomoko, Satake Erina, Takeuchi Arisa, Taguchi Ayumi, Urata Yoko, Fujii Tomoyuki, Osuga Yutaka

机构信息

Department of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.

出版信息

J Obstet Gynaecol Res. 2018 Feb;44(2):191-198. doi: 10.1111/jog.13559. Epub 2018 Jan 5.

DOI:10.1111/jog.13559
PMID:29316073
Abstract

Endometriosis is characterized by the implantation and growth of endometriotic tissues outside the uterus. It is widely accepted the theory that endometriosis is caused by the implantation of endometrial tissue from retrograde menstruation; however, retrograde menstruation occurs in almost all women and other factors are required for the establishment of endometriosis, such as cell survival, cell invasion, angiogenesis, and cell growth. Immune factors in the local environment may, therefore, contribute to the formation and progression of endometriosis. Current evidence supports the involvement of immune cells in the pathogenesis of endometriosis. Peritoneal neutrophils and macrophages secrete biochemical factors that help endometriotic cell growth and invasion, and angiogenesis. Peritoneal macrophages and NK cells in endometriosis have limited capability of eliminating endometrial cells in the peritoneal cavity. An imbalance of T cell subsets leads to aberrant cytokine secretions and inflammation that results in the growth of endometriosis lesions. It is still uncertain whether these immune cells have a role in the initial cause and/or stimulate actions that enhance disease; however, in either case, modulating the actions of these cells may prevent initiation or disease progression. Further studies are needed to deepen the understanding of the pathology of endometriosis and to develop novel management approaches of benefit to women suffering from this disease.

摘要

子宫内膜异位症的特征是子宫内膜组织在子宫外着床并生长。子宫内膜异位症由逆行月经中的子宫内膜组织着床引起,这一理论已被广泛接受;然而,几乎所有女性都会发生逆行月经,而子宫内膜异位症的发生还需要其他因素,如细胞存活、细胞侵袭、血管生成和细胞生长。因此,局部环境中的免疫因素可能会促使子宫内膜异位症的形成和发展。目前的证据支持免疫细胞参与子宫内膜异位症的发病机制。腹膜中的中性粒细胞和巨噬细胞分泌有助于子宫内膜异位细胞生长、侵袭和血管生成的生化因子。子宫内膜异位症患者腹膜中的巨噬细胞和自然杀伤细胞清除腹腔内子宫内膜细胞的能力有限。T细胞亚群失衡会导致细胞因子异常分泌和炎症,从而促使子宫内膜异位症病灶生长。这些免疫细胞在初始病因中是否起作用和/或是否刺激疾病进展仍不确定;然而,无论哪种情况,调节这些细胞的作用都可能预防疾病的发生或进展。需要进一步研究以加深对子宫内膜异位症病理的理解,并开发对患有这种疾病的女性有益的新治疗方法。

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