Decrease in activated regulatory T cell populations in the endometrium during ovulation in endometriosis

子宫内膜异位症患者排卵期间子宫内膜中活性调节性 T 细胞群减少

阅读:5
作者:Maya Fujii, Yukiko Tanaka, Hiroyuki Okimura, Eiko Maeda, Masahide Hamaguchi, Michiaki Fukui, Jo Kitawaki, Taisuke Mori

Abstract

Endometriosis is a serious disorder that can lead to infertility. The immune system, particularly regulatory T cells (Tregs), is involved in endometriosis and infertility; however, endometriosis-associated infertility is poorly understood. Tregs, which have an immunosuppressive function, fluctuate during the menstrual cycle. They are functionally heterogeneous and can be divided into subsets, with only activated Tregs (aTregs) having a true immunosuppressive function. The purpose of this study is to investigate the role of aTregs in endometriosis and how they contribute to endometriosis-associated infertility. We enrolled 72 women with (n = 39) and without (n = 33) endometriosis. Subpopulations of Tregs were examined in normal endometrium (NE), eutopic endometrium from women with endometriosis (EE), normal peritoneal fluid (N-PF), and peritoneal fluid from women with endometriosis (E-PF) via flow cytometry. The proportion of aTregs during the ovulatory phase was higher in NE than in EE (P < 0.05), and that during ovulatory and secretory phases was significantly higher in NE than in N-PF (P < 0.01 and 0.05, respectively). aTreg populations did not significantly differ between EE and E-PF. During the ovulatory phase, the proportion of resting Treg (rTreg) in the N-PF was significantly higher than during the proliferative phase (P < 0.05). The E-PF of rTreg populations did not differ significantly throughout the menstrual cycle. We found that Treg subsets were altered in the endometrium and PF of patients with endometriosis during the menstrual cycle. Our findings, particularly the reduction of aTregs in the EE, may provide an insight into the mechanism of endometriosis-associated infertility.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。