Zare Moghaddam Maryam, Zare Fateme, Sandoghsaz Reyhane, Khalili Abbas, Shams Ali
Department of Immunology, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Reproductive Immunology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Int J Reprod Biomed. 2024 May 15;22(3):235-244. doi: 10.18502/ijrm.v22i3.16168. eCollection 2023 Mar.
Endometriosis is a chronic estrogen-related inflammatory disorder that is known by proliferating endometrial cells in a place outside the uterus. The high presence of immune cells in the peritoneal fluid of women with endometriosis confirms the involvement of the immune system in the pathogenesis of the disease. Mucosal-associated invariant T (MAIT) cells play an undeniable impact on mucosal immunity by the production of interleukin-17, interferon-gamma (IFN-γ), and tumor necrosis factor-alpha. The function of the cells in the pathogenesis of endometriosis is less investigated.
This study aims to investigate the infiltration of MAIT cells by using the determination levels of gene expression in eutopic and ectopic tissue of endometriosis lesions.
In this case-control study, the tested samples include 20 eutopic and 20 ectopic tissues of women with endometriosis and 20 uterine endometrial tissues of women in the control group. Expressions of the tumor necrosis factor-alpha, interleukin-17A, and -γ genes were analyzed by quantitative reverse transcriptase-polymerase chain reaction.
According to the results, gene expression did not show substantial elevation in the uterine and eutopic endometrial tissues compared to internal gene control as well as in ectopic tissues. Correlation analysis approved a positive relationship between expression genes and -γ levels in ectopic tissues.
Considering the low-expression specific gene of MAIT cells in ectopic tissue, it can be concluded that these cells are present in the endometriotic environment to a certain extent, and there is a possibility of their role in the progression of endometriosis by secreting IFN- .
子宫内膜异位症是一种与雌激素相关的慢性炎症性疾病,其特征是子宫内膜细胞在子宫外的部位增殖。子宫内膜异位症患者腹腔液中免疫细胞的大量存在证实了免疫系统参与了该疾病的发病机制。黏膜相关恒定T(MAIT)细胞通过产生白细胞介素-17、干扰素-γ(IFN-γ)和肿瘤坏死因子-α,对黏膜免疫产生不可忽视的影响。这些细胞在子宫内膜异位症发病机制中的作用研究较少。
本研究旨在通过测定子宫内膜异位症病变的在位和异位组织中基因表达水平,研究MAIT细胞的浸润情况。
在这项病例对照研究中,测试样本包括20例子宫内膜异位症患者的在位和异位组织以及20例对照组女性的子宫子宫内膜组织。通过定量逆转录聚合酶链反应分析肿瘤坏死因子-α、白细胞介素-17A和-γ基因的表达。
结果显示,与内参基因相比,在位和异位子宫内膜组织以及异位组织中的基因表达均未显示出显著升高。相关性分析证实了异位组织中表达基因与-γ水平之间存在正相关。
考虑到MAIT细胞特异性基因在异位组织中的低表达,可以得出结论,这些细胞在一定程度上存在于子宫内膜异位症环境中,并且有可能通过分泌IFN- 在子宫内膜异位症的进展中发挥作用。