Human Va7.2-Ja33 mucosal-associated invariant T cells in endometrial ectopic tissues tend to produce interferon-gamma: A new player in endometriosis etiology: A case-control study

Maryam Zare Moghaddam, Fateme Zare, R. Sandoghsaz, Abbas Khalili, Ali Shams
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Abstract

Background: 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. Objective: This study aims to investigate the infiltration of MAIT cells by using the determination levels of Vα7.2-Jα33 gene expression in eutopic and ectopic tissue of endometriosis lesions. Materials and Methods: 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 Vα-Jα tumor necrosis factor-alpha, interleukin-17A, and IFN-γ genes were analyzed by quantitative reverse transcriptase-polymerase chain reaction. Results: According to the results, Vα7.2-Jα33 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 Vα7.2-Jα33 expression genes and IFN-γ levels in ectopic tissues. Conclusion: 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-γ. Key words: Endometriosis, MAIT, IFN-γ, TNF-α, TCR V alpha 7.2-J alpha33, IL-17
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子宫内膜异位组织中的人Va7.2-Ja33粘膜相关不变T细胞倾向于产生γ干扰素:子宫内膜异位症病因中的新角色:病例对照研究
背景: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腔以外的地方增殖。患有子宫内膜异位症的妇女腹腔液中存在大量免疫细胞,这证实免疫系统参与了该疾病的发病机制。粘膜相关不变 T 细胞(MAIT)通过产生白细胞介素-17、γ 干扰素(IFN-γ)和肿瘤坏死因子-α,对粘膜免疫产生了不可否认的影响。但对这些细胞在子宫内膜异位症发病机制中的功能研究较少。研究目的本研究旨在通过测定异位和异位子宫内膜异位症病灶组织中 Vα7.2-Jα33 基因表达水平,研究 MAIT 细胞的浸润情况。材料与方法:在这项病例对照研究中,检测样本包括子宫内膜异位症妇女的 20 例异位组织和 20 例异位组织,以及对照组妇女的 20 例子宫内膜组织。通过反转录聚合酶链反应定量分析 Vα-Jα 肿瘤坏死因子-α、白细胞介素-17A 和 IFN-γ 基因的表达。结果显示结果显示,与内部基因对照组相比,子宫内膜组织和异位内膜组织中的Vα7.2-Jα33基因表达量并未出现大幅升高,异位组织中的Vα7.2-Jα33基因表达量也未出现大幅升高。相关性分析表明,异位组织中 Vα7.2-Jα33 表达基因与 IFN-γ 水平呈正相关。结论考虑到异位组织中MAIT细胞特异性基因的低表达,可以认为这些细胞在一定程度上存在于子宫内膜异位症的环境中,有可能通过分泌IFN-γ在子宫内膜异位症的进展过程中发挥作用。关键词子宫内膜异位症 MAIT IFN-γ TNF-α TCR V alpha 7.2-J alpha33 IL-17
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