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
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
