Human V α 7.2-J α 33 mucosal-associated invariant T cells in endometrial ectopic tissues tend to produce interferon-gamma: A new player in endometriosis etiology: A case-control study

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 V $\alpha$ 7.2-J $\alpha$ 33 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 V $\alpha$ 7.2-J $\alpha$ 33 tumor necrosis factor-alpha, interleukin-17A, and IFN-γ genes were analyzed by quantitative reverse transcriptase-polymerase chain reaction.

Results: According to the results, V $\alpha$ 7.2-J $\alpha$ 33 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 V $\alpha$ 7.2-J $\alpha$ 33 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- $\gamma$ .

Keywords: Endometriosis, MAIT, IFN-γ, TNF-α; IL-17.; TCR V alpha 7.2-J alpha33.

Figure 1

Results of PCR product electrophoresis, 1% agarose gel was used for cDNA electrophoresis. A) Include bands of V $\alpha$ 7.2-J $\alpha$ 33 with a length of 104 bp and IFN- $\gamma$ with a length of 220 bp. B) Include bands of TNF- $\alpha$ with a length of 143 bp, and IL-17A with a length of 102 bp.

Figure 2

IFN-γ melt curve.

Figure 3

Expression of IFN-γ mRNA in ectopic, eutopic, and healthy women. Statistical analysis showed significant elevation levels of IFN-γ in ectopic lesions compared to the eutopic lesion and control females.

Figure 4

Expression TNF- $\alpha$ mRNA in the endometriotic lesion and normal endometrium. Higher level of TNF- $\alpha$ in eutopic lesions compared to ectopic lesions in endometriosis participants with p = 0.01.

Figure 5

Expression IL-17 mRNA in the endometriotic lesion and normal endometrium. A higher level of IL-17 in the ectopic lesion was observed compared to the eutopic lesion and control with p = 0.002.

Figure 6

Expression V $\alpha$ 7.2-J $\alpha$ 33 mRNA in the endometriotic lesion and normal endometrium. No statistically significant difference was observed in V $\alpha$ 7.2-J $\alpha$ 33 mRNA expression in endometriotic lesions compared to control.