Abstract
It has been postulated that the immune system is impaired in individuals with endometriosis, with attention directed to natural killer (NK) cells. Specifically, it has been hypothesized that altered numbers of peripheral NK cells in blood are associated with the presence of endometriotic lesions. This study aimed to evaluate the level of the peripheral NK cell surface marker CD107a in endometriosis in the presence of IL-2 stimulation. Peripheral blood mononuclear cells (PBMCs) were obtained from 7 women with endometriosis and 7 women without endometriosis. The PBMCs were divided into two groups and either treated with recombinant IL-2 or left untreated. The cytotoxic activity of the PBMCs toward target cells (K562) was evaluated. Then, both groups were cocultured for 4 days. The expressions of CD107a, TNF-α, and IFN-γ were determined using flow cytometry analysis. There was no difference in the expression of CD107a prior to IL-2 stimulation in PBMCs from women with endometriosis compared to those from women without endometriosis. However, we observed upregulation of the expression of the surface marker CD107a after treatment in the endometriosis group. In addition, there was a significant difference in CD107a expression in the endometriosis group before versus after stimulation with IL-2 (p < 0.01). We also found no difference in the production of TNF-α and IFN-γ before versus after treatment with IL-2 in either groups. The levels of CD107a were significantly enhanced in peripheral blood taken from women with endometriosis after treatment with IL-2.
Highlights
Endometriosis is one of the most common benign gynecological disorders and is histologically characterized by the presence of endometrial tissue outside the uterus [1]
Cell viability is defined as cells that reflect the number of cells that are negative for staining with trypan blue compared to the positive one. e total number of cells and the viability of the cells are shown in Table 1. e number of cells significantly decreased in the control group after cryopreservation; no significant difference was seen in the endometriosis group before and after cryopreservation (Table 1)
Peripheral Blood Mononuclear Cell (PBMC) were evaluated in the endometriosis group and the control group prior to IL-2 treatment. ere was no difference in the expression of CD107a, tumor necrosis factor-α (TNF-α), or IFN-c between the endometriosis group and the control group (Table 2)
Summary
Endometriosis is one of the most common benign gynecological disorders and is histologically characterized by the presence of endometrial tissue outside the uterus [1]. Endometriosis causes dysmenorrhea, dyspareunia, pelvic pain, and infertility in women of reproductive age [2]. Despite its high prevalence and incapacitating symptoms, the exact pathogenic mechanisms of endometriosis are not completely understood. Immunological dysfunction in the peritoneal environment is believed to be a crucial factor in the development of endometriosis, as the displaced endometrial cells are able to avoid immune recognition [3]. Several studies have shown that inflammation contributes to the pathophysiology of the disease, mainly by altering the functions of immune cells and increasing the levels of proinflammatory cytokines in the peritoneal cavity, endometrium, and blood [4].
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