Abstract
Endometriosis is a chronic inflammation that is one of the most common benign gynecological diseases. It is a steroid-dependent condition in which tissue histologically similar to the endometrium with glands and stroma grow outside the uterine cavity, causing pelvic pain, dysmenorrhea and infertility. It is estimated that approximately 10-15% of women of reproductive age, 40% of women with pelvic pain and 50% of women with fertility problems have this disease. It is also known that endometriosis, especially advanced disease, may impair fertility and currently it is estimated that about 20-50% of women with endometriosis are infertile. However, the mechanisms responsible for these effects are unknown. However, a number of studies have described changes in the immune different in women with endometriosis and infertility parameters. Autoimmune and inflammatory diseases are a group of complex diseases, affecting up to 5% of the population, is characterized by loss of tolerance to self-antigens, causing tissue destruction and whose pathogenesis involves a combination of multiple genetic and environmental factors. An important question to be investigated is based on the autoimmune system changes of patients with endometriosis. Immunological theories suggest that changes in the immune system could prevent the ability to eliminate the endometrium of the pelvic cavity. Recently, COX2 enzyme and prostaglandins have been associated with various pathologies of the reproductive tract, including endometriosis. A transcript of the COX2 gene is rapidly activated by growth factors and oncogenes play important roles in inflammation and tumorigenesis. Studies have shown that Th17 cells are present in endometriotic tissue and interleukin-17A (IL-17) stimulates the secretion of interleukin-8 (IL-8) and increases the expression of COX2 from endometriotic stromal cells, suggesting the role IL-17 in the development of endometriosis. Furthermore, there are reports that concentrations of IL-17A peritoneal fluid correlate with the severity of endometriosis and infertility associated with endometriosis, reinforcing that IL-17A and Th17 are involved in the pathogenesis of the disease. Recently, several studies have reported the association of a polymorphism in the promoter of IL-17A and autoimmune diseases and cancer gene region, with conflicting results. Inspired by these findings, the aim of the study is to evaluate the expression of IL-17A in the endometrium of women with endometriosis and controls and correlate it with the rs2275913 polymorphism / -197G> A in the promoter region of the gene. (AU)
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