دانلود رایگان مقاله انگلیسی ایمونولوژی آندومتریوز - الزویر 2018

abstract

The pathophysiology of endometriosis is not completely understood, but an aberrant immune response in the peritoneal environment seems to be crucial for the proliferation of ectopic endometrial cells e as those cells escape apoptosis and peritoneal cavity immunosurveillance. The growth of endometrial implants leads to the recruitment of a large number and diversity of immune cells and intense inflammation with increased proinflammatory cytokines, growth factors, and angiogenesis. There is substantial evidence of aberrant function of almost all types of immune cells in women with endometriosis: decreased T cell reactivity and NK cytotoxicity, polyclonal activation of B cells and increased antibody production, increased number and activation of peritoneal macrophages, and changes in inflammatory mediators. New clinical treatments for endometriosis are an urgent need, especially nonhormonal drugs. The study of immunology may clarify its role in the pathogenesis of endometriosis and contribute to the development of new therapeutic strategies.

Inflammatory mediators: cytokines, chemokines, and growth factors

Increased soluble factors such as autoantibodies, cytokines, growth factors, adhesion molecules, enzymes, hormones, prostaglandins, and reactive oxygen species [16,21,63e66], have been described in the blood, peritoneal fluid, and lesions of patients with endometriosis. This fact is probably a consequence of the high number of leukocytes, macrophages, and other immune cells in the peritoneal cavity of these patients. These proteins work as mediators of the immune system [67], regulating the proliferation and the differentiation of immune cells, the release of enzymes and acute phase proteins, immunoglobulin secretion, and the cytotoxic activities of immune cells [20]. Studies have shown that the higher concentration of inflammatory mediators in the peritoneal fluid in endometriosis has toxic effects on oocyte pick up by the fimbria, spermeoocyte interaction, and embryo implantation, leading to an aberrant reproductive function in these women. These effects were reversed during hormonal treatment [3]. Many cytokines e IL-1 [68,69], IL-4 [70], IL-6 [71], IL-8 [72,73], IL-10 [36], IL-33 [74], and TNFa [75] e and growth factors e transforming growth factor (TGF-b) [71], insulin-like growth factor (IGF-1) [76,77], hepatocyte growth factor (HGF) [78], epidermal growth factor (EGF) [79], platelet-derived growth factor (PDGF) [80,81], and vascular endothelial growth factor (VEGF) [24,82]e are significantly increased in endometriosis [83]. In addition, studies have shown that there are changes in the Th1/Th2 balance toward Th2 in endometriosis [22,43].