مقاله انگلیسی رایگان در مورد ایمونولوژی آندومتریوز – الزویر 2018

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 Endometriosis is a hormono-dependent inflammatory gynecological disease whose pathophysiology is not completely understood. A peritoneal environment that allows the proliferation of ectopic endometrial cells associated with an aberrant immune response seems to contribute to the development of the disease. Although several immunological abnormalities have already been reported, the role of the immune system in endometriosis is not well established [1]. Disturbances in immune homeostasis are associated with increase in implantation, proliferation, and angiogenesis of the ectopic endometrial tissue [2]. However, it is not clear whether the modifications of the immune response lead to the development of the disease or if they are consequences of the ectopic endometrial growth [3]. The study of immunological dysfunctions in the context of endometriosis may help in understanding its role in the pathogenesis of the disease and could contribute to the development of new therapeutic strategies in the future.

Immunosurveillance: importance of immunological disorders in the survival and proliferation of ectopic endometrial cells

One of the main theories of the pathogenesis of endometriosis is the retrograde menstruation e the dissemination of endometrial cells through the uterine tubes e first described by Sampson (1927) [4]. However, it is known that this phenomenon occurs in most women of reproductive age, but not all of them develop the disease. Once they reach the peritoneal cavity, the endometrial cells in healthy women do not implant and are eliminated by an “immunosurveillance” system through apoptosis [3]. It was proposed that, in women with endometriosis, changes in cell-mediated and humoral immunity may contribute to the development of the disease [5]. These changes probably prevent the clearance of the endometrial cells that reach the peritoneal cavity and allow their implantation and development [3]. The exact mechanisms of immunosurveillance evasion by ectopic endometrial cells remain unclear, and some hypotheses have been formulated to explain this phenomenon. The production of proteins by the implants e such as the soluble form of the ICAM (intercellular adhesion molecule)-1, the sICAM1 e could interfere in their recognition by the leukocytes. It has been described that the expression of ICAM-1 mRNA and the secretion of sICAM-1 are increased in endometriotic stromal cells compared to those in stromal cells from eutopic endometrium. The circulating sICAM-1 binds to leukocyte function antigen-1 (LFA-1) and makes leukocytes less available to recognize the aberrant endometrial cells through their cell surface ICAM-1 [6].