Abstract
Endometriosis is a benign, chronic, estrogen-dependent condition, present in 10% of women of reproductive age. The condition is associated with chronic pelvic pain and infertility that influence their quality of life, as well as married life and has important socio-economic consequences. Despite its high morbidity, its etiopathogenesis is incompletely known. A large number of studies suggest that the ability of endometrial implants to grow in ectopic locations may be correlated with the altered immune response towards the endometriotic tissue. There are enough data to show that immune system mediators, such as cytokines and chemokines, are playing key roles in the onset and olso on progression of endometriosis. There are studies that prove the association between endometriosis and autoimmune diseases. The present paper aims to investigate the implications of the immune response in the etiopathogenesis of endometriosis. The study of cellular or humoral immunity deficits, the presence of autoantibodies associated with this condition, can facilitate the understanding of the mechanisms that lead to the appearance and spread of endometriosis. We hope that this information will ultimately provide the basis for the development of new effective approaches in endometriosis management.
Highlights
Endometriosis is a benign, chronic, estrogen-dependent gynecological condition, present especially in women of reproductive age, with important implications on their quality of life, married life, and with special socio-economic consequences through the costs involved in diagnosis and her treatment.Symptoms of endometriosis often include dysmenorrhea, non-menstrual pelvic pain, and infertility [1,2]
Cytokines and chemokines involved in inflammation, angiogenesis, and tissue growth are increased in plasma and peritoneal fluid in women with endometriosis [15,16]
We have provided information on the implications of this dysfunction, to understand how the immune system is potentially dysfunctional in patients with endometriosis
Summary
Endometriosis is a benign, chronic, estrogen-dependent gynecological condition, present especially in women of reproductive age, with important implications on their quality of life, married life, and with special socio-economic consequences through the costs involved in diagnosis and her treatment. Symptoms of endometriosis often include dysmenorrhea, non-menstrual pelvic pain, and infertility [1,2]. The main methods of treating endometriosis include surgical removal of ectopic tissue and/or hormonal treatment to suppress ovarian function with adverse side effects [5]. The etiology of endometriosis is complex but insufficiently known. It appears to be multifactorial, including ectopic endometrial tissue, altered immunity, unbalanced cell proliferation and apoptosis, aberrant endocrine signaling, and genetic factors [6,7]. Immune system abnormalities have been consistently demonstrated in women with endometriosis, a chronic inflammatory response to the pres-. Cytokines and chemokines involved in inflammation, angiogenesis, and tissue growth are increased in plasma and peritoneal fluid in women with endometriosis [15,16]. We hope that current and future research will identify some of the mechanisms of endometriosis, providing us with new therapeutic possibilities
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