Immunology as a risk factor and its role in the development of endometriosis
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AbstractEndometriosis is a common and complex gynecological disorder characterized by the occurrence of endometrial epithelial and stromal cells outside the uterus. However, its pathogenesis is still not fully understood. The most common working hypothesis is Sampson's implantation theory [1]. It was proposed that the endometrial fragments during menstruation can regurgitate through the fallopian tubes and survive in the peritoneal cavity. The retrograde menstruation has been demonstrated by the vital endometrial cells in peritoneal cavity and occurs in approximately 76% to 90% women during proliferative period [2, 3]. However, the implantation theory still cannot explain why only less than 10% of women suffer from endometriosis [4]. Additional factors involved in the development of endometriosis are implicated. Accumulated studies suggested that abnormal peritoneal immune responses may beneficial the implantation of endometrium [4]. In healthy women, refluxed endometrial cells are normally eliminated by the physiological immune surveillance. In women with endometriosis, the increased immune cells are not able to eradiated the ectopic endometrial cells, but facilitate and promote their survival and growth by producing excessive pathological growth factors and cytokines. The underlying mechanism of immune ignorance is still not very clear. In this chapter, we discussed the immunology as a risk factor and its role in the development of endometriosis. We summarized the latest research findings toward the immune response in the pathogenesis of endometriosis, elaborated the difficulties of both human and animal studies, and also proposed roadmaps for further research and development. © 2013 by Nova Science Publishers, Inc. All rights reserved.
All Author(s) ListZhang T., Wang C.C.
All Editor(s) Listed. by Marta Juarez.
Detailed descriptioned. by Marta Juarez.
Pages111 - 139
LanguagesEnglish-United Kingdom

Last updated on 2020-03-08 at 03:28