title: Immunological factors and their role in the genesis and development of endometriosis.
abstract: The article presents an overview of immunological factors and their role in the genesis and development of endometriosis, with emphasis on inflammatory cytokines and growth and adhesion factors. Although retrograde menstruation is a common phenomenon among women of reproductive age, not all women with retrograde menstruation suffer the disease. Development of endometriosis seems to be a complex process, facilitated by several factors, including quantity and quality of endometrial cells in peritoneal fluid (PF), increased inflammatory activity in PF, increased endometrial-peritoneal adhesion and angiogenesis, reduced immune surveillance and clearance of endometrial cells, and increased production of autoantibodies against endometrial cells. Potential biomarkers like cytokines and autoantibodies, upregulated during development of endometriosis, seem useful in the development of a non-surgical diagnostic tool. In this review work, the immune role in endometriosis is examined through the role of immunological factors in the genesis and development of the disease. Furthermore, it could be concluded that, although endometriosis can be treated using hormonal suppression, there is a need today for non-hormonal drugs, probably to modulate immune function, in order to confront the disease and alleviate pain or infertility without inhibition of ovulation.
authors.affiliation: Third Department of Obstetrics and Gynecology, University of Athens Medical School, Attikon Hospital, Athens, Greece. harrysiri@hotmail.com
authors.forename: Charalambos
authors.initials: C
authors.lastname: Siristatidis
authors.forename: Christos
authors.initials: C
authors.lastname: Nissotakis
authors.forename: Charalambos
authors.initials: C
authors.lastname: Chrelias
authors.forename: Helen
authors.initials: H
authors.lastname: Iacovidou
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Salamalekis
mesh_terms: D001202:Ascitic Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D001323:Autoantibodies; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology; D004715:Endometriosis / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D005260:Female; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D007378:Interleukins / Q000276:immunology; D020738:Leptin / Q000502:physiology; D008264:Macrophages / Q000378:metabolism; D020782:Matrix Metalloproteinases / Q000502:physiology; D017382:Reactive Oxygen Species; D048069:Tumor Necrosis Factors / Q000276:immunology
chemical_list: D001323:Autoantibodies; D016207:Cytokines; D006133:Growth Substances; D007378:Interleukins; D020738:Leptin; D017382:Reactive Oxygen Species; D048069:Tumor Necrosis Factors; D020782:Matrix Metalloproteinases