Abstract
Endometriosis is a benign gynecologic disorder characterized by the ectopic growth of misplaced endometrial cells. The retrograde menstruation theory, also known as Sampson's theory, proposes that viable endometrial tissue is refluxed through the fallopian tubes during menstruation and implants on peritoneal surface or pelvic organs. This peritoneal reflux could be a necessary but not sufficient condition for the development of endometriosis. Different studies have suggested that immunological mechanisms are involved in the pathophysiology of endometriosis. Clearly, the immune system is involved in endometriosis. It is not clear, however, what leads to the initiation, promotion, and progression of the disease. In some women who become endometriotic, the system of immunological clearance is inefficient or overwhelmed. This incapacity can be a result from either from the endometrium itself and/or from one or several anomalies in the factors present in the peritoneal environment such as: (1) cytokines; (2) natural killer cells; (3) macrophages; (4) dendritic cells; (5) T cell response. Facing these challenges, our goal in this study is to evaluate the cells and molecules present in the endometrial environment that could participate on the on/off circuit of the immunological clearance and that promotes the progression of endometriosis (AU)