In This Study we Aim to Explore the Immune Nature of Endometriosis as Manifested in the Peripheral Blood, Endometriosis Lesions, Normal Peritoneum and Normal Endometrium of Patients Suffering From Documented Endometriosis.

Endometriosis affects 15-20% of women in their reproductive life. Endometriosis is a chronic disabling inflammatory disease, characterized by implantation and growth of endometrial tissue (glandular epithelium and stroma) outside the uterine cavity.

Retrograde menstruation was found in 80%-90% of women. In most women these endometrial cells undergo apoptosis. In patients suffering from endometriosis this cells induce an inflammatory response. Pelvic endometriosis is associated with intrinsic anomalies of the refluxed endometrium, increased secretion of pro-inflammatory cytokines, neoangiogenesis, and impaired function of cell-mediated natural immunity.

Endometriosis has also been considered to be an autoimmune disease, owing to the presence of auto antibodies, the association with other autoimmune diseases and recurrent immune-mediated abortion.

Evidence suggests that Foxp3-expressing CD4+CD25+ regulatory T cells play a crucial role in the suppression of inflammatory disease. However, their role in the suppression of endometriosis has not yet been addressed.

We aim to study this aberrant regulation of endometrial cell apoptosis by investigating the peripheral blood immune system of patients suffering from endometriosis.