Abstract
Endometriosis is a common gynecological disease that affects women of reproductive age in which the uterine endometrium grows outside the uterus. Origin of the ectopic endometrium is thought to be the retrograde endometrium through the oviducts. However, factors that determine the adherence and proliferation of the ectopic endometrium have not been revealed. Importantly, systemic autoimmune diseases are considered a key factor in the endometriosis onset. Herein, we established a surgical endometriosis rodent model using autoimmune disease-prone MRL/MpJ-Fas(lpr/lpr) (MRL/lpr) and MRL/+ mice to provide basic evidence of the relationship between autoimmune disease and endometriosis. Endometriosis lesions were successfully induced in two regions after transplanting uterine tissues from donor mice into the peritoneal cavity of recipient mice: the peritoneum or adipose tissue around the transplantation point (proximal lesions) and the gastrosplenic ligament or intestinal mesentery far from the transplantation site (distal lesions). Distal lesions were observed only in MRL/lpr mice, whereas endometriosis lesions showed no genotype- or region-related differences in the histology and distribution of sex hormone receptors and T cells. In contrast, transplanted uterine tissues in donor MRL/lpr mice exhibited a large infiltration of T cells in the lamina propria. Splenomegaly was more common in recipient than that in donor MRL/lpr mice. These results suggest that the infiltration of endogenous T cells in the endometrium alters the growth features of ectopic endometrium, possibly affecting the severity of endometriosis in patients with systemic autoimmune diseases.