The development of endometriosis in a murine model is dependent on the presence of dendritic cells

Endometriosis is a common condition associated with pelvic pain and infertility. This study group has previously shown that supplementation of dendritic cells led to enhancement of endometriosis lesion growth and angiogenesis. This study determined whether endometriosis is dependent on the presence of endogenous dendritic cells. Surgical induction of endometriosis was performed in CD11c+ DTR/GFP transgenic (Tg) female mice in which dendritic cells were ablated upon injection of diphtheria toxin (DT). Mice were allocated into four groups (n = 5 each): group I, wild-type mice treated with vehicle; group II, wild-type mice treated with DT; group III, Tg mice treated with DT; and group IV, Tg mice treated with vehicle. After 10 days, mice were killed and endometriosis lesions were analysed by flow cytometry. DT treatment led to ablation of dendritic cells in spleens and endometriosis lesions in Tg mice while no ablation was observed in controls. Corresponding to dentritic cell ablation, endometriosis lesions in group III were ∼5-fold smaller than in the control groups (ANOVA P < 0.0001). This study suggests that endometriosis development is dependent on the presence of endogenous dendritic cells. Therapies designed to inhibit dentritic cell infiltration as possible treatments for endometriosis warrant further study.Endometriosis is a common condition associated with pelvic pain and infertility. We have previously shown that supplementation of a specialized group of bone marrow-derived immune cells – dendritic cells – led to enhancement of endometriosis lesion growth and to enhanced blood vessel formation within the lesions. Here we determined whether endometriosis is dependent on the presence of endogenous dendritic cells. Surgical induction of endometriosis was performed in a specialized transgenic mouse model in which dendritic cells could be specifically ablated upon injection of diphtheria toxin. Our results show that, corresponding to dendritic cell ablation, endometriosis lesions in this group were ∼5-fold smaller than in all control groups. Our study indicates that endometriosis development is dependent on the presence of endogenous dendritic cells. Therapies designed to inhibit dendritic cell infiltration as possible treatments for endometriosis warrant further studies.