title: The development of endometriosis in a murine model is dependent on the presence of dendritic cells.
abstract: 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 dendritic 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 dendritic cell infiltration as possible treatments for endometriosis warrant further study.
authors.affiliation: Tel-Aviv Sourasky Medical Center, 6 Weizmann Street, Tel Aviv 64239, Israel.
authors.forename: Niv
authors.initials: N
authors.lastname: Pencovich
authors.affiliation: Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, MA 02115, USA; Vascular Biology Program, Department of Surgery, Children's Hospital Boston, both at Harvard Medical School, Boston, MA 02115, USA.
authors.forename: Janelle
authors.initials: J
authors.lastname: Luk
authors.affiliation: Laboratory for Reproductive Immunology, Department of Obstetrics and Gynecology, Hillel Yaffe Medical Center, Faculty of Medicine, Technion - Israel Institute of Technology, P.O. Box 169, Hadera 38100, Israel.
authors.forename: Shay
authors.initials: S
authors.lastname: Hantisteanu
authors.affiliation: Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, MA 02115, USA.
authors.forename: Mark D
authors.initials: MD
authors.lastname: Hornstein
authors.affiliation: Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, MA 02115, USA; Vascular Biology Program, Department of Surgery, Children's Hospital Boston, both at Harvard Medical School, Boston, MA 02115, USA; Laboratory for Reproductive Immunology, Department of Obstetrics and Gynecology, Hillel Yaffe Medical Center, Faculty of Medicine, Technion - Israel Institute of Technology, P.O. Box 169, Hadera 38100, Israel; IVF Unit, Department of Obstetrics and Gynecology, Hillel Yaffe Medical Center, Faculty of Medicine, Technion - Israel Institute of Technology, P.O. Box 169, Hadera 38100, Israel. Electronic address: ofainaru@techunix.technion.ac.il.
authors.forename: Ofer
authors.initials: O
authors.lastname: Fainaru
mesh_terms: D000818:Animals; D003713:Dendritic Cells / Q000502:physiology*; D004167:Diphtheria Toxin; D004195:Disease Models, Animal; D004715:Endometriosis / Q000473:pathology*; D005260:Female; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic
chemical_list: D004167:Diphtheria Toxin
keywords: angiogenesis; dendritic cells; endometriosis; infertility; mouse model; myeloid cells