Volume 107, Issue 1, Pages 167-173
Gentaro Izumi, Ph.D., M.D., Kaori Koga, Ph.D., M.D., Masashi Takamura, Ph.D., M.D., Tomoko Makabe, M.D., Miwako Nagai, Ph.D., M.D., Yoko Urata, Ph.D., M.D., Miyuki Harada, Ph.D., M.D., Tetsuya Hirata, Ph.D., M.D., Yasushi Hirota, Ph.D., M.D., Tomoyuki Fujii, Ph.D., M.D., Yutaka Osuga, Ph.D., M.D.
To characterize peritoneal dendritic cells (DCs) in endometriosis and to clarify their role in its etiology.
Sixty-three women (35 patients with endometriosis and 28 control women) who had undergone laparoscopic surgery.
Peritoneal DCs from endometriosis and control samples were analyzed for the expression of cell surface markers. Monocyte-derived dendritic cells (Mo-DCs) were cultured with dead endometrial stromal cells (dESCs) to investigate changes in phagocytic activity and cytokine expression.
Main Outcome Measure(s)
Cell surface markers and cytokine expression and identification with the use of flow cytometry or reverse-transcription polymerase chain reaction (RT-PCR). Changes in cytokine expression and phagocytic activity of Mo-DCs cultured with dESCs and d-mannan were measured with the use of flow cytometry and RT-PCR.
The proportion of mannose receptor (MR)–positive myeloid DC type 1 was higher in endometriosis samples than in control samples. The blocking of MR reduced phagocytosis of dESCs by Mo-DCs. Mo-DCs cultured with dESCs expressed higher levels of interleukin (IL) 1β and IL-6 than control samples.
Peritoneal DCs in endometriosis tissue express high levels of MR, which promotes phagocytosis of dead endometrial cells and thereby contributes to the etiology of endometriosis.