Immunosuppression mediated by myeloid‐derived suppressor cells (MDSCs) in endometriosis
Other conference paper


In endometriosis, immune cells cannot eradicate ectopic endometrial cells, but rather facilitate and promote their survival and growth. Underlying mechanism of endometrium immune escape is still undefined. MDSCs are a population of myeloid suppressive cells negatively regulate immune responses. We aimed to study role of MDSCs in immunosuppression of endometriosis.
Endometriosis was induced by syngeneic endometrium intraperitoneal transplantation. MDSCs were quantified in bone marrow, spleen, peripheral blood, peritoneal fluid, lymph nodes and endometriotic lesions during early development of endometriosis. Further the endometriosis MDSCs were isolated and depleted for immunological studies. Then growth and development of the endometriotic lesions were assessed.
Materials and methods:
MDSCs were isolated by sorter. T‐cell proliferation were determined by T‐cells coculture. Arginase activity were measured by urea production. NO/ROS production were detected by DCFDA lablelling. MDSCs were depleted by peptibody immunisation. Cytokine/chemokine were profiled by antibody arrays. MDSC functions were confirmed
by specific receptor inhibitor and transgenic mouse models.
Mouse CD11b+Gr1+ MDSCs were predominately increased in peritoneum within 7 days of transplantation. T‐cell proliferation was significantly suppressed, and arginase activity and NO/ROS production were significantly increased in the isolated endometriosis MDSCs. Depletion of MDSCs significantly enlarged endometriotic lesion size and
enhanced proliferation of endometriotic stroma and glandular epithelium. Cytokines IL3 and IL6 and chemokines CCL2, CXCL12 and CXC15 were significantly increased in peritoneal fluid and expressed in endometriotic lesions. Inhibition and deficient of CXCR2 limited migration of MDSCs in vitro and in vivo and promote growth and
development of endometriosis in vivo. Similarly human HLA‐DR‐CD11b+CD33+ MDSCs were significantly higher in peripheral blood of women with severe endometriosis than women without endometriosis and then significantly decreased 1 week after surgical removal of the endometrial implants.
MDSCs play a role in the endometriosis immunity that MDSCs negatively regulate the immune responses and promote the growth and development of endometriosis, and CXCL1/2 are involved in migration of MDSCs during early development of endometriosis.
著者Wang Chi Chiu , Zhang Tao , Man Chi Wai Gene, Liang Bo , Nagarkatti PS, Nagarkatti M
會議名稱The 13th World Congress on Endometriosis
關鍵詞immunology, immunosuppression, MDSC

上次更新時間 2018-18-01 於 03:06