CD33(+) CD14(+) CD11b(+) HLA-DR(-) monocytic myeloid-derived suppressor cells recruited and activated by CCR9/CCL25 are crucial for the pathogenic progression of endometriosis.

Endometriosis (EM) is a chronic immunoinflammatory disease associated with an abnormal immunotolerant microenvironment. Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that play a major role in immunosuppression in cancer, inflammation and other diseases. This paper aims to elucidate whether or not MDSCs are involved in regulating this microenvironment in EM and how this regulation occurs. Immunochemistry (IHC) and qPCR were conducted to measure CD11b and ARG1 expression in the ectopic endometrium samples from EM patients. CCL25 levels in EM PF and the expression of CCR9 on M-MDSCs were measured by ELISA. M-MDSC migration was determined towards rhCCL25, α-CCR9, α-CCL25 and EM PF through in vitro chemotaxis assay. CD33+ CD14+ CD11b+ HLA-DR- M-MDSCs isolated from EM PBMCs were added to CD8+ T cells stimulated with α-CD3/α-CD28 antibody. After 72 hours of co-culture, proliferation was measured to rate the immunosuppressive function of M-MDSCs. Finally, levels of IL-10, GM-CSF and arginase activity in the cultured supernatants were detected. IHC and qPCR results revealed higher CD11b and ARG1 expression in EM endometrium than normal endometrium. MDSCs accumulated in the EM microenvironment, in which M-MDSCs were the predominant type. CD33+ CD14+ CD11b+ HLA-DR- M-MDSCs expressed high CCR9 levels and were recruited through CCL25. M-MDSCs from EM PBMCs inhibited proliferation and activity in autologous T cells. rhCCL25 promoted IL-10 and GM-CSF secretion and arginase enzymatic activity in CD33+ CD14+ CD11b+ HLA-DR- M-MDSCs. CD33+ CD14+ CD11b+ HLA-DR- M-MDSCs recruited and activated by CCR9/CCL25 play a crucial role in the pathogenic progression of endometriosis, thus providing a potential target for EM treatment.

Sun Y ，Shao J ，Jiang F ，Wang Y ，Yan Q ，Yu N ，Zhang J ，Zhang J ，Li M ，He Y ... -  《-》

Expansion of monocytic myeloid-derived suppressor cells in endometriosis patients: A pilot study.

Endometriosis is a chronic inflammation disease and is closely associated with immune dysregulation. Myeloid-derived suppressor cells (MDSCs) are a negative regulator of the immune system. The aim of this study was to evaluate the possible role of MDSCs in endometriosis patients. We collected the peripheral blood and peritoneal fluid from endometriosis patients and controls and analyzed M-MDSCs level using specific monoclonal antibodies recognizing HLA-DR, CD33, CD11b, CD14 markers by flow cytometry. We found that there existed abnormal expansion of monocytic MDSCs (M-MDSCs) (HLA-DR-/lowCD33+CD11b+ CD14+) in peripheral blood and peritoneal fluid of patients with endometriosis. Functional studies revealed that M-MDSCs from endometriosis patients significantly suppressed T-cell responses and produced high level of reactive oxygen species (ROS). The elevation of M-MDSCs from endometriosis patients may contribute to the disease progression.

Chen H ，Qin S ，Lei A ，Li X ，Gao Q ，Dong J ，Xiao Q ，Zhou J ... -  《-》

CD45(+)CD33(low)CD11b(dim) myeloid-derived suppressor cells suppress CD8(+) T cell activity via the IL-6/IL-8-arginase I axis in human gastric cancer.

Mao FY ，Zhao YL ，Lv YP ，Teng YS ，Kong H ，Liu YG ，Wu XL ，Hao CJ ，Chen W ，Duan MB ，Han B ，Ma Q ，Wang TT ，Peng LS ，Zhang JY ，Cheng P ，Su CY ，Fu XL ，Zou QM ，Guo G ，Guo XL ，Zhuang Y ... -  《Cell Death & Disease》

Population alterations of L-arginase- and inducible nitric oxide synthase-expressed CD11b+/CD14⁻/CD15+/CD33+ myeloid-derived suppressor cells and CD8+ T lymphocytes in patients with advanced-stage non-small cell lung cancer.

Liu CY ，Wang YM ，Wang CL ，Feng PH ，Ko HW ，Liu YH ，Wu YC ，Chu Y ，Chung FT ，Kuo CH ，Lee KY ，Lin SM ，Lin HC ，Wang CH ，Yu CT ，Kuo HP ... -  《-》

A circulating subpopulation of monocytic myeloid-derived suppressor cells as an independent prognostic/predictive factor in untreated non-small lung cancer patients.

Vetsika EK ，Koinis F ，Gioulbasani M ，Aggouraki D ，Koutoulaki A ，Skalidaki E ，Mavroudis D ，Georgoulias V ，Kotsakis A ... -  《-》