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Start Over Author "Ma, Xinting" Topic myeloid-derived suppressor cells
2 results on '"Ma, Xinting"'

1. MDSCs drive the process of endometriosis by enhancing angiogenesis and are a new potential therapeutic target.

Author

Zhang T, Zhou J, Man GCW, Leung KT, Liang B, Xiao B, Ma X, Huang S, Huang H, Hegde VL, Zhong Y, Li Y, Kong GWS, Yiu AKW, Kwong J, Ng PC, Lessey BA, Nagarkatti PS, Nagarkatti M, and Wang CC

Subjects
Animals, Arginase metabolism, Cells, Cultured, Chemokines metabolism, Cytokines metabolism, Disease Models, Animal, Endometrium blood supply, Female, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Reactive Oxygen Species metabolism, Receptors, Interleukin-8B genetics, Receptors, Interleukin-8B metabolism, Angiogenesis Inducing Agents immunology, Endometriosis immunology, Endometrium immunology, Granulocytes immunology, Myeloid-Derived Suppressor Cells immunology
Abstract

Endometriosis affects women of reproductive age via unclear immunological mechanism(s). Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of myeloid cells with potent immunosuppressive and angiogenic properties. Here, we found MDSCs significantly increased in the peripheral blood of patients with endometriosis and in the peritoneal cavity of a mouse model of surgically induced endometriosis. Majority of MDSCs were granulocytic, produced ROS, and arginase, and suppressed T-cell proliferation. Depletion of MDSCs by antiGr-1 antibody dramatically suppressed development of endometrial lesions in mice. The chemokines CXCL1, 2, and 5 were expressed at sites of lesion while MDSCs expressed CXCR-2. These CXC-chemokines promoted MDSC migration toward endometriotic implants both in vitro and in vivo. Also, CXCR2-deficient mice show significantly decreased MDSC induction, endometrial lesions, and angiogenesis. Importantly, adoptive transfer of MDSCs into CXCR2-KO mice restored endometriotic growth and angiogenesis. Together, this study demonstrates that MDSCs play a role in the pathogenesis of endometriosis and identifies a novel CXC-chemokine and receptor for the recruitment of MDSCs, thereby providing a potential target for endometriosis treatment., (© 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Published
2018
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2. MDSCs drive the process of endometriosis by enhancing angiogenesis and provide a new potential approach for treatment

Author

Zhang, Tao, Zhou, Juhua, Man, Gene Chi Wai, Leung, Kam Tong, Liang, Bo, Xiao, Bo, Ma, Xinting, Huang, Shaoyan, Huang, Huaxiang, Hegde, Venkatesh L., Zhong, Yin, Li, Yanmin, Kong, Grace Wing Shan, Yiu, Alice KaWah, Kwong, Joseph, Ng, Pak Cheung, Nagarkatti, Prakash S., Nagarkatti, Mitzi, and Wang, Chi Chiu

Subjects
Mice, Knockout, Arginase, Myeloid-Derived Suppressor Cells, Endometriosis, Article, Receptors, Interleukin-8B, Mice, Inbred C57BL, Disease Models, Animal, Endometrium, Mice, Animals, Cytokines, Humans, Angiogenesis Inducing Agents, Female, Chemokines, Reactive Oxygen Species, Cells, Cultured, Granulocytes
Abstract

Endometriosis affects women of reproductive age via unclear immunological mechanism(s). Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of myeloid cells with potent immunosuppressive and angiogenic properties. Here, we found MDSCs significantly increased in the peripheral blood of patients with endometriosis and in the peritoneal cavity of a mouse model of surgically induced endometriosis. Majority of MDSCs were granulocytic, produced ROS, and arginase, and suppressed T-cell proliferation. Depletion of MDSCs by antiGr-1 antibody dramatically suppressed development of endometrial lesions in mice. The chemokines CXCL1, 2, and 5 were expressed at sites of lesion while MDSCs expressed CXCR-2. These CXC-chemokines promoted MDSC migration toward endometriotic implants both in vitro and in vivo. Also, CXCR2-deficient mice show significantly decreased MDSC induction, endometrial lesions, and angiogenesis. Importantly, adoptive transfer of MDSCs into CXCR2-KO mice restored endometriotic growth and angiogenesis. Together, this study demonstrates that MDSCs play a role in the pathogenesis of endometriosis and identifies a novel CXC-chemokine and receptor for the recruitment of MDSCs, thereby providing a potential target for endometriosis treatment.

Published
2018

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