Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal–fetal interface

查看全文 作　　者：Xiao-Qiu [1]Wang;Wen-Jie [1]Zhou;Xin-Xin [1]Hou;Qiang [2]Fu;Da-Jin [1]Li

机构地区：[1]Laboratory for Reproductive Immunology,Key Laboratory of Reproduction Regulation of NPFPC,SIPPR,Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,Hospital and Institute of Obstetrics and Gynecology,IRD,Fudan University,Shanghai Medical College,Shanghai,China;[2]College of Basic Medicine,Binzhou Medical University,Yantai,Shandong,China

出　　处：《Cellular & Molecular Immunology》索引2018年第15卷第12期,共9页

基　　金：This study was funded by grant number MOST 2015CB943300 awarded to Da-Jin Li;a grant from the National Natural Science Foundation of China,number 81200425,awarded to Xiao-Qiu Wang;a grant from the National Natural Science Foundation of China,number 81471548,awarded to D.-J.L.;a grant from the National Natural Science Foundation of China,number 81571512,awarded to Q.F.;a grant from The Department of Science and Technology in Shandong Province,number ZR2015JL027,awarded to Q.F. 摘　　要：Decidual macrophages (dMΦ) are distinct from the conventional macrophages present in other tissues and express M2macrophage markers, but the molecular mechanisms of formation and the roles of M2 MΦ during pregnancy have not beencompletely elucidated. The crosstalk between decidual natural killer cells (dNK) and dMΦ plays an important role in themaintenance of maternal–fetal immune tolerance. Here, CXCL16 derived from first-trimester trophoblast cells induces thepolarization of human M2 macrophages. The M2 MΦ polarized by CXCL16 exhibit decreased interleukin-15 production, whichfacilitates the inactivation of NK cells. The cytotoxicity of NK cells is attenuated by the CXCL16-polarized M2 MΦ. The data shown inthe present study provide evidence to support the hypothesis that CXCL16 secreted by trophoblast cells is a key molecule involvedin decidual M2 MΦ polarization, which in turn regulates the killing ability of NK cells, thereby contributing to the homeostatic andimmune-tolerant milieu required for successful fetal development. 关键词：CXCL16 TROPHOBLASTS macrophage polarization NK cells maternal-fetal interface

相关文献

参考文献（52）
引证文献（21）
耦合文献（55）

参考文献(52)

引证文献(21)

耦合文献(55)

互联网出版许可证新出网证(渝)字10号全国400电话 - 免长途话费

Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal–fetal interface

参考文献(52)

引证文献(21)

耦合文献(55)

用户提示