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.
College of Basic Medicine, Binzhou Medical University, Yantai, Shandong, China.
Cell Mol Immunol. 2018 Dec;15(12):1038-1046. doi: 10.1038/s41423-018-0019-x. Epub 2018 Mar 27.
Decidual macrophages (dMΦ) are distinct from the conventional macrophages present in other tissues and express M2 macrophage markers, but the molecular mechanisms of formation and the roles of M2 MΦ during pregnancy have not been completely elucidated. The crosstalk between decidual natural killer cells (dNK) and dMΦ plays an important role in the maintenance of maternal-fetal immune tolerance. Here, CXCL16 derived from first-trimester trophoblast cells induces the polarization of human M2 macrophages. The M2 MΦ polarized by CXCL16 exhibit decreased interleukin-15 production, which facilitates the inactivation of NK cells. The cytotoxicity of NK cells is attenuated by the CXCL16-polarized M2 MΦ. The data shown in the present study provide evidence to support the hypothesis that CXCL16 secreted by trophoblast cells is a key molecule involved in decidual M2 MΦ polarization, which in turn regulates the killing ability of NK cells, thereby contributing to the homeostatic and immune-tolerant milieu required for successful fetal development.
蜕膜巨噬细胞（dMΦ）不同于存在于其他组织中的传统巨噬细胞，表达 M2 巨噬细胞标志物，但形成的分子机制以及 M2 MΦ 在妊娠期间的作用尚未完全阐明。蜕膜自然杀伤细胞（dNK）和 dMΦ 之间的串扰在维持母胎免疫耐受中起重要作用。在这里，来自早孕期滋养层细胞的 CXCL16 诱导人 M2 巨噬细胞的极化。由 CXCL16 极化的 M2 MΦ 表现出白细胞介素-15 产生减少，从而促进 NK 细胞失活。CXCL16 极化的 M2 MΦ 减弱了 NK 细胞的细胞毒性。本研究提供的证据支持这样一种假设，即滋养层细胞分泌的 CXCL16 是参与蜕膜 M2 MΦ 极化的关键分子，进而调节 NK 细胞的杀伤能力，从而有助于成功胎儿发育所需的稳态和免疫耐受环境。
