Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal-fetal interface.
Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal-fetal interface.
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滋养层来源的 CXCL16 诱导 M2 巨噬细胞极化，进而使母胎界面的 NK 细胞失活
DOI：
10.1038/s41423-018-0019-x
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发表时间：
2018-12
影响因子：
24.1
通讯作者：
Li DJ
中科院分区：
文献类型：
--
作者：
Wang XQ;Zhou WJ;Hou XX;Fu Q;Li DJ
蜕膜巨噬细胞（dMΦ）不同于存在于其他组织中的常规巨噬细胞，并表达M2巨噬细胞标志物，但M2 MΦ在妊娠期间形成的分子机制和作用尚未完全阐明。蜕膜自然杀伤细胞（dNK）与dMΦ之间的相互作用在维持母胎免疫耐受中起重要作用。在这里，CXCL 16来源于早期妊娠滋养层细胞诱导人M2巨噬细胞的极化。由CXCL 16极化的M2 MΦ表现出减少的白细胞介素-15产生，这促进NK细胞的失活。NK细胞的细胞毒性被CXCL 16极化的M2 MΦ减弱。本研究中显示的数据提供了证据支持以下假设：滋养层细胞分泌的CXCL 16是参与蜕膜M2 MΦ极化的关键分子，其反过来调节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。
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.
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DOI：
10.1084/jem.20010938
发表时间：
2002-02-04
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Gerosa F;Baldani-Guerra B;Nisii C;Marchesini V;Carra G;Trinchieri G
通讯作者：
Trinchieri G
影响因子：
15.3
作者：
Ashkar, A A;Di Santo, J P;Croy, B A
通讯作者：
Croy, B A
影响因子：
4.4
作者：
Manaster, Irit;Mizrahi, Saar;Mandelboim, Ofer
通讯作者：
Mandelboim, Ofer
影响因子：
4.6
作者：
Heikkinen, J;Möttönen, M;Lassila, O
通讯作者：
Lassila, O
DOI：
10.1128/cdli.11.5.879-888.2004
发表时间：
2004-09-01
期刊：
CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY
影响因子：
--
作者：
Choi, SS;Chhabra, VS;Roberts, RL
通讯作者：
Roberts, RL