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Distinctive phenotypes and functions of innate lymphoid cells in human decidua during early pregnancy.
Nature Communications ( IF 16.6 ) Pub Date : 2020-01-20 , DOI: 10.1038/s41467-019-14123-z
Oisín Huhn 1, 2, 3, 4 , Martin A Ivarsson 4, 5 , Lucy Gardner 4 , Mike Hollinshead 4 , Jane C Stinchcombe 6 , Puran Chen 5 , Norman Shreeve 1, 2 , Olympe Chazara 2, 4, 7 , Lydia E Farrell 2, 4 , Jakob Theorell 8, 9 , Hormas Ghadially 3 , Peter Parham 10, 11 , Gillian Griffiths 6 , Amir Horowitz 12 , Ashley Moffett 2, 4 , Andrew M Sharkey 2, 4 , Francesco Colucci 1, 2
Affiliation  

During early pregnancy, decidual innate lymphoid cells (dILCs) interact with surrounding maternal cells and invading fetal extravillous trophoblasts (EVT). Here, using mass cytometry, we characterise five main dILC subsets: decidual NK cells (dNK)1-3, ILC3s and proliferating NK cells. Following stimulation, dNK2 and dNK3 produce more chemokines than dNK1 including XCL1 which can act on both maternal dendritic cells and fetal EVT. In contrast, dNK1 express receptors including Killer-cell Immunoglobulin-like Receptors (KIR), indicating they respond to HLA class I ligands on EVT. Decidual NK have distinctive organisation and content of granules compared with peripheral blood NK cells. Acquisition of KIR correlates with higher granzyme B levels and increased chemokine production in response to KIR activation, suggesting a link between increased granule content and dNK1 responsiveness. Our analysis shows that dILCs are unique and provide specialised functions dedicated to achieving placental development and successful reproduction.

中文翻译:

妊娠早期人类蜕膜中先天淋巴细胞的独特表型和功能。

在妊娠早期,蜕膜先天淋巴细胞 (dILC) 与周围的母体细胞相互作用并侵入胎儿绒毛外滋养细胞 (EVT)。在这里,使用大规模细胞术,我们表征了五个主要的 dILC 亚群:蜕膜 NK 细胞 (dNK)1-3、ILC3s 和增殖 NK 细胞。刺激后,dNK2 和 dNK3 产生比 dNK1 更多的趋化因子,包括可作用于母体树突细胞和胎儿 EVT 的 XCL1。相反,dNK1 表达受体,包括杀伤细胞免疫球蛋白样受体 (KIR),表明它们对 EVT 上的 HLA I 类配体有反应。与外周血 NK 细胞相比,蜕膜 NK 具有独特的组织结构和颗粒含量。KIR 的获得与更高的颗粒酶 B 水平和响应 KIR 激活的趋化因子产生增加相关,表明增加的颗粒含量和 dNK1 反应性之间存在联系。我们的分析表明,dILC 是独一无二的,并提供专门用于实现胎盘发育和成功繁殖的专门功能。
更新日期:2020-01-22
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