子宫自然杀伤细胞中 PBX1 的表达驱动胎儿生长。
PBX1 expression in uterine natural killer cells drives fetal growth.
机构信息
Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China.
出版信息
Sci Transl Med. 2020 Apr 1;12(537). doi: 10.1126/scitranslmed.aax1798.
Abundant decidual natural killer (dNK) cells at the maternal-fetal interface are important during early pregnancy. However, functional subsets of dNK cells remain poorly understood. We describe a CD49aPBX homeobox 1 (PBX1) dNK cell subset that promotes fetal development in humans and mice. The expression of PBX1 in dNK cells is up-regulated via the activated AKT1 pathway through the interaction of major histocompatibility complex G with the immunoglobulin-like transcript 2 receptor. PBX1 drives pleiotrophin and osteoglycin transcription in dNK cells, further promoting fetal development. Decreased PBX1 expression or the PBX1 mutant correlated with fetal growth restriction and pregnancy failure in patients with unexplained recurrent spontaneous abortion (URSA). Inactivation of in mouse dNK cells impairs fetal development by decreasing growth-promoting factors from CD49aPBX1 dNK cells. Impairment of PBX1 in dNK cells has positive correlation with URSA pathogenesis and may provide a potential marker for this condition.
在妊娠早期，丰富的母胎界面上的天然杀伤（dNK）细胞是很重要的。然而，dNK 细胞的功能亚群仍了解甚少。我们描述了一个 CD49aPBX 同源盒 1（PBX1）dNK 细胞亚群，它在人类和小鼠中促进胎儿发育。通过主要组织相容性复合体 G 与免疫球蛋白样转录物 2 受体的相互作用，激活 AKT1 通路可上调 dNK 细胞中 PBX1 的表达。PBX1 驱动 dNK 细胞中的多效蛋白和骨粘连蛋白转录，进一步促进胎儿发育。在不明原因复发性自然流产（URSA）患者中，PBX1 表达降低或 PBX1 突变与胎儿生长受限和妊娠失败相关。在小鼠 dNK 细胞中失活会通过减少 CD49aPBX1 dNK 细胞中的生长促进因子来损害胎儿发育。dNK 细胞中 PBX1 的损伤与 URSA 发病机制呈正相关，可能为此病症提供一个潜在的标志物。
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