Firstly, dNK promote vasculargrowth

Firstly, dNK promote vascular
growth in the decidua through the production of vascular
endothelial growth factor (VEGF) and placental growth factor
(PlGF) (9, 13, 17–19) as well as of angiopoietin 1, angiopoietin
2, and TGF-b1 (15, 20). The release of these proangiogenic factors by dNK cells depends on the engagement of both NKp30 and
NKp44 activating receptors by their specific ligands present on
stromal decidual cells and extravillous trophoblast (17). Engagement of another NK cell receptor, KIR2DL4, by soluble HLA-G
specific ligand was shown to induce the production of proangiogenic cytokines (21). Since KIR2DL4 is expressed by dNK either
at the cell surface (22) or intracellularly (21), and soluble HLAG is secreted by trophoblast (23), this receptor-ligand couple is
likely to contribute to the remodeling of the maternal vasculature
in early pregnancy. The same authors have demonstrated that the
KIR2DL4-induced senescence secretome of PB-NK can promote
vascular remodeling and angiogenesis (24). Analysis of the dNK
cell transcriptome revealed a strong similar senescence signature
(24). Secondly, dNK release interleukin-8 (IL-8) and interferoninducible protein-10 (IP-10) chemokines that favor the migration
of the extravillous cytotrophoblast into the decidua basalis by
interacting with the CXCR3 and CXCR1 receptors expressed by the
trophoblast cells (17). Migration of extravillous trophoblast cells
results in the invasion of spiral arteries thus contributing to the
uterine vascular remodeling crucial for the placental development
and outcome of pregnancy (25). Such production of chemoattractants by dNK is due to the engagement of NKp30 and NKp44 by
their specific ligands expressed by trophoblast and stromal decidual cells (17). Similar interactions between dNK and trophoblas

結果 (中文) 1:

Firstly, dNK promote vasculargrowth in the decidua through the production of vascularendothelial growth factor (VEGF) and placental growth factor(PlGF) (9, 13, 17–19) as well as of angiopoietin 1, angiopoietin2, and TGF-b1 (15, 20). The release of these proangiogenic factors by dNK cells depends on the engagement of both NKp30 andNKp44 activating receptors by their specific ligands present onstromal decidual cells and extravillous trophoblast (17). Engagement of another NK cell receptor, KIR2DL4, by soluble HLA-Gspecific ligand was shown to induce the production of proangiogenic cytokines (21). Since KIR2DL4 is expressed by dNK eitherat the cell surface (22) or intracellularly (21), and soluble HLAG is secreted by trophoblast (23), this receptor-ligand couple islikely to contribute to the remodeling of the maternal vasculaturein early pregnancy. The same authors have demonstrated that theKIR2DL4-induced senescence secretome of PB-NK can promotevascular remodeling and angiogenesis (24). Analysis of the dNKcell transcriptome revealed a strong similar senescence signature(24). Secondly, dNK release interleukin-8 (IL-8) and interferoninducible protein-10 (IP-10) chemokines that favor the migrationof the extravillous cytotrophoblast into the decidua basalis byinteracting with the CXCR3 and CXCR1 receptors expressed by thetrophoblast cells (17). Migration of extravillous trophoblast cells结果在螺旋动脉从而有助于入侵子宫血管重塑对胎盘发展至关重要和 (25) 妊娠结局。这样的趋化因子由丹麦生产是 NKp30 和 NKp44 的参与滋养层细胞和间质蜕膜细胞 (17) 表示其特异性配体。丹麦与 trophoblas 类似相互作用

結果 (中文) 3:

首先，DNK促进血管生长
蜕膜中通过血管
内皮生长因子（VEGF）生产和胎盘生长因子
（PLGF）（9，13，17–19）以及血管生成素1，促血管生成素
和TGF-β（15，2，20）。通过对这些dNK细胞促血管生成因子的释放取决于NKp30和
订婚他们在
NKp44间质蜕膜细胞和绒毛外滋养细胞特异性配体激活的受体（17）。参与另一个NK细胞受体，KIR2DL4，可溶性HLA-G
特异配体诱导的促血管生成细胞因子的产生（21）。由于是由DNK要么
KIR2DL4在细胞表面或细胞内的表达（22）（21），和可溶性hlag分泌的滋养细胞（23），该受体的配体对
可能有助于母体血管重塑
妊娠早期。同一作者已经证明，
KIR2DL4的pb-nk诱导衰老
分泌促进血管重塑和血管生成（24）。的DNK
分析细胞转录组显示了强烈的类似衰老的签名
（24）。其次，DNK释放白细胞介素-8（IL-8）和interferoninducible蛋白10（IP-10）趋化因子，青睐的绒毛外滋养层细胞的迁移
为底蜕膜的
与受体CXCR3和CXCR1的
滋养层细胞表达的相互作用（17）。绒毛外滋养细胞迁移
结果螺旋动脉的浸润，从而有助于为胎盘发育的胎盘发育和妊娠结局（25），子宫血管重构的关键。这样的DNK趋化因子的生产是由它们的特异性配体
由滋养细胞和间质蜕膜细胞中的表达导致NKp30和NKp44订婚（17）。DNK和trophoblas相似之间的相互作用