Federal State Research Institute of Maternity and Childhood named V.N. Gorodkov, Ivanovo, Russia.
Scand J Immunol. 2014 Sep;80(3):198-208. doi: 10.1111/sji.12196.
The immunological paradox of pregnancy, when maternal immune system recognizes but does not reject the semiallogenic foetus, is not yet fully understood. The aim of this work was to detail the mechanisms of the interaction of decidual CD56+ NK, infiltrating the maternal part of placenta, and trophoblast cells of foetal origin. Samples of the endometrial tissue from 13 healthy non-pregnant women, 37 placentas, obtained after medical abortion of viable pregnancy at 7-10 weeks of gestation, and 26 samples of placentas from first-trimester recurrent spontaneous abortion (RSA) were used as the material for investigation. Phenotype of NK was assessed by flow cytometry. The influence of trophoblast cells upon IFNγ and GrB mRNAs expression by dNK was investigated by RT-PCR. The influence of dNK upon trophoblast cells migration and invasion was studied using collagen and Matrigel systems. In RSA group comparing to the normal pregnancy, the decrease of dNK with inhibitory receptors (NKG2A) and elevation of activated dNK were seen. In normal pregnancy, but not in RSA, trophoblast cells increased the expression of IFNγ and GrB mRNAs by CD56+ dNK. Both in normal and RSA pregnancy, dNK inhibited the migration and invasion of trophoblast cells. Initially, low invasive and migration capacities of trophoblast cells were seen during RSA. Thus, unbalanced activation of dNK can lead to the impairment of dNK and trophoblast cells interaction during RSA.
妊娠的免疫学悖论,即母体免疫系统识别但不排斥半同种异体胎儿,目前尚未完全理解。本研究的目的是详细描述浸润胎盘母体部分的蜕膜 CD56+NK 与胎儿来源的滋养层细胞相互作用的机制。我们使用了 13 名健康未怀孕女性、37 名妊娠 7-10 周因医学原因流产的胎盘以及 26 名早孕期复发性自然流产(RSA)胎盘的子宫内膜组织样本作为研究材料。通过流式细胞术评估 NK 的表型。通过 RT-PCR 研究滋养层细胞对 dNK 中 IFNγ 和 GrB mRNA 表达的影响。使用胶原和 Matrigel 系统研究 dNK 对滋养层细胞迁移和侵袭的影响。与正常妊娠相比,RSA 组中具有抑制性受体(NKG2A)的 dNK 减少,而激活的 dNK 增加。在正常妊娠中,但在 RSA 中没有,滋养层细胞增加了 CD56+ dNK 中 IFNγ 和 GrB mRNA 的表达。在正常和 RSA 妊娠中,dNK 均抑制滋养层细胞的迁移和侵袭。最初,在 RSA 中观察到滋养层细胞的侵袭和迁移能力较低。因此,dNK 的不平衡激活可能导致 RSA 期间 dNK 和滋养层细胞相互作用受损。