Kusumi Maki, Yamashita Takahiro, Fujii Tomoyuki, Nagamatsu Takeshi, Kozuma Shiro, Taketani Yuji
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
J Reprod Immunol. 2006 Jun;70(1-2):33-42. doi: 10.1016/j.jri.2005.12.008. Epub 2006 Feb 20.
The balance of inhibitory and activating natural killer (NK) receptors on maternal decidual NK cells, most of which are CD56bright, is thought to be crucial for the proper growth of trophoblasts in placenta. A lectin-like NK receptor, CD94/NKG2, is the receptor for human leukocyte antigen (HLA)-E, which is expressed on trophoblasts. To clarify the mechanism regulating the activity of decidual NK cells during pregnancy, we investigated the expression patterns of inhibitory NK receptor, CD94/NKG2A, and activating receptor, CD94/NKG2C, on decidual NK cells in an early stage of normal pregnancy and compared them with those on peripheral NK cells, most of which are CD56dim. The rate of NKG2A-positive cells was significantly higher for decidual CD56bright NK cells than for peripheral CD56dim NK cells, but the rates of NKG2C-positive cells were comparable between the two cell types. Interestingly, peripheral CD56dim NK cells reciprocally expressed inhibitory NKG2A and activating NKG2C, but decidual CD56bright NK cells that expressed activating NKG2C simultaneously expressed inhibitory NKG2A. The co-expression of inhibitory and activating NKG2 receptors may fine-tune the immunoregulatory functions of the decidual NK cells to control the trophoblast invasion in constructing placenta.
母体蜕膜自然杀伤(NK)细胞上抑制性和激活性受体的平衡被认为对胎盘滋养层细胞的正常生长至关重要,其中大多数蜕膜NK细胞为CD56bright。一种凝集素样NK受体CD94/NKG2是人类白细胞抗原(HLA)-E的受体,HLA-E在滋养层细胞上表达。为了阐明孕期调节蜕膜NK细胞活性的机制,我们研究了正常妊娠早期蜕膜NK细胞上抑制性NK受体CD94/NKG2A和激活性受体CD94/NKG2C的表达模式,并将其与外周血NK细胞(大多数为CD56dim)上的表达模式进行比较。蜕膜CD56bright NK细胞中NKG2A阳性细胞的比例显著高于外周血CD56dim NK细胞,但两种细胞类型中NKG2C阳性细胞的比例相当。有趣的是,外周血CD56dim NK细胞相互表达抑制性NKG2A和激活性NKG2C,但同时表达激活性NKG2C的蜕膜CD56bright NK细胞也表达抑制性NKG2A。抑制性和激活性NKG2受体的共表达可能会微调蜕膜NK细胞的免疫调节功能,以控制胎盘形成过程中滋养层细胞的侵入。