Hayakawa Yoshihiro, Smyth Mark J
Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Vic. 3002, Australia.
Semin Immunol. 2006 Jun;18(3):176-85. doi: 10.1016/j.smim.2006.03.005. Epub 2006 May 3.
NKG2D is a type II transmembrane-anchored glycoprotein expressed as a disulfide-linked homodimer on the surface of all mouse and human natural killer cells (NK cells). Stimulation of NK cells through NKG2D triggers cell-mediated cytotoxicity and in some cases induces the production of cytokines. NKG2D binds to family of ligands with structural homology to MHC class I, however, unlike conventional MHC class I molecules, NKG2D ligands often display up-regulated surface expression on stressed cells and are frequently over expressed by tumors. Recent evidence clearly implicates that NKG2D recognition plays an important role in tumor immune surveillance and that NKG2D primarily acts to trigger perforin-mediated apoptosis. The data begin to place the NKG2D pathway into the context of other recognition-effector systems used by NK cells.
NKG2D是一种II型跨膜锚定糖蛋白，以二硫键连接的同型二聚体形式表达于所有小鼠和人类自然杀伤细胞（NK细胞）表面。通过NKG2D刺激NK细胞可触发细胞介导的细胞毒性，在某些情况下还会诱导细胞因子的产生。NKG2D与具有MHC I类结构同源性的配体家族结合，然而，与传统的MHC I类分子不同，NKG2D配体在应激细胞上通常表现为表面表达上调，并且在肿瘤中经常过度表达。最近的证据清楚地表明，NKG2D识别在肿瘤免疫监视中起重要作用，并且NKG2D主要作用是触发穿孔素介导的细胞凋亡。这些数据开始将NKG2D途径置于NK细胞使用的其他识别效应系统的背景中。
