Nitta T, Yagita H, Sato K, Okumura K
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
J Exp Med. 1989 Nov 1;170(5):1757-61. doi: 10.1084/jem.170.5.1757.
The CD56 differentiation antigen, recognized by anti-Leu-19 and NKH-1 mAbs, is a 200-220-kD glycoprotein that is expressed predominantly on human NK cells and a minor subset of T lymphocytes mediating MHC-unrestricted cytotoxicity. The recent finding that CD56 is an isoform of the neural cell adhesion molecule (N-CAM) prompted us to examine the adhesive function of CD56 in the NK-target cell interaction. Synergistic inhibitory effects of anti-CD56 mAbs with anti-LFA-1 and/or anti-LFA-3 mAbs were demonstrated on NK cell-mediated cytotoxicity and on NK cell binding to target cells only when the target cells also express CD56. These findings indicate that CD56 on NK cells can serve as the third pathway of cell adhesion other than those mediated by the CD2/LFA-3 and LFA-1/ICAM-1 interactions, and is involved in NK cell cytotoxicity when interacting with the cells bearing N-CAM.
抗Leu-19和NKH-1单克隆抗体识别的CD56分化抗原是一种200 - 220kD的糖蛋白,主要表达于人类自然杀伤(NK)细胞和介导MHC非限制性细胞毒性的一小部分T淋巴细胞上。最近发现CD56是神经细胞黏附分子(N-CAM)的一种异构体,这促使我们研究CD56在NK-靶细胞相互作用中的黏附功能。仅当靶细胞也表达CD56时,抗CD56单克隆抗体与抗LFA-1和/或抗LFA-3单克隆抗体对NK细胞介导的细胞毒性以及NK细胞与靶细胞的结合具有协同抑制作用。这些发现表明,NK细胞上的CD56可以作为除由CD2/LFA-3和LFA-1/ICAM-1相互作用介导的途径之外的第三条细胞黏附途径,并且在与携带N-CAM的细胞相互作用时参与NK细胞的细胞毒性作用。