Deckert M, Kubar J, Zoccola D, Bernard-Pomier G, Angelisova P, Horejsi V, Bernard A
INSERM U343, Faculté de Médecine, Nice, France.
Eur J Immunol. 1992 Nov;22(11):2943-7. doi: 10.1002/eji.1830221128.
The T cell surface molecule CD2 forms, with its counter-receptor CD58 (LFA-3), a powerful adhesion/activation pathway. There is some evidence that CD2 might bind more than a single ligand. Chinese hamster ovary cells (CHO) expressing human CD59 after cDNA transfection (CD59+CHO) form rosettes with human T cells; these rosettes are inhibited in a dose-dependent fashion by the CD59 monoclonal antibody (mAb) H19 and by the CD2 mAb O275 known to block natural rosettes, but not by the CD2R mAb D66, a poor rosette blocker. CD2+CHO transfectants form rosettes with human erythrocytes; these rosettes are inhibited by the CD59 mAb H19 in addition to CD2 mAb O275 and CD58 mAb; murine thymoma cells expressing human CD2 form rosettes with CD59+CHO cells that again are blocked by CD59 H19 and by CD2 O275 mAb. In a marked contrast with H19, two others CD59 mAb, YTH 53.1 and MEM 43, which react with a different epitope on CD59, led to a 50%-70% increase of the number of cells forming rosettes. In addition to rosette experiments, the binding of 125I-labeled CD59 molecules to CD2+CHO cells was specifically inhibited by unlabeled CD59 molecule and CD2 mAb. Furthermore, the binding of CD59 molecules to resting T cells induced expression of CD2R epitopes. These results directly show that CD2 binds CD59 and that subtle molecular changes occur upon binding.
T细胞表面分子CD2与其反受体CD58(淋巴细胞功能相关抗原-3,LFA-3)形成一条强大的黏附/激活途径。有证据表明,CD2可能结合不止一种配体。经cDNA转染后表达人CD59的中国仓鼠卵巢细胞(CHO)(CD59+CHO)与人T细胞形成玫瑰花结;这些玫瑰花结被CD59单克隆抗体(mAb)H19和已知可阻断天然玫瑰花结的CD2 mAb O275以剂量依赖方式抑制,但不被玫瑰花结阻断能力较差的CD2R mAb D66抑制。CD2+CHO转染细胞与人红细胞形成玫瑰花结;除CD2 mAb O275和CD58 mAb外,这些玫瑰花结还被CD59 mAb H19抑制;表达人CD2的鼠胸腺瘤细胞与CD59+CHO细胞形成玫瑰花结,同样被CD59 H19和CD2 O275 mAb阻断。与H19形成鲜明对比的是,另外两种与CD59上不同表位反应的CD59 mAb,YTH 53.1和MEM 43,导致形成玫瑰花结的细胞数量增加50%-70%。除玫瑰花结实验外,未标记的CD59分子和CD2 mAb可特异性抑制125I标记的CD59分子与CD2+CHO细胞的结合。此外,CD59分子与静息T细胞的结合诱导了CD2R表位的表达。这些结果直接表明CD2结合CD59,且结合时会发生细微的分子变化。