Beverley P C, Healey D, Broadhurst K, Sattentau Q J
ICRF Human Tumour Immunology Group, University College, London, UK.
J Autoimmun. 1989 Jun;2 Suppl:243-9. doi: 10.1016/0896-8411(89)90136-4.
Attempts to raise protective immunity to HIV have been notably ineffective. However the conservation of binding of different virus strains to CD4 suggests that the HIV envelope glycoprotein (gp120) should have a conserved site for CD4. Attempts to raise neutralizing anti-idiotypes to CD4 monoclonal antibodies (MoAbs) have generated polyclonal sera which block HIV-induced syncytium formation in vitro but have low titres. Mapping of CD4 epitopes recognized by CD4 MoAbs and gp120 indicates that none of the present CD4 MoAbs bind to exactly the same site as gp120, which may explain the relative lack of success of the anti-idiotype approach to date.
增强对HIV的保护性免疫的尝试一直成效显著。然而，不同病毒株与CD4结合的保守性表明，HIV包膜糖蛋白（gp120）应该有一个与CD4结合的保守位点。制备针对CD4单克隆抗体（MoAbs）的中和抗独特型抗体的尝试产生了多克隆血清，这些血清在体外可阻断HIV诱导的合胞体形成，但效价较低。对CD4 MoAbs和gp120识别的CD4表位进行图谱分析表明，目前的CD4 MoAbs没有一个与gp120结合在完全相同的位点，这可能解释了迄今为止抗独特型方法相对缺乏成功的原因。
