Van Seventer G A, Van Lier R A, Kuijpers K C, Spits H, Melief C J
Central Laboratory of the Netherlands, Red Cross Blood Transfusion Service, Amsterdam.
Eur J Immunol. 1988 Dec;18(12):1973-8. doi: 10.1002/eji.1830181216.
We investigated the function of the CD8 moiety in antigen-specific and alternative activation of HLA class I- and HLA class II-allospecific CD8+ cytotoxic T lymphocyte (CTL) clones. Monoclonal antibodies (mAb) directed against the CD8 structure were only found to inhibit antigen-specific cytotoxicity of class I-allospecific CD8+ CTL clones and not of a class II-allospecific CD8+ CTL clone. However, cytotoxicity induced by CD3 mAb (used at suboptimal concentrations) or CD2 mAb in both types of CTL clone was blocked by CD8 mAb. The class II-allospecific CD8+ CTL clone was uniformly more difficult to inhibit than the class I-allospecific CD8+ CTL clones and, moreover, also easier to induce to exert nonspecific cytotoxicity by CD2 mAb and CD3 mAb. The absence of CD8 mAb blocking of antigen-specific cytotoxicity of the class II-specific CD8+ CTL clone is, therefore, assumed to result from too strong a triggering signal to be overcome by the down-regulatory signal of the CD8 antigen. These combined findings suggest a down-regulatory function of CD8 not only in T cell receptor (TcR)/CD3 activation, but also in TcR/CD3-controlled alternative activation routes such as the CD2 activation pathway.
我们研究了CD8部分在HLA I类和HLA II类同种异体特异性CD8+细胞毒性T淋巴细胞（CTL）克隆的抗原特异性激活和替代激活中的作用。仅发现针对CD8结构的单克隆抗体（mAb）可抑制I类同种异体特异性CD8+CTL克隆的抗原特异性细胞毒性，而对II类同种异体特异性CD8+CTL克隆则无此作用。然而，在两种类型的CTL克隆中，由CD3 mAb（以次优浓度使用）或CD2 mAb诱导的细胞毒性均被CD8 mAb阻断。II类同种异体特异性CD8+CTL克隆通常比I类同种异体特异性CD8+CTL克隆更难被抑制，此外，通过CD2 mAb和CD3 mAb诱导其发挥非特异性细胞毒性也更容易。因此，假定II类特异性CD8+CTL克隆的抗原特异性细胞毒性缺乏CD8 mAb阻断是由于触发信号过强，以至于CD8抗原的下调信号无法克服。这些综合发现表明，CD8不仅在T细胞受体（TcR）/CD3激活中具有下调功能，而且在TcR/CD3控制的替代激活途径（如CD2激活途径）中也具有下调功能。
