Fleischer B, Sturm E, De Vries J E, Spits H
Department of Medical Microbiology and Immunology, University of Ulm, FRG.
J Immunol. 1988 Aug 15;141(4):1103-7.
The expression and function of the T cell activation molecule Tp103 on human cloned cytotoxic CD3+ and CD3- cells were studied. All in vitro growing CD3+ and CD3- clones expressed Tp103 regardless of their phenotype and the expression of a CD3-associated TCR complex. Whereas the CD2 pathway was functional in all these clones, only CD3-expressing clones could be triggered via Tp103 to kill target cells. In contrast, both CD2 and Tp103 pathways were suppressed after modulation of the TCR complex with anti-CD3 mAb. This indicates that the function of Tp103 but not of CD2 is dependent on the expression of a functional Ag receptor on cytotoxic T cells. Furthermore, modulation of the Ag receptor induces a state of unresponsiveness in cytotoxic T cells that cannot be attributed to just the removal of the CD3/TCR complex from the cell membrane.
研究了人克隆的细胞毒性CD3 +和CD3-细胞上T细胞活化分子Tp103的表达及功能。所有体外生长的CD3 +和CD3-克隆均表达Tp103，无论其表型以及与CD3相关的TCR复合物的表达情况如何。虽然CD2途径在所有这些克隆中均起作用，但只有表达CD3的克隆可通过Tp103被触发以杀伤靶细胞。相反，用抗CD3单克隆抗体调节TCR复合物后，CD2和Tp103途径均被抑制。这表明Tp103而非CD2的功能依赖于细胞毒性T细胞上功能性抗原受体的表达。此外，抗原受体的调节会在细胞毒性T细胞中诱导一种无反应状态，这不能仅仅归因于从细胞膜上去除CD3/TCR复合物。
