Ohno H, Ushiyama C, Taniguchi M, Germain R N, Saito T
Division of Molecular Genetics, School of Medicine, Chiba University, Japan.
J Immunol. 1991 Jun 1;146(11):3742-6.
T lymphocytes can be activated clonotypically through TCR/CD3 complex or polyclonally via the CD2 molecule. Whether CD2-mediated activation is dependent on TCR/CD3 expression or signaling is controversial. We have re-explored this issue by using a series of CD2-transfected, TCR/CD3 surface membrane-negative human and mouse T cells. Our results clearly show that such T cells can be triggered for IL-2 secretion and increases in intracellular Ca2+ through the CD2 molecule in the absence of surface expression of TCR/CD3 complexes. These responses are only observed when cells express high levels of CD2 and there is a critical threshold of CD2 expression necessary for such activation in the absence of CD3. Concomitant expression of TCR/CD3 complex markedly lowers the level of CD2 required for activation via the latter pathway. These results provide a clear resolution of the controversy concerning the requirement for surface CD3 expression in T cell activation through CD2 and further suggest a possible role for CD2 in activation of TCR/CD3-negative cells.
T淋巴细胞可通过TCR/CD3复合物以克隆型方式被激活，或通过CD2分子以多克隆方式被激活。CD2介导的激活是否依赖于TCR/CD3的表达或信号传导存在争议。我们通过使用一系列转染了CD2、TCR/CD3表面膜阴性的人和小鼠T细胞重新探讨了这个问题。我们的结果清楚地表明，在没有TCR/CD3复合物表面表达的情况下，此类T细胞可通过CD2分子被触发分泌白细胞介素-2并使细胞内钙离子增加。只有当细胞表达高水平的CD2时才会观察到这些反应，并且在没有CD3的情况下，存在激活所需的CD2表达临界阈值。TCR/CD3复合物的共表达显著降低了通过后一种途径激活所需的CD2水平。这些结果明确解决了关于通过CD2激活T细胞时表面CD3表达要求的争议，并进一步表明CD2在激活TCR/CD3阴性细胞中可能发挥的作用。
