Dang N H, Torimoto Y, Sugita K, Daley J F, Schow P, Prado C, Schlossman S F, Morimoto C
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
J Immunol. 1990 Dec 15;145(12):3963-71.
In this paper, we examined in detail the ability of anti-1F7 to modulate 1F7 (CD26) surface expression as well as analyzed the functional relationship between the surface expression of CD3, CD2, and CD26 and human T cell activation. We showed that anti-1F7-induced modulation is an energy-dependent process that occurs via capping and internalization of the Ag-antibody complex. Although the recovery rate for Ag reexpression of 1F7 following optimal modulation is relatively delayed, reexpression of 1F7 is greatly accelerated following phorbol ester treatment. Most importantly, we demonstrated that modulation of the CD26 Ag leads to an enhancement in the proliferative activity of modulated human T cells treated with anti-CD3 or anti-CD2, which is preceded by an enhancement in Ca2+ mobilization. CD26 modulation also led to an increase in anti-CD3- or anti-CD2-mediated T cell clone proliferation. Finally, whereas modulation of the CD26 Ag has an effect on CD3- or CD2-induced T cell activation, modulation of the CD3/TCR complex inhibits the proliferative response of T cells incubated with anti-CD3 plus anti-1F7 or anti-CD2 plus anti-1F7. However, modulation of the CD2 structure does not affect anti-CD3- plus anti-1F7-induced human T cell activation. The above results thus provide additional evidence that the CD26 Ag plays an integral role in the regulation of human T cell activation.
在本文中，我们详细研究了抗1F7调节1F7（CD26）表面表达的能力，并分析了CD3、CD2和CD26的表面表达与人T细胞活化之间的功能关系。我们发现抗1F7诱导的调节是一个能量依赖的过程，通过抗原-抗体复合物的聚集和内化发生。虽然最佳调节后1F7抗原重新表达的恢复率相对延迟，但佛波酯处理后1F7的重新表达大大加速。最重要的是，我们证明了CD26抗原的调节导致用抗CD3或抗CD2处理的被调节人T细胞增殖活性增强，这之前伴随着Ca2+动员的增强。CD26调节也导致抗CD3或抗CD2介导的T细胞克隆增殖增加。最后，虽然CD26抗原的调节对CD3或CD2诱导的T细胞活化有影响，但CD3/TCR复合物的调节抑制了与抗CD3加抗1F7或抗CD2加抗1F7一起孵育的T细胞的增殖反应。然而，CD2结构的调节不影响抗CD3加抗1F7诱导的人T细胞活化。因此，上述结果提供了额外的证据，证明CD26抗原在人T细胞活化的调节中起不可或缺的作用。
