Morimoto C, Matsuyama T, Rudd C E, Forsgren A, Letvin N L, Schlossman S F
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.
Eur J Immunol. 1988 May;18(5):731-7. doi: 10.1002/eji.1830180512.
The monoclonal antibody anti-2H4 recognizes a 220-kDa and 200-kDa glycoprotein and subdivides T4+ cells into distinct subpopulations: the T4+2H4+ inducer of suppression and the T4+2H4- inducer of help. The T4+2H4+ subset has been shown to play a crucial role in the activation of T8+ suppressor cells. In the present study, we attempted to determine whether the 2H4 molecule itself may be involved in initial triggering of suppressor inducer function. The results show that the addition of anti-2H4 antibody to a mixture of B and T cells resulted in a marked suppression of pokeweed mitogen-driven Ig synthesis. When anti-2H4 was added to B cell cultures containing T4+2H4+ or T4+2H4- cells but lacking T8 cells, no suppression was generated. In addition to the requirement for T8 cells, no suppression was generated if T4+2H4+ cells were absent. These results suggest that the anti-2H4 antibody contributes to the activation of the T4+2H4+ lymphocyte subset, which in turn induces T8 cells to suppress B cell Ig synthesis. Biochemical analysis of the T4+2H4+ subset of lymphocytes indicated that the in vitro addition of anti-2H4 antibody resulted in an increased expression of the 220-kDa and 200-kDa structure on T4 cells. We conclude that perturbation of the 2H4 molecule may potentiate the activation of the suppressor inducer subset and that the T200 molecule may be directly involved in suppressor inducer function.
单克隆抗体抗 - 2H4可识别一种220 kDa和一种200 kDa的糖蛋白，并将T4 + 细胞细分为不同的亚群：T4 + 2H4 + 抑制诱导细胞和T4 + 2H4 - 辅助诱导细胞。已证明T4 + 2H4 + 亚群在T8 + 抑制细胞的激活中起关键作用。在本研究中，我们试图确定2H4分子本身是否可能参与抑制诱导功能的初始触发。结果表明，向B细胞和T细胞的混合物中添加抗 - 2H4抗体可显著抑制商陆有丝分裂原驱动的Ig合成。当将抗 - 2H4添加到含有T4 + 2H4 + 或T4 + 2H4 - 细胞但缺乏T8细胞的B细胞培养物中时，未产生抑制作用。除了需要T8细胞外，如果不存在T4 + 2H4 + 细胞，也不会产生抑制作用。这些结果表明，抗 - 2H4抗体有助于T4 + 2H4 + 淋巴细胞亚群的激活，进而诱导T8细胞抑制B细胞Ig合成。对淋巴细胞T4 + 2H4 + 亚群的生化分析表明，体外添加抗 - 2H4抗体导致T4细胞上220 kDa和200 kDa结构的表达增加。我们得出结论，2H4分子的扰动可能增强抑制诱导亚群的激活，并且T200分子可能直接参与抑制诱导功能。
