Bruserud O, Hamann W, Patel S, Pawelec G
Second Department of Internal Medicine, Tübingen University Medical Clinic, F.R.G.
Int J Immunopharmacol. 1991;13(8):1127-35. doi: 10.1016/0192-0561(91)90164-3.
Dipyridamole inhibited the proliferation of functionally heterogeneous CD4+ TCR alpha beta+ T-cell clones prepared from CML-patients 4-6 weeks after allogeneic bone marrow transplantation. The effect was seen when testing concentrations corresponding to the therapeutic serum level. Dipyridamole caused a dose-dependent inhibition of PHA-stimulated proliferation both for clones dependent on exogenous IL2 and clones undergoing autocrine proliferation. The inhibition was seen when using different accessory cells (PBM or BCL), and also when dipyridamole was present during IL2- or IL4-dependent proliferation of activated T-cells. The effect of dipyridamole was also investigated for 76 T-cell clones (76 CD4+ and 7 CD8+ clones) prepared by different cloning procedures from three patients. Although these clones were heterogeneous with regard to cytotoxic function, lymphokine production or lymphokine responsiveness, dipyridamole inhibited IL2-dependent proliferation of all clones. In addition dipyridamole inhibited proliferation of CML cells.
双嘧达莫抑制了同种异体骨髓移植后4 - 6周从慢性粒细胞白血病患者制备的功能异质性CD4+ TCRαβ+ T细胞克隆的增殖。在测试与治疗性血清水平相对应的浓度时观察到了这种效果。双嘧达莫对依赖外源性白细胞介素2的克隆和进行自分泌增殖的克隆均引起剂量依赖性抑制PHA刺激的增殖。当使用不同的辅助细胞（外周血单核细胞或B细胞系）时观察到了这种抑制作用，并且当双嘧达莫存在于活化T细胞的白细胞介素2或白细胞介素4依赖性增殖过程中时也观察到了这种抑制作用。还对通过不同克隆程序从三名患者制备的76个T细胞克隆（76个CD4+和7个CD8+克隆）研究了双嘧达莫的作用。尽管这些克隆在细胞毒性功能、淋巴因子产生或淋巴因子反应性方面存在异质性，但双嘧达莫抑制了所有克隆的白细胞介素2依赖性增殖。此外，双嘧达莫抑制了慢性粒细胞白血病细胞的增殖。
