THC抑制IL—2激活NK细胞的机理

THC(delta-9-tetrahydrocannabinol)是毒品大麻(marijuana)的主要心理活性成分,对白细胞介素-2(IL-2)激活NK细胞活性有非常显著的抑制作用。为了探讨THC抑制NK活性的机理,本实验用重组人IL-2-鼠NK细胞系统,从配体-受体结合的角度研究了THC对IL-2激活NK细胞活性的影响。结果表明:16μmol～32μmolTHC处理(台盼兰排除和~3H-TdR掺入法证明对NK细胞无毒性作用),能显著降低NK细胞与IL-2的特异结合;减少NK细胞表面的IL-2受体数目;但THC并不显著改变IL-2与受体结合的平衡解离常数(kd值);也不影响Tac单克隆抗体与β链Tac位点的结合。

Mechansim of Suppression of IL_2 Driven NK Activiation by THC

Previous studies have shown that AHC (delta-9-tetrahydrocannabinol), the major Psy-choactive marijuana component, significantly suppresses IL-2(intetleukin-2) activated NK cytolytic activity. To determine the mechanism of this sppressiion, we examined THC effects on IL-2-driven NK activiation from the ligand-receptor point of view by using recombinant human IL-2 and mouse mol NK cell line system. The results showed that pretreatment with THC (16HM-32HM) of NK/A2 cells, which was not directly toxic for the cells as judged by trypan blue exclusion and 3H-TdR incraton studies, inhibited the specific binding of IL-2 to the cells, decreased the number of IL-2 receptors on the cell surfaces, had no considerable effect on kd values of IL-2 binding to receptors, and did not adverslly affect Tac epitopes in a significant way as indicated by anti-Tac flow cytometric analysis.