Derocq J M, Ségui M, Marchand J, Le Fur G, Casellas P
Department of Immunology, Sanofi Recherche, Montpellier, France.
FEBS Lett. 1995 Aug 7;369(2-3):177-82. doi: 10.1016/0014-5793(95)00746-v.
This study examined the effect of cannabinoid ligands on human tonsillar B-cells activated either through cross-linking of surface immunoglobulins or ligation of the CD40 antigen. The two synthetic cannabinoids, CP55,940 and WIN55212-2, as well as delta 9-tetrahydrocannabinol (THC), the psychoactive component of marijuana, caused a dose-dependent increase of B-cell proliferation and displayed EC50 at low nanomolar concentrations. This cannabinoid-induced enhancing activity was inhibited by pertussis toxin which suggested a G-protein-coupled receptor process. In addition, the absence of antagonistic effect of SR141716A, a specific CB1 receptor antagonist, together with the demonstration that human B-cells displayed large amount of CB2 receptor mRNAs, led us to assume that the growth enhancing activity observed on B-cells at very low concentrations of cannabinoids could be mediated through the CB2 receptor.
本研究检测了大麻素配体对通过表面免疫球蛋白交联或CD40抗原连接而活化的人扁桃体B细胞的影响。两种合成大麻素CP55,940和WIN55212-2，以及大麻的精神活性成分Δ9-四氢大麻酚（THC），导致B细胞增殖呈剂量依赖性增加，并在低纳摩尔浓度下显示出半数有效浓度（EC50）。这种大麻素诱导的增强活性被百日咳毒素抑制，这表明其是一个G蛋白偶联受体过程。此外，特异性CB1受体拮抗剂SR141716A不存在拮抗作用，以及人B细胞显示出大量CB2受体mRNA的证明，使我们推测在极低浓度大麻素下观察到的对B细胞的生长增强活性可能是通过CB2受体介导的。
